Hormones of endocrines/ dental crown & bridge courses

HORMONES OF ENDOCRINESHORMONES OF ENDOCRINES
PARATHYROID GLANDPARATHYROID GLAND
ADRENAL GLANDADRENAL GLAND
GONADSGONADS
PANCREASPANCREAS
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
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CONTENTSCONTENTS
 IntroductionIntroduction
 Parathyriod glandsParathyriod glands
Physiologic anatomyPhysiologic anatomy
DevelopmentDevelopment
HistologyHistology
Blood supplyBlood supply
Veinous drainageVeinous drainage
Lymphatic drainageLymphatic drainage
Nerve supplyNerve supply
Chemistry of parathyriod hormoneChemistry of parathyriod hormone

 Calcium metabolismCalcium metabolism
ImportanceImportance
Normal valueNormal value
Regulation of blood calcium levelRegulation of blood calcium level
calcitonincalcitonin
 Applied physiologic disordersApplied physiologic disorders
HyperparathyriodismHyperparathyriodism
HypoparathyriodismHypoparathyriodism
 Adrenal glandsAdrenal glands
Functional anatomyFunctional anatomy
Blood supplyBlood supply
Veinous drainageVeinous drainage
Lymphatic drainageLymphatic drainage www.indiandentalacademy.com

HistologyHistology
Adrenal cortexAdrenal cortex
Adrenal medullaAdrenal medulla
 Physiologic disorders of adrenal glandPhysiologic disorders of adrenal gland
 GonadsGonads
TestesTestes
ovariesovaries
 Applied physiologic disorders gonadsApplied physiologic disorders gonads
 PancreasPancreas
 Physiologic anatomyPhysiologic anatomy
 Pancreatic hormonesPancreatic hormones
 Applied physiologic disorders of pancreasApplied physiologic disorders of pancreas

INTRODUCTIONINTRODUCTION
 A hormone is a chemical substance that is secretedA hormone is a chemical substance that is secreted
into the internal body fluids by one cell or group ofinto the internal body fluids by one cell or group of
cells and has a physiological control effects oncells and has a physiological control effects on
other cells of the body.other cells of the body.

PARATHYROID GLANDPARATHYROID GLAND

PHYSIOLIGIC ANATOMY OFPHYSIOLIGIC ANATOMY OF
PARATHYROID GLANDSPARATHYROID GLANDS
Normally there are four parathyroid glands humanNormally there are four parathyroid glands human
being which are located immediately behind thebeing which are located immediately behind the
thyroid glands. One behind each of the upper andthyroid glands. One behind each of the upper and
each of the lower poles of the thyroid glands.each of the lower poles of the thyroid glands.
(superior and inferior parathyroids)(superior and inferior parathyroids)

 Each parathyroid gland is about 6mm long andEach parathyroid gland is about 6mm long and
3mm wide and 2mm thick and has macroscopic3mm wide and 2mm thick and has macroscopic
appearance of dark brown fat.appearance of dark brown fat.
 The parathyroid glands are difficult to locateThe parathyroid glands are difficult to locate
during thyroid operations because they oftenduring thyroid operations because they often
look like just another lobule of thyroid gland.look like just another lobule of thyroid gland.
 Superior parathyroid glands are more constant inSuperior parathyroid glands are more constant in
site than inferior and usually mid way alongsite than inferior and usually mid way along
posterior thyroid border dorsal to recurrentposterior thyroid border dorsal to recurrent
laryngeal nervelaryngeal nerve

 Inferior thyroid glands may beInferior thyroid glands may be
 Within thyroid sheath- below inferior thyroidWithin thyroid sheath- below inferior thyroid
arteryartery
 Outside the sheath- above the inferior thyroidOutside the sheath- above the inferior thyroid
arteryartery
 Within the thyroid gland near its inferior poleWithin the thyroid gland near its inferior pole

HISTOLOGYHISTOLOGY
 Principle or chief cells - major source ofPrinciple or chief cells - major source of
parathyroid harmone.(PTH)parathyroid harmone.(PTH)
 Oxyphillic cells – not knownOxyphillic cells – not known
DEVELOPMENTDEVELOPMENT
 Parathyroid develop from endoderm in theParathyroid develop from endoderm in the
pharyngeal pouches. The inferior parathyroidpharyngeal pouches. The inferior parathyroid
from the 3from the 3rdrd
and therefore reffered to asand therefore reffered to as
parathyroids III, the superior from the 4parathyroids III, the superior from the 4THTH
andand
termed as parathyroid IVtermed as parathyroid IV

 BLOOD SUPPLYBLOOD SUPPLY
The parathyroid glands receive a rich blood supplyThe parathyroid glands receive a rich blood supply
from inferior thyroid artery and from thefrom inferior thyroid artery and from the
anastomosis between superior and inferioranastomosis between superior and inferior
thyroid arteries.thyroid arteries.
 VEINOUS DRAINAGEVEINOUS DRAINAGE
Drained by superior middle and inferior thyroidDrained by superior middle and inferior thyroid
veins.veins.
 LYMPHATIC DRAINAGELYMPHATIC DRAINAGE
Superior parathyroid drains into upper deep cervicalSuperior parathyroid drains into upper deep cervical
lymph nodes. Inferior parathyroid drains intolymph nodes. Inferior parathyroid drains into
lower deep cervical nodeslower deep cervical nodeswww.indiandentalacademy.com

 NERVE SUPPLYNERVE SUPPLY
Vasomotor nerves are derived from the middleVasomotor nerves are derived from the middle
and superior cervical ganglia, directly orand superior cervical ganglia, directly or
through inferior thyroid plexusthrough inferior thyroid plexus
Parathyroid activity is controlled by bloodParathyroid activity is controlled by blood
calcium levels; low levels stimulate and highcalcium levels; low levels stimulate and high
levels inhibit the activity of the gland.levels inhibit the activity of the gland.

 CHEMISTRY OF PARATHYDOIDCHEMISTRY OF PARATHYDOID
HARMONEHARMONE
It is first synthesized on the ribosomes in the formIt is first synthesized on the ribosomes in the form
of preproharmone, a polypeptide chain of 110of preproharmone, a polypeptide chain of 110
aminoacids. This is cleaved first to a proharmoneaminoacids. This is cleaved first to a proharmone
with 90 aminoacids, then to the harmone itselfwith 90 aminoacids, then to the harmone itself
with 84 aminoacids by endoplasmic reticulumwith 84 aminoacids by endoplasmic reticulum
and golgi apparatus and finally packaged inand golgi apparatus and finally packaged in
secretory granules in the cytoplasm of thesecretory granules in the cytoplasm of the
cells.The final hormone has a mol wt of aboutcells.The final hormone has a mol wt of about
9500.9500.

