Lecture#: 2

c 0

0 n -i 0

M~dical Committee Tho Univct•ftv of Jordon

·Endocrine system

Subject :Pituitary gland

. Doctor : Salim Khresh~~1

#2

·· Done By : Slides ~-~,:.iC',<

Date : 14/3/2013

f'mav(m\r iculnr nucleus

Nourosecreto/

Supra-opllco-·

H ypothatarnus~

I hypophyseal1

__ __

tract

Tubero-hypophyseal tract

Infundibulum

( po,tuior pituifCtrJ NEUROHYPOPHYSIS

Figure 10-0 Tortora/ Anagnoslakos: Principles of Anatomy ami Physiology, 5/e Copyt!Qhl @l 11lt'7 l•y !loopm A !1<1w, Puhli"h•·l~. Inc. /\ll1\qhl~ "•t.OI'IOd .

anterior pituitcu; ADENOHYPOPHYSIS

. The Pituitary ( hypoph~s;S) GlA.ID

~~Jl,!(_ 9_1~~3;:.~~7-~~ }J. ~1~-'~,.~taTlit' .. B.f .. ~~~·~ -\:() l9ra~ it\ w~\,ht-~l\~'t lie~

/ ..__/

Capillnry of pituitnry porti:ll system

__ Anterior pituitnry coli

Fig. 28.5 Rc-lu.tiollShip bctweel\ hypothalamic ncuroncs and an­terior pituirary cells. (From lt. Guillcmin & lt Burgus ( 1972) Scie111;jic Amef'ic,w '1.27 ()) :2 11-:D.)

Axon of hypothnlamo­----- hypophyseal twct

Posterior pituitary cell (stornge cell)

Fig. 2H.H l{olc of chc posterior piwitary cells in the storage of the lwrmones oxycociu awl A[) (I clahor;~tcd by hypothalamic neuroncs (F,-om H. (;uilklllill & It. 1\urgus ( 197:2) Sdcntific American 227 (5) 211-j}).

Superior hypophyseal

~ artery

;\nterior lobe

Hormone­secreting cell

Th:rc! ventricle

lvledian eminence

Posterior lobe

Inferior --""""'"""' hypophyseal

artery

FIGURE 31.2 The blood supply to the anterior pituitary. This illustration shows the relationship of the pituitary blood supply to hypothalamic magnocellular neurons and to hypothalamic neurosecretory cells that produce releasing hormones. The rnagnocellular neuron (larger, dark blue cell body) releases AVP or oxytocin at its axon terminals into capillaries that give rise to the venous drainage of the posterior lobe. The neurons with smaller, light blue cell bodies are secreting releasing factors into capillary networks that give rise to the long and short hypophyseal portal vessels, respectively. Releasing hormones are shown reaching the hormone-secreting cells of the anterior lobe via the portal vessels.

e HF5¥szAw·:.;1:H>o:'··"( :'·. ,~-· ::! tzwn:swuwaauw

~

I • Somatolroph & r-Most cells that prod!ce 9" gro~-~~ h_qrmsH~e 1 an~} · Lactotr •• ph

prolactin are separate cells.

However, some ·norm1al 1

and tum·or cells ~ are single cells that Growth

produce both

.9£9wlh hormone

t . . Sllmulates

;=:-:::;.::1 body

growth

. ·-:·~'!" ..

Initiates milk

production by mammary

glands

Prolactin (PAL)

Stimulates . adrenal

cortex to secrete

its hormones

Increases skin

pigmentation

~~:·;.. . . @.:~ Gonaclotwnh

~\~;;..~~,...

Corticolipotrcph

1\

Stimulates lhvroid

gland to secrete its hormones

,\lelanocyte­stimulating hormone

(MSH)

Stimulates sperm

production in testes

~\.~I""

Thyrotroph

l Thyroid­

slirnulaling hormone

(TSH)

Stimulates egg

procluclion in o·1aries

/r-, 1 .. · - ' "t.·:( l

''", r.:::,J I \ ' / ___ ,.,..

F-ollicl~~-

shmulali<~g hormone

(FSHj

/

1:::-, ~-:~ I!?J \

("' v J

re-T;- · ... . M~1L90!1.?.Q_~~~Qph c:lls pr~?ucg _g_gtH follicle-stimulating h~~monE:: and lutl=!inizing hormone. However ______ , ----·-----~·-···----·· .....

~-!_~y~ -~~J?.§:-ate cells m~'l_ exis_!, ·1· son_:Je pr~uci_~g_fql_li_~lc~ ' ·--~---~··-~····--··--··•·<·-·-······-·-··---·----~--~-"-'"

S1 ·I r"'.l' •j ~ '·1ng ~1G ,....ll"n.. "'r-r~ 1 t•'e: .. ;-.: 00 L • '-' cil 1 Jrl. v ·.:: o. "; -l;~r~;~~c ... ----- cr ...... :. -·-~·.-;.~·::-:='---=;-===:-:.: .. ~~-_--~,-'::.-·--

(LH) -~ prOCJUCiii~J

\ ~lei ni~gJ.~-=~71_9:18. ··

Prepares ulertJ~ lor

in1plantat:o:1 or a lcrtili;:cd

ovum

S!irnulJtrs secrc lion of lcstos:crone

by tes:cs

FIGURE '19-6 Cells of the adenohypophysis as reve~led by- special strains.l

ovui;J(inn. and

slirnulates formation or

corpus luteum in ovaries

.Ailll.!J lOr: t'I~UIL<JI)' '-lldiiU '-UIIL<.llll::. .)t,:\l<.:lol

·Different Cell Types That Synthesi~e and ·secrete Hormones. Usually, there is one cell type for each major honnone forrncd in t:he anterior pituitary gland. \\'ith special stains <!lto:tchcd to high-af[inity antibodies th;il

bind wilh the distinctive hormones, at least five cell types c;:n be differen Lic:t.ed.

Table 75.-1 Cell•.; <wd f~rrrnones of the /Interior Pituitary Gland 11nd Thc1r PhysiologJCiil rimctions

Cell

Somatotmpes

Corticotropes

Thyrotropes

Gor.adotropes

Lactctrop!'S Mammotmpes

Hormone · · Chemistry

Growth hormone (GH; Single chain of 'Ul amino <;:)rnatotropin) acids

Adrenocorticotropic hormone Single chain of 39 (ACTH; corticotropin) amino ucids

Thyroid-stimulating hormone (7SH; thyrotropin)

Fc!lide-stimulating hormone (:SH)

Luteinizing hormone {LH)

Prolactin (PRL}

Glycoprotein of two subunits. u (89 amino acids) and 0 (112 amino acids)

Glycoprotein of two subunit;;, a (89 amino i!cids) and )J ( 112 amino acids) Glycoprotein of two subunits, o. (89 amino acids) and J~ (115 amino adds)

Sing!e chain of 19B amino acids

Physiological Action

Stimulates body growth; stimulates secretion of IGF-1; stimulates lipolysis; inhibits actions of insulin on carbohydrate and lipid metabolism

Stimulates production of glucocorticoids and androgens by the adrenal cortex: maintains size of zona fasciculata and zona reticularis of cort\~x

Stimulates production of thyroid hormones by thyroid follicular cells; maintains size of follicular cells

Stimul<Jtes deve~opment of ovarian follicles; regulates spermatogenesis in the testis Causes ovulation and formation of the corpus luteurn in the ovary; stimulates production of estrogen and progesterone by the ovary; st.irnulates testosterone production by the testis

Stimulates milk secretion and production

;c:~:. ~~lSU!in-[ih} ?,'O'