CALCIUM METABOLISMCALCIUM METABOLISM
IMPORTANCE OF CALCIUMIMPORTANCE OF CALCIUM
 Neuronal activityNeuronal activity
 Skeletal muscle activitySkeletal muscle activity
 Cardiac activityCardiac activity
 Smooth muscle activitySmooth muscle activity
 Secretory activity of the glandsSecretory activity of the glands
 Coagulation of bloodCoagulation of blood

 NORMAL VALUESNORMAL VALUES
In a normal young healthy adult there is aboutIn a normal young healthy adult there is about
1100gms of calcium in the body. It forms about1100gms of calcium in the body. It forms about
1.5% of total body wt.99% of calcium is present in1.5% of total body wt.99% of calcium is present in
bones and the rest is present in plasma.the normalbones and the rest is present in plasma.the normal
blood calcium level is 9.4mg% and it rangesblood calcium level is 9.4mg% and it ranges
between 9 and 11mg%between 9 and 11mg%

REGULATION OF BLOOD CALCIUMREGULATION OF BLOOD CALCIUM
LEVELLEVEL
Regulated by three harmonesRegulated by three harmones
 ParathormoneParathormone
 1, 25 dihyroxy cholecalciferol1, 25 dihyroxy cholecalciferol
 calcitonincalcitonin

 ACTIONS OF PARATHORMONEACTIONS OF PARATHORMONE
 By increasing the resorption of calcium from theBy increasing the resorption of calcium from the
bonesbones
 By decreasing the excretion of calcium throughBy decreasing the excretion of calcium through
the kidneysthe kidneys
 By increasing the absorption of calcium fromBy increasing the absorption of calcium from
gastrointestinal tract.gastrointestinal tract.

 EFFECT ON BONEEFFECT ON BONE
 Rapid phase –Rapid phase – this occurs within minutes after thethis occurs within minutes after the
release of parathormone from parathyroid glands.release of parathormone from parathyroid glands.
Immediately after reaching the bone, theImmediately after reaching the bone, the
parathormone gets attached with the receptors onparathormone gets attached with the receptors on
the cell membrane of osteoblasts andthe cell membrane of osteoblasts and
osteocytes.The harmone-receptor complexosteocytes.The harmone-receptor complex
increases the permeability of the membranes ofincreases the permeability of the membranes of
these cells for calcium ions. This increases thethese cells for calcium ions. This increases the
calcium pump mechanism allowing calcium ions tocalcium pump mechanism allowing calcium ions to
move from these cells to plasmamove from these cells to plasma

 Slow phase –Slow phase – slow phase of calciumslow phase of calcium
resorption from bone is by activation ofresorption from bone is by activation of
osteoclasts.The osteoclasts are largeosteoclasts.The osteoclasts are large
phagocytic multinucleated cells derivedphagocytic multinucleated cells derived
from monocytes or monocyte like cellsfrom monocytes or monocyte like cells
present in the bone marrow. whenpresent in the bone marrow. when
osteoclasts are activated by parathormone,osteoclasts are activated by parathormone,
some proteolytic enzymes are releasedsome proteolytic enzymes are released
from lysosomes of the cells.from lysosomes of the cells.

Apart from the proteolytic enzymes, severalApart from the proteolytic enzymes, several
acids such as citric acid and lactic acid areacids such as citric acid and lactic acid are
also released. All these substances digest oralso released. All these substances digest or
resorb the organic matrix of the bone,resorb the organic matrix of the bone,
releasing the calcium ions. The calcium ionsreleasing the calcium ions. The calcium ions
slowly move into the plasma. Thus,slowly move into the plasma. Thus,
parathormone releases calcium from boneparathormone releases calcium from bone
by activating the osteoclasts.by activating the osteoclasts.

 EFFECTS ON KIDNEYEFFECTS ON KIDNEY
Parathormone increases the reabsorption of calciumParathormone increases the reabsorption of calcium
from the renal tubules along with magnesium ionsfrom the renal tubules along with magnesium ions
and hydrogen ions. At the same time it increasesand hydrogen ions. At the same time it increases
the excretion of phosphates from the renalthe excretion of phosphates from the renal
tubules.tubules.

 EFFECTS ON GASTROINTESTINALEFFECTS ON GASTROINTESTINAL
TRACTTRACT
Parathormone increases the absorption of calciumParathormone increases the absorption of calcium
ions from gastrointestinal tracts. It is because ofions from gastrointestinal tracts. It is because of
the formation of 1,25 dihydroxy cholecalciferolthe formation of 1,25 dihydroxy cholecalciferol
from vitamin D by kidney. It also increases thefrom vitamin D by kidney. It also increases the
absorption of phosphate ions. For the absorptionabsorption of phosphate ions. For the absorption
of calcium from the gastrointestinal tract vitaminof calcium from the gastrointestinal tract vitamin
D is very essential. For activation of vitamin DD is very essential. For activation of vitamin D
parathormone is necessary.parathormone is necessary.

 ACTIVATION OF VITAMIN DACTIVATION OF VITAMIN D
There are various forms of vitamin D. But the mostThere are various forms of vitamin D. But the most
important one is the vitamin Dimportant one is the vitamin D3.3.This is also knownThis is also known
as cholecalciferol.as cholecalciferol.
Vitamin DVitamin D33 is synthesized in the skin fromis synthesized in the skin from
7dehydrocholestrol by the action of ultraviolet7dehydrocholestrol by the action of ultraviolet
rays from the sunlight. It is also obtained from therays from the sunlight. It is also obtained from the
dietary sources.dietary sources.

Activation of vitamin DActivation of vitamin D33 occurs in two stepsoccurs in two steps
FIRST STEP –FIRST STEP – cholecalciferol is converted intocholecalciferol is converted into
25,hydroxy cholecalciferol in the liver. This25,hydroxy cholecalciferol in the liver. This
process can be limited and can be inhibited by 25,process can be limited and can be inhibited by 25,
hydroxy cholecalciferol itself by feedbackhydroxy cholecalciferol itself by feedback
mechanism. this inhibition is essential for twomechanism. this inhibition is essential for two
reasons.reasons.
 Regulation of the amount of active vitamin DRegulation of the amount of active vitamin D
 Storage of vitamin D for months together. this isStorage of vitamin D for months together. this is
because if vitamin Dbecause if vitamin D33 is converted into 25,hydroxyis converted into 25,hydroxy
cholecalciferol. It remains in the body only for 2-5cholecalciferol. It remains in the body only for 2-5
days. Where as vitamin Ddays. Where as vitamin D33 can be stored in thecan be stored in the
liver for months together.liver for months together.

 SECOND STEP –SECOND STEP – 25,hydroxy cholecalciferol25,hydroxy cholecalciferol
is converted into 1,25,dihydroxyis converted into 1,25,dihydroxy
cholecalciferol in kidney. And this is thecholecalciferol in kidney. And this is the
active form of vitamin Dactive form of vitamin D33. this step needs the. this step needs the
presence of parathormone.presence of parathormone.

 ROLE OF CALCIUM ION INROLE OF CALCIUM ION IN
REGULATING 1,25,DIHYDROXYREGULATING 1,25,DIHYDROXY
CHOLECALCIFEROLCHOLECALCIFEROL
If more calcium is present in blood,it inhibits theIf more calcium is present in blood,it inhibits the
formation of 1,25 dihydroxy cholecalciferol. Theformation of 1,25 dihydroxy cholecalciferol. The
mechanism involved in the inhibition of themechanism involved in the inhibition of the
formation of 1,25 dihydroxy cholecalciferol.formation of 1,25 dihydroxy cholecalciferol.
 Increase in calcium ion concentration directlyIncrease in calcium ion concentration directly
suppresses the conversion of 25 hydroxysuppresses the conversion of 25 hydroxy
cholecalciferol. This effect is very mild.cholecalciferol. This effect is very mild.

 Increase in calcium ion concentration decreasesIncrease in calcium ion concentration decreases
the parathyroid secretion. Decrease inthe parathyroid secretion. Decrease in
parathormone secretion in turn suppresses theparathormone secretion in turn suppresses the
conversion of 25 hydroxy cholecalciferol. Lack ofconversion of 25 hydroxy cholecalciferol. Lack of
these in turn, decreases the absorption of calciumthese in turn, decreases the absorption of calcium
ions from the intestine, from the bones and fromions from the intestine, from the bones and from
the renal tubules as well. This makes the calciumthe renal tubules as well. This makes the calcium
level in plasma to fall back to normal.level in plasma to fall back to normal.

 ACTIONS OF 1, 25 DIHYDROXYACTIONS OF 1, 25 DIHYDROXY
CHOLECALCIFEROLCHOLECALCIFEROL
 It increases the absorption of calcium from theIt increases the absorption of calcium from the
intestine. It does this by increasing the calciumintestine. It does this by increasing the calcium
binding protiens in the intestinal epithelial cells.binding protiens in the intestinal epithelial cells.
These protiens act as a carrier protiens forThese protiens act as a carrier protiens for
facilitated diffusion by which the calcium ions arefacilitated diffusion by which the calcium ions are
transported.transported.
 Increases the synthesis of alkaline phosphatase inIncreases the synthesis of alkaline phosphatase in
the intestinal epitheliumthe intestinal epithelium
 Increases the synthesis of calcium inducedIncreases the synthesis of calcium induced
adinosine triphosphatase in the intestinaladinosine triphosphatase in the intestinal
epitheliumepithelium

 REGULATION OF PARATHORMONEREGULATION OF PARATHORMONE
SECRETIONSECRETION
 Increases in calcium concentration in the bloodIncreases in calcium concentration in the blood
decreases parathormone secretion and suchdecreases parathormone secretion and such
conditions in which the secretion ofconditions in which the secretion of parathormoneparathormone
isis decreased aredecreased are 1) increased levels of calcium in diet1) increased levels of calcium in diet
2) increased vitamin D in diet2) increased vitamin D in diet
3) increased resorption of calcium3) increased resorption of calcium
from the bones ( diseases of bones)from the bones ( diseases of bones)
 Decrease in calcium ion concentration of the bloodDecrease in calcium ion concentration of the blood
increases parathormone secretion as in cases ofincreases parathormone secretion as in cases of
rickets, pregnancy and lactationrickets, pregnancy and lactationwww.indiandentalacademy.com

 CALCITONINCALCITONIN
 Secreted by the parafollicular cells situatedSecreted by the parafollicular cells situated
amongst the follicles in thyriod glandamongst the follicles in thyriod gland
 It is a polypeptide chain with 32 aminoacids.It is a polypeptide chain with 32 aminoacids.
 Molecular weight is about 3,400Molecular weight is about 3,400

 ACTIONS OF CALCITONINACTIONS OF CALCITONIN
 Calcitonin decreases the blood calcium level byCalcitonin decreases the blood calcium level by
acting on bones, kidney and intestine.acting on bones, kidney and intestine.
 ON BONES –ON BONES – calcitonin facilitates thecalcitonin facilitates the
deposition of calcium on bones. It alsodeposition of calcium on bones. It also
suppresses the activity of osteoclasts, which aresuppresses the activity of osteoclasts, which are
responsible for resorption of calcium fromresponsible for resorption of calcium from
bones. It inhibits development of osteoclasts inbones. It inhibits development of osteoclasts in
bone.bone.

 ON KIDNEY –ON KIDNEY – calcitonin increases thecalcitonin increases the
excretion of calcium through urine, byexcretion of calcium through urine, by
inhibiting the reabsorption of calcium from theinhibiting the reabsorption of calcium from the
renal tubules.renal tubules.
 ON INTESTINE –ON INTESTINE – prevents the absorptionprevents the absorption
of calcium from intestine into bloodof calcium from intestine into blood

APPLIED PHYSIOLOGIC DISORDERS OFAPPLIED PHYSIOLOGIC DISORDERS OF
PARATHYRIOD GLANDSPARATHYRIOD GLANDS
 HORMONEHORMONE
EXCESSEXCESS
PRIMARY SECONDARY
Primary
Hyperparathyroidism
(adenoma, hyperplasia
Occasionally carcinoma)
Tertiary
hyperparathyriodism
Secondary
hyperparathyroidism

 HORMONEHORMONE
DEFFICIENCYDEFFICIENCY
 HORMONEHORMONE
RESISTANCERESISTANCE
 NON-FUNCTIONINGNON-FUNCTIONING
TUMOURTUMOUR
Post surgical
Auto immune
-
Parathyroid carcinoma

 PRIMARY HYPERPARATHYROIDISMPRIMARY HYPERPARATHYROIDISM
CLNICAL FEATURES :CLNICAL FEATURES :
 More common in women over 50 years of ageMore common in women over 50 years of age
 Manifests its symptoms primarily in the bonesManifests its symptoms primarily in the bones
and kidneysand kidneys
 Pathological fractures may be the first symptomPathological fractures may be the first symptom
of the disease, although bone pain and jointof the disease, although bone pain and joint
stiffness are frequently early symptomsstiffness are frequently early symptoms
 Skeletal lesionsSkeletal lesions

 HypercalcaemiaHypercalcaemia
 HypophosphatemiaHypophosphatemia
 Demineralization of bonesDemineralization of bones
 NephrocalcinosisNephrocalcinosis
 Calcium levels – 12 -15mg/dlCalcium levels – 12 -15mg/dl

 OSTEITIS FIBROSA CYSTICAOSTEITIS FIBROSA CYSTICA
(VON RECKLINGHAUSENS DISEASE)(VON RECKLINGHAUSENS DISEASE)
 Generalised decalcification of skeletonGeneralised decalcification of skeleton
 Single or multiple cysts or pseudo tumors ofSingle or multiple cysts or pseudo tumors of
bonebone
 Early radiological changes first appear in theEarly radiological changes first appear in the
skull and phalanges, with loss of density and subskull and phalanges, with loss of density and sub
periosteal erosionsperiosteal erosions

 INVESTIGATIONS :INVESTIGATIONS :
 BIOCHEMICAL : raised serum calcium and raisedBIOCHEMICAL : raised serum calcium and raised
parathormone, increased alkaline phosphataseparathormone, increased alkaline phosphatase
level, increased chloride level and decreaselevel, increased chloride level and decrease
phosphate levelsphosphate levels
 RADIOLOGICAL : In the jaws, the bone inRADIOLOGICAL : In the jaws, the bone in
hyperparathyroidism has been described as havinghyperparathyroidism has been described as having
‘ground-glass’ appearance.‘ground-glass’ appearance.
 A pepper-pot appearance may be seen on lateralA pepper-pot appearance may be seen on lateral
radiographs of the skullradiographs of the skull

 TREATMENT :TREATMENT :
 The only long term therapy is surgery, withThe only long term therapy is surgery, with
exicision of a solitary parathyroid adenoma orexicision of a solitary parathyroid adenoma or
debulking of hyperplastic glandsdebulking of hyperplastic glands
 Post operative hypocalcaemia may occurPost operative hypocalcaemia may occur
during first two weeks.during first two weeks.

 HYPOPARATHYROIDISM ANDHYPOPARATHYROIDISM AND
HYPOCALCEMIAHYPOCALCEMIA
 Most common cause of hypoparathyroidism isMost common cause of hypoparathyroidism is
damage to parathyroid glands or their blooddamage to parathyroid glands or their blood
supply during thyroid surgerysupply during thyroid surgery
 idiopathic hypoparathyroidismidiopathic hypoparathyroidism
 pseudo hypoparathyroidismpseudo hypoparathyroidism

 CLINICAL FEATURES :CLINICAL FEATURES :
 TETANY :TETANY :
 Tetany occurs in all syndromes in whichTetany occurs in all syndromes in which
ionised calcium concentrations are lowionised calcium concentrations are low
 When calcium levels fall below 6mg/dl signsWhen calcium levels fall below 6mg/dl signs
of tetany developsof tetany develops
 Low ionised calcium concentrations causesLow ionised calcium concentrations causes
increased excitability of peripheral nerves.increased excitability of peripheral nerves.
Magnesium depletion should also beMagnesium depletion should also be
considered as a possible contributing factor,considered as a possible contributing factor,
particularly in malabsorption, diureticparticularly in malabsorption, diuretic
therapy or alcohol excesstherapy or alcohol excesswww.indiandentalacademy.com

 In children a characteristic traid of carpopedalIn children a characteristic traid of carpopedal
spasm, stridor and convulsions occurspasm, stridor and convulsions occur
 Stridor is caused by spasm of the glottisStridor is caused by spasm of the glottis
 Adults complain of tingiling in the hands ,feet andAdults complain of tingiling in the hands ,feet and
around the moutharound the mouth
 Signs :trousseaus signSigns :trousseaus sign
 chvosteks signchvosteks sign

 LATENT TETANY present when signs ofLATENT TETANY present when signs of
overt tetany are lacking, trousseus sign isovert tetany are lacking, trousseus sign is
elicitedelicited
 IN MILD TETANY this sign can beIN MILD TETANY this sign can be
produced by occluding the circulation for fewproduced by occluding the circulation for few
minutes with blood pressure cuffminutes with blood pressure cuff
 TREATMENT OF TETANYTREATMENT OF TETANY : 20ml of 10%: 20ml of 10%
calcium gluconate injected into vein slowlycalcium gluconate injected into vein slowly
raise the serum calcium concentrationraise the serum calcium concentration
immediatelyimmediately

ADRENAL GLANDADRENAL GLAND

FUNCTIONAL ANATOMY OF ADRENALFUNCTIONAL ANATOMY OF ADRENAL
GLANDSGLANDS
 Two adrenal glands or supra renal glandsTwo adrenal glands or supra renal glands
situated on the upper pole of each kidneysituated on the upper pole of each kidney
each gland weighs about 4gms and iseach gland weighs about 4gms and is
made of two distinct parts.made of two distinct parts.
 Adrenal cortex (derived from mesodermAdrenal cortex (derived from mesoderm
of developing embryo and producesof developing embryo and produces
steroid hormones. Eg aldosterone )steroid hormones. Eg aldosterone )
 Adrenal medulla (derived from ectodermAdrenal medulla (derived from ectoderm
and produces catecholamines)and produces catecholamines)

 BLOOD SUPPLY :BLOOD SUPPLY : supplied by threesupplied by three
groups of arteries the superior, middle andgroups of arteries the superior, middle and
inferior suprarenal from the inferior phrenic,inferior suprarenal from the inferior phrenic,
abdominal aorta and renal artery.abdominal aorta and renal artery.
 VEINOUS DRAINAGEVEINOUS DRAINAGE : Medullary veins: Medullary veins
emerge from the hilum to form a suprarenalemerge from the hilum to form a suprarenal
vein, draining to the inferior venacava (rightvein, draining to the inferior venacava (right
side) and left renal vein.side) and left renal vein.
 LYMPHATIC DRAINAGE :LYMPHATIC DRAINAGE : the lymphthe lymph
vessels end in lateral aortic nodesvessels end in lateral aortic nodes
 NERVE SUPPLY :NERVE SUPPLY : mainly myelinatedmainly myelinated
preganglionic sympathetic fibers distributedpreganglionic sympathetic fibers distributed
to the medullary chromaffin cellsto the medullary chromaffin cells

ADRENAL CORTEXADRENAL CORTEX
The adrenal cortex is sub divided into threeThe adrenal cortex is sub divided into three
zoneszones
 Zona glomerulosa ( mineralocorticoids)Zona glomerulosa ( mineralocorticoids)
 Zona fasciculata ( glucocorticoids )Zona fasciculata ( glucocorticoids )
 Zona reticularis ( gonadocorticoids )Zona reticularis ( gonadocorticoids )

MINERALOCORTICOIDSMINERALOCORTICOIDS
HORMONE DAILY OUTPUT PLASMA LEVEL
ALDOSTERONE 0.5 microgms 0.006 microgm
11-DEOXYCORTICOSTERONE 0.2 microgms 0.006 microg

 ACTIONSACTIONS
 Control water and eletrolyte homeostasis,Control water and eletrolyte homeostasis,
particularly the concentrations of sodium andparticularly the concentrations of sodium and
potassium ionspotassium ions
 95% of the mineralocorticoid activity is due to95% of the mineralocorticoid activity is due to
aldosteronealdosterone
 Aldosterone acts on certain tubule cells in theAldosterone acts on certain tubule cells in the
kidney to increase their reabsorption of sodium.kidney to increase their reabsorption of sodium.
By stimulating return of NaBy stimulating return of Na++
from the body . Thefrom the body . The
sodium reabsorption leads to reabsorption of Clsodium reabsorption leads to reabsorption of Cl--
and HCOand HCO33
--
and retention of water.and retention of water.
 At the same time , aldostrone increases theAt the same time , aldostrone increases the
excretion of Kexcretion of K++
. So more K. So more K++
is lost in the urine.is lost in the urine.
Thus removing acids from the body andThus removing acids from the body and
preventing acidosis.preventing acidosis.

CONTROL OF ALDOSTERONECONTROL OF ALDOSTERONE
SECRETION :SECRETION : involves several mechanismsinvolves several mechanisms
operating simultaneously.operating simultaneously.
 Renin angiotensin pathwayRenin angiotensin pathway
 Potassium concentrationPotassium concentration

GLUCOCORTICOIDSGLUCOCORTICOIDS
 The glucocorticoids regulate metabolism andThe glucocorticoids regulate metabolism and
resistance to stress.resistance to stress.
 Glucocorticoids areGlucocorticoids are
• Cortisol (hydrocortisone)Cortisol (hydrocortisone)
• CorticosteroneCorticosterone
• CortisoneCortisone
 Cortisol is most abundant and is responsible forCortisol is most abundant and is responsible for
95%of glucocorticoid activity.95%of glucocorticoid activity.

 THE GLUCOCORTICOIDS HAVE THETHE GLUCOCORTICOIDS HAVE THE
FOLLOWING EFFECTS.FOLLOWING EFFECTS.
 Glucocorticoids, together with other harmones,Glucocorticoids, together with other harmones,
promote normal metabolism. Their role is topromote normal metabolism. Their role is to
make sure ATP is available. They increase themake sure ATP is available. They increase the
rate at which the proteins are catabolised andrate at which the proteins are catabolised and
amino acids are removed from cells primarilyamino acids are removed from cells primarily
muscle fibers, and transported to the liver.muscle fibers, and transported to the liver.

 If the body’s reserves of glycogen and fat areIf the body’s reserves of glycogen and fat are
low, the liver may convert lactic acid(lactate)low, the liver may convert lactic acid(lactate)
or certain amino acids to glucose. Thisor certain amino acids to glucose. This
conversion of substances other than glycogenconversion of substances other than glycogen
are another carbohydrate into glucose is calledare another carbohydrate into glucose is called
gluconeogenesisgluconeogenesis
 They also stimulate lypolysis, the breakdownThey also stimulate lypolysis, the breakdown
of triglycerides into fatty acids and glycerolof triglycerides into fatty acids and glycerol
and release of fatty acids from adipose tissue.and release of fatty acids from adipose tissue.

 They provide resistance to stress. AddedThey provide resistance to stress. Added
glucose is used by tissues to produce ATP toglucose is used by tissues to produce ATP to
combating various stresses: fasting, fright,combating various stresses: fasting, fright,
temperature extremes, high altitude, bleeding,temperature extremes, high altitude, bleeding,
infection, surgery, trauma, and almost anyinfection, surgery, trauma, and almost any
debilitating diseases.debilitating diseases.
 They also make blood vessels more sensitive toThey also make blood vessels more sensitive to
vessel constricting chemicals. They therebyvessel constricting chemicals. They thereby
raise the blood pressure.raise the blood pressure.

 They are anti inflammatory compounds thatThey are anti inflammatory compounds that
inhibit the cells and secretions that participate ininhibit the cells and secretions that participate in
inflammatory responses. They reduce theinflammatory responses. They reduce the
number of mast cells, thus reducing the releasenumber of mast cells, thus reducing the release
of histamine; stabilize lysosomal membranes toof histamine; stabilize lysosomal membranes to
reduce the release of enzymes; decreases thereduce the release of enzymes; decreases the
blood capillary permeability; and depressesblood capillary permeability; and depresses
phagocytosis.phagocytosis.

 High doses depresses the immune responses.forHigh doses depresses the immune responses.for
this reason they are taken by organ transplantthis reason they are taken by organ transplant
recipients to retard tissue rejection by therecipients to retard tissue rejection by the
immune system.immune system.
 They retard connective tissue regeneration andThey retard connective tissue regeneration and
thereby slow wound healing.thereby slow wound healing.

 REGULATION OF GLUCOCORTICOIDREGULATION OF GLUCOCORTICOID
SECRETIONSECRETION

GONADOCORTICOIDSGONADOCORTICOIDS
 The adrenal cortex secretes both female andThe adrenal cortex secretes both female and
male gonadocorticoids. These are estrogens andmale gonadocorticoids. These are estrogens and
androgens.androgens.
 Estrogens are several closely related female sexEstrogens are several closely related female sex
harmones that are also produced by the ovariesharmones that are also produced by the ovaries
and placenta.and placenta.
 The androgens secreted by adrenal cortex areThe androgens secreted by adrenal cortex are
• DehydroepiandrosteroneDehydroepiandrosterone
• AndrostenedioneAndrostenedione
• TestosteroneTestosterone

ADRENAL MEDULLAADRENAL MEDULLA
 Adrenal medulla consists of harmoneAdrenal medulla consists of harmone
producing cells called chromaffin cells whichproducing cells called chromaffin cells which
surround large blood vessels.surround large blood vessels.
 Adrenal medullary harmones are amines andAdrenal medullary harmones are amines and
derivatives of catecholes. So these harmonesderivatives of catecholes. So these harmones
are called catecholamines.are called catecholamines.
• Adrenaline or epinephrineAdrenaline or epinephrine
• Nor adrenaline or nor epinephrineNor adrenaline or nor epinephrine
• DopamineDopamine

 Plasma levels of catecholamines are as follows.Plasma levels of catecholamines are as follows.
• Adrenaline : 3microgm/dlAdrenaline : 3microgm/dl
• Nor adrenaline : 30 microgm/dlNor adrenaline : 30 microgm/dl
• dopamine : 3.5microgm/dldopamine : 3.5microgm/dl

 SYNTHESIS OF CATECHOLAMINESSYNTHESIS OF CATECHOLAMINES

 ACTIONS OF ADRENALINE ANDACTIONS OF ADRENALINE AND
NOR ADRENALINENOR ADRENALINE
 The actions of adrenaline and nor adrenalineThe actions of adrenaline and nor adrenaline
are exerted through some receptors presentare exerted through some receptors present
target organs. These receptors are calledtarget organs. These receptors are called
adrenergic receptors.adrenergic receptors.
 Alpha adrenergic receptorsAlpha adrenergic receptors
 Beta adrenergic receptorsBeta adrenergic receptors

 ALPHA ADRENERGIC RECEPTORS :ALPHA ADRENERGIC RECEPTORS :
 Alpha adrenergic receptors give more response toAlpha adrenergic receptors give more response to
nor adrenaline than to adrenalinenor adrenaline than to adrenaline
 Alpha 1 receptors exert their actions by activatingAlpha 1 receptors exert their actions by activating
the second messenger inositol triphosphate (IPthe second messenger inositol triphosphate (IP33))
through phaspholipase cthrough phaspholipase c
 Alpha 2 receptors exert their effect by inhibitingAlpha 2 receptors exert their effect by inhibiting
adenyl cyclase and reducing intracellular cyclicadenyl cyclase and reducing intracellular cyclic
AMP.AMP.

 BETA ADRENERGIC RECEPTORSBETA ADRENERGIC RECEPTORS
 Beta 1 receptors have mostly same degree ofBeta 1 receptors have mostly same degree of
response to both adrenaline and nor adrenalineresponse to both adrenaline and nor adrenaline
 Beta 2 receptors are larger than beta1 receptorsBeta 2 receptors are larger than beta1 receptors
and show more response to adrenaline than norand show more response to adrenaline than nor
adrenalineadrenaline
 Both beta 1 and beta 2 receptors produce theirBoth beta 1 and beta 2 receptors produce their
actions by activating adenyl cyclase through Gactions by activating adenyl cyclase through G
proteins and increasing intracellular cyclic AMPproteins and increasing intracellular cyclic AMP

 EFFECT ON METABOLISM ( VIAEFFECT ON METABOLISM ( VIA
ALPHA AND BETA RECEPTORS)ALPHA AND BETA RECEPTORS)
 General metabolism :General metabolism : adrenaline increasesadrenaline increases
oxygen consumption and carbon dioxideoxygen consumption and carbon dioxide
removal. It increases basal metabolic rate.removal. It increases basal metabolic rate.
 Carbohydrate metabolism :Carbohydrate metabolism : adrenalineadrenaline
increases blood glucose level. It is by increasingincreases blood glucose level. It is by increasing
glycogenolysis in liver and muscleglycogenolysis in liver and muscle
 Fat metabolism :Fat metabolism : adrenaline causesadrenaline causes
metabolism of free fatty acids from adiposemetabolism of free fatty acids from adipose
tissuetissue..

 Effect on blood :Effect on blood : adrenaline reduces bloodadrenaline reduces blood
coagulation timecoagulation time
 Effect on heart : ( via beta receptors)Effect on heart : ( via beta receptors)
Adrenaline has got stronger effects than norAdrenaline has got stronger effects than nor
adrenaline on heart it increases overall activityadrenaline on heart it increases overall activity
of heart rate (chronotrophic effect ), force ofof heart rate (chronotrophic effect ), force of
contraction (inotropic effect) and excitability ofcontraction (inotropic effect) and excitability of
heart muscleheart muscle..

 Effect on blood vessels :(Effect on blood vessels :( via alpha and beta 2via alpha and beta 2
receptors )receptors )
 Nor adrenaline has got stronger effects on bloodNor adrenaline has got stronger effects on blood
vessels. It causes constriction of blood vesselsvessels. It causes constriction of blood vessels
through out the body so it is calledthrough out the body so it is called
‘General vasoconstrictor’‘General vasoconstrictor’
 Adrenaline also causes constriction of bloodAdrenaline also causes constriction of blood
vessels however, it causes dilatation ofvessels however, it causes dilatation of
blood vessels in skeletal muscle, liver andblood vessels in skeletal muscle, liver and
heart through beta2 receptorsheart through beta2 receptors

 Effects on blood pressure :Effects on blood pressure : ( via alpha and( via alpha and
beta receptors ) adrenaline increase systolicbeta receptors ) adrenaline increase systolic
blood pressure by increasing the force ofblood pressure by increasing the force of
contraction and diastolic blood pressure bycontraction and diastolic blood pressure by
reducing the peripheral resistance.reducing the peripheral resistance.
 Effects on respiration :Effects on respiration : adrenaline increaseadrenaline increase
the rate and force of respirationthe rate and force of respiration
 Effect on skin :Effect on skin : adrenaline causes severeadrenaline causes severe
contraction of arrector pilicontraction of arrector pili

Effects on smooth muscles :Effects on smooth muscles : catecholaminescatecholamines
causes contraction of smooth muscles in thecauses contraction of smooth muscles in the
following organsfollowing organs
 Splenic capsuleSplenic capsule
 Sphincters of gastrointestinal tractSphincters of gastrointestinal tract
 GallbladderGallbladder
 UterusUterus
 Dilator pupillae of irisDilator pupillae of iris

 Effects on central system : (via beta receptorsEffects on central system : (via beta receptors))
 Adrenaline increases the activity of brain duringAdrenaline increases the activity of brain during
fight or flight process after exposure to stress.fight or flight process after exposure to stress.
 Other effects :Other effects : on salivary glands catecholamineson salivary glands catecholamines
cause vasoconstriction and slight increase incause vasoconstriction and slight increase in
secretionsecretion
 On nerve fibers: adrenaline decreases the latency ofOn nerve fibers: adrenaline decreases the latency of
action potential in the nerve fiber.action potential in the nerve fiber.

 DOPAMINE :DOPAMINE :
 Dopamine is secreted by adrenal medulla and also byDopamine is secreted by adrenal medulla and also by
dopaminergic neurons in some areas of braindopaminergic neurons in some areas of brain
particularly basalganglia.particularly basalganglia.
 In brain this hormone acts as neurotransmitterIn brain this hormone acts as neurotransmitter
The injected dopamine produces following effectsThe injected dopamine produces following effects
 Vasoconstriction by releasing nor epinephrineVasoconstriction by releasing nor epinephrine
 Increase in heart rateIncrease in heart rate
 Increase in systolic blood pressure does not effectIncrease in systolic blood pressure does not effect
diastolic blood pressurediastolic blood pressure

ADRENAL GLANDSADRENAL GLANDS
 DISORDERS OFDISORDERS OF
ADRENAL CORTEXADRENAL CORTEX
 HyperaldosteronismHyperaldosteronism
(mineralocorticoid excess)(mineralocorticoid excess)
 Cushing's syndromeCushing's syndrome
(glucocorticoid excess)(glucocorticoid excess)
 Addisions diseaseAddisions disease
(Hypo secretion of glucocorticoid)(Hypo secretion of glucocorticoid)
 Addisonian crisis or adrenal crisisAddisonian crisis or adrenal crisis
DISORDERS OF
ADRENAL MEDULLA
Pheochromocytoma
(hyper secretion of
Catacholamines)

GONADSGONADS

GONADSGONADS
 The organs of the male and female reproductiveThe organs of the male and female reproductive
systems may be grouped by function the testissystems may be grouped by function the testis
and ovaries also called gonads (gonos – seed)and ovaries also called gonads (gonos – seed)
 Function in production of gametes – sperm cellsFunction in production of gametes – sperm cells
and ovaand ova
 The production of gametes and fluid and thereThe production of gametes and fluid and there
discharge into ducts classify the gonads asdischarge into ducts classify the gonads as
exocrine glands, where as the production ofexocrine glands, where as the production of
hormones classifies them as endocrine glandhormones classifies them as endocrine gland

TESTESTESTES
The testes are a paired organs with in a sac of skinThe testes are a paired organs with in a sac of skin
called scrotum, which hangs from the groin area ofcalled scrotum, which hangs from the groin area of
the trunk. Composed mainly coils of spermthe trunk. Composed mainly coils of sperm
producing seminiferous tubules, there is aproducing seminiferous tubules, there is a
scattering of endocrine interstitial cells found inscattering of endocrine interstitial cells found in
areas between the tubules. This interstitial cellsareas between the tubules. This interstitial cells
produce androgens (male sex hormones). Theproduce androgens (male sex hormones). The
principle androgen isprinciple androgen is testosteronetestosterone

 DEVELOPMENT :DEVELOPMENT :
Testis develop high on embroys posteriorTestis develop high on embroys posterior
abdominal wall and usually begin their descentabdominal wall and usually begin their descent
into the scrotum through the inguinal canalsinto the scrotum through the inguinal canals
during the later half of the seventh month of fetalduring the later half of the seventh month of fetal
developmentdevelopment

 TESTOSTERONE :TESTOSTERONE :
 Synthesized from cholesterol in the testis.Synthesized from cholesterol in the testis.
 It is a principle androgen but in someIt is a principle androgen but in some
target cells is not active until it is reducedtarget cells is not active until it is reduced
and converted into another androgenand converted into another androgen
called dihydrotestosterone (DHT). Socalled dihydrotestosterone (DHT). So
testosterone is both a hormone and atestosterone is both a hormone and a
prohormone (hormone precursor)prohormone (hormone precursor)

 PRINCIPLE ACTIONSPRINCIPLE ACTIONS
 Development and maintenance of male sexualDevelopment and maintenance of male sexual
charactersticscharacterstics
 Regulation of spermatogenesisRegulation of spermatogenesis
 Stimulation of descent of testis before birthStimulation of descent of testis before birth
Testosterone secretion is regulated principally byTestosterone secretion is regulated principally by
gonodotropin (especially LH) levels in thegonodotropin (especially LH) levels in the
blood.blood.

 INHIBININHIBIN
 is a protein hormone secreted by sustentacularis a protein hormone secreted by sustentacular
(sertoli) cells that has a direct effect on the(sertoli) cells that has a direct effect on the
anterior pitutary by inhibiting secretion ofanterior pitutary by inhibiting secretion of
FSH to control sperm productionFSH to control sperm production

OVARIESOVARIES
 The female gonads, called the ovaries, areThe female gonads, called the ovaries, are
paired oval bodies located in the pelvic cavitypaired oval bodies located in the pelvic cavity
that produce several type of hormonesthat produce several type of hormones
 EstrogensEstrogens
 ProgesteroneProgesterone
 InhibinInhibin
 RelaxinRelaxin

 ESTROGENS :ESTROGENS : promote development andpromote development and
maintenance of female sexual characteristics.maintenance of female sexual characteristics.
With other hormones they are responsible forWith other hormones they are responsible for
breast development and the proper sequencebreast development and the proper sequence
events in female reproductive cycle (menstrualevents in female reproductive cycle (menstrual
cycle)cycle)
 PROGESTERONEPROGESTERONE : (PREGNANCY-: (PREGNANCY-
PROMOTING STEROID) secreted by corpusPROMOTING STEROID) secreted by corpus
luteum. Maintains the lining of uterus necessaryluteum. Maintains the lining of uterus necessary
for successful pregnancy (gestation)for successful pregnancy (gestation)

 INHIBIN :INHIBIN : inhibits secretion of FSHinhibits secretion of FSH
towards the end of menstrual cycletowards the end of menstrual cycle
 RELAXIN:RELAXIN: relaxes pubic symphysis andrelaxes pubic symphysis and
helps dilate uterine cervix near the end ofhelps dilate uterine cervix near the end of
pregnancypregnancy

GONADSGONADS
 IN MALESIN MALES
 HypogonadismHypogonadism
 CryptorchidismCryptorchidism
 Male infertilityMale infertility
 GynaecomastiaGynaecomastia
 Erectile impotenceErectile impotence
 IN FEMALESIN FEMALES
HirsutismHirsutism
AmenorrhoeaAmenorrhoea

PANCREASPANCREAS

 PHYSIOLOGIC ANATOMY OFPHYSIOLOGIC ANATOMY OF
PANCREASPANCREAS
 Pancreas is a flattened organ located posterior andPancreas is a flattened organ located posterior and
slightly inferior to stomach. The adult pancreasslightly inferior to stomach. The adult pancreas
consists of a head, body and tail. The head of theconsists of a head, body and tail. The head of the
gland lies in the C- shaped beginning of the smallgland lies in the C- shaped beginning of the small
intestine (duodenum), with its body extendingintestine (duodenum), with its body extending
horizontally behind the stomach and its tailhorizontally behind the stomach and its tail
touching the spleen.touching the spleen.

 Pancreas contains a combination of four primaryPancreas contains a combination of four primary
type of endocrine cells, all joined to each other bytype of endocrine cells, all joined to each other by
gap junctions. Each type of cell secretes a differentgap junctions. Each type of cell secretes a different
hormone, but the gap junctions allow for somehormone, but the gap junctions allow for some
co-ordination of these functions as a singleco-ordination of these functions as a single
secretory unitsecretory unit
 Alpha cells (A cells )Alpha cells (A cells )
 Beta cells (B cells )Beta cells (B cells )
 Delta cells ( D cells )Delta cells ( D cells )
 Pancreatic polypeptide cells ( F or PP, cells )Pancreatic polypeptide cells ( F or PP, cells )

 HORMONES OF PANCREASHORMONES OF PANCREAS
 InsulinInsulin
 GlucagonGlucagon
 SomatostatinSomatostatin
 Pancreatic polypeptidePancreatic polypeptide

INSULIN :INSULIN :
 Insulin was discovered in 1922 by Charles HerbertInsulin was discovered in 1922 by Charles Herbert
Best and Fedric BantingBest and Fedric Banting
CHEMISTRY :CHEMISTRY : it is a small protien. It has ait is a small protien. It has a
molecular weight of 5808. It is composed of twomolecular weight of 5808. It is composed of two
amino acid chains A and B. A chain contains 21amino acid chains A and B. A chain contains 21
amino acids and B chain contains 30 amino acidsamino acids and B chain contains 30 amino acids
which are linked by disulphide bridges. If twowhich are linked by disulphide bridges. If two
chains are lost functional activity of insulin is lost.chains are lost functional activity of insulin is lost.

 MAJOR ACTIONS OF INSULIN :MAJOR ACTIONS OF INSULIN :
Actions on cell membrane permeabilityActions on cell membrane permeability
 Insulin promotes the entry of glucose into all cellsInsulin promotes the entry of glucose into all cells
of the body excepting the cells of the liver, brainof the body excepting the cells of the liver, brain
and the RBCsand the RBCs
 Insulin also promotes the entry of amino acidsInsulin also promotes the entry of amino acids
and fatty acids within the cellsand fatty acids within the cells
 Entry of KEntry of K++
inside the cell is facilitated by insulininside the cell is facilitated by insulin

 ACTIONS ON METABOLISMACTIONS ON METABOLISM
Carbohydrate :Carbohydrate :
 insulin inhibit gluoneogenesis and glycogenolysisinsulin inhibit gluoneogenesis and glycogenolysis
 Insulin promotes glycogenesisInsulin promotes glycogenesis
Fat :Fat :
 Promotes lipogenesisPromotes lipogenesis
 Inhibits formation of ketone bodiesInhibits formation of ketone bodies

Protein :Protein :
 Promotes protien synthesisPromotes protien synthesis
 Facilitates actions of several enzymes egFacilitates actions of several enzymes eg
hexokinasehexokinase
Nucleic acids :Nucleic acids :
 Promotes synthesis of DNA and RNAPromotes synthesis of DNA and RNA

 MODE OF ACTION OF INSULIN :MODE OF ACTION OF INSULIN :
 On the target cells, the insulin combines with aOn the target cells, the insulin combines with a
membrane receptor protein and, executes it actionmembrane receptor protein and, executes it action
by activating the intracellular enzyme system.by activating the intracellular enzyme system.
 Insulin receptor is a complex protein with aInsulin receptor is a complex protein with a
molecular weight of 3,40,000.molecular weight of 3,40,000.
 Insulin receptor is tetramer formed by 4 glycoproteinInsulin receptor is tetramer formed by 4 glycoprotein
subunits. Two of the subunits which, protrudesubunits. Two of the subunits which, protrude
outside the cell are called alpha subunits. The otheroutside the cell are called alpha subunits. The other
two subunits protruding inside the cell are the betatwo subunits protruding inside the cell are the beta
subunitssubunits

 The alpha and beta subunits are linked to each otherThe alpha and beta subunits are linked to each other
by disulfide bonds.by disulfide bonds.
 The intracellular surfaces of beta subunits have theThe intracellular surfaces of beta subunits have the
enzyme activity – protein kinase (tyrosine kinase )enzyme activity – protein kinase (tyrosine kinase )
activityactivity
 The activation of tyrosine kinase occurs due to aThe activation of tyrosine kinase occurs due to a
process called autophosphorylation of beta subunitsprocess called autophosphorylation of beta subunits
on tyrosine residues.on tyrosine residues.
 The activated tyrosine kinase acts on manyThe activated tyrosine kinase acts on many
intracellular enzymes so that some of the enzymesintracellular enzymes so that some of the enzymes
are activated and others are inactivatedare activated and others are inactivated

 REGULATION OF INSULINREGULATION OF INSULIN
SECRETIONSECRETION
 Regulation by substratesRegulation by substrates
 Hormonal controlHormonal control
 Neural controlNeural control

 NORMAL BLOOD GLUCOSE LEVEL :NORMAL BLOOD GLUCOSE LEVEL :InIn
normal persons, blood glucose levels is controlled withnormal persons, blood glucose levels is controlled with
in a narrow range. After the over night fasting, in earlyin a narrow range. After the over night fasting, in early
morning, the blood glucose level ranges between 80 andmorning, the blood glucose level ranges between 80 and
90 mg/dl of blood. Between first and second hour after90 mg/dl of blood. Between first and second hour after
meals (post prandial ), the blood glucose level rises tomeals (post prandial ), the blood glucose level rises to
120 –140 mg/dl. The glucose level in the blood is120 –140 mg/dl. The glucose level in the blood is
brought back to normal at the end of the second hourbrought back to normal at the end of the second hour
after the meal.after the meal.

 GlucagonGlucagon ::
 It is a polypeptide chain, containing 29 aminoIt is a polypeptide chain, containing 29 amino
acids, with a molecular weight of 2495.acids, with a molecular weight of 2495.
 The main target tissue of glucagon is the liverThe main target tissue of glucagon is the liver
 Actions :Actions :
 Accelerates the conversion of glycogen intoAccelerates the conversion of glycogen into
glucoseglucose
 Enhances gluconeogenesisEnhances gluconeogenesis

Somatostatin :Somatostatin : inhibits the secretion of glucagon,inhibits the secretion of glucagon,
insulin and pancreatic polypeptideinsulin and pancreatic polypeptide
 It also inhibits the secretion of growthIt also inhibits the secretion of growth
hormonehormone
 Pancreatic polypeptide :Pancreatic polypeptide : exact function notexact function not
known.known.

 APPLIED PHYSIOLOGIC DISORDERSAPPLIED PHYSIOLOGIC DISORDERS
 Diabetes mellitusDiabetes mellitus
 HyperinsulinismHyperinsulinism

 DIABETES MELLITUS :DIABETES MELLITUS :
 Most common endocrine disorderMost common endocrine disorder
 Is a group of disorder that all lead to an elevation ofIs a group of disorder that all lead to an elevation of
glucose in the blood (hyperglycemia). As hyperglycemiaglucose in the blood (hyperglycemia). As hyperglycemia
increases, there is loss of glucose in the urineincreases, there is loss of glucose in the urine
(glucosuria )(glucosuria )
 Polyuria, polydipsia, polyphagiaPolyuria, polydipsia, polyphagia
 Type I diabetes mellitusType I diabetes mellitus
 Type II diabetes mellitusType II diabetes mellitus

HYPERINSULINISM :HYPERINSULINISM :
 Most often results when a diabetic injects too muchMost often results when a diabetic injects too much
of insulin.of insulin.
 Rarely it results from a malignant tumor orRarely it results from a malignant tumor or
hyperplasia of the pancreatic islets.hyperplasia of the pancreatic islets.
 The principal symptom is hypoglycemia, decreasedThe principal symptom is hypoglycemia, decreased
blood glucose levels stimulates the secretion ofblood glucose levels stimulates the secretion of
epinephrine and glucagon. As a consequence,epinephrine and glucagon. As a consequence,
anxiety, sweating, tremor, increased heart rate,anxiety, sweating, tremor, increased heart rate,
hunger and weakness occurs.hunger and weakness occurs.

 CONCLUSIONCONCLUSION

BIBILIOGRAPHYBIBILIOGRAPHY

 Internal medicine for dentistry - Louse F. Rose &Internal medicine for dentistry - Louse F. Rose &
Donald Kaye 2Donald Kaye 2ndnd
editionedition
 principles of anatomy and physiology –Gerard J. Tortoraprinciples of anatomy and physiology –Gerard J. Tortora
7th edition7th edition
 Anatomy and physiology – Gary A. Thibodeau 2Anatomy and physiology – Gary A. Thibodeau 2ndnd
editionedition
 Textbook of medical physiology – Guyton & HallTextbook of medical physiology – Guyton & Hall
99thth
editionedition
 Principles and practice of medicine – DavidsonPrinciples and practice of medicine – Davidson
1818THTH
editionedition

 A text book of oral pathology – ShaferA text book of oral pathology – Shafer
44thth
editionedition
 physiology – Robert M. Bernephysiology – Robert M. Berne
33rdrd
editionedition

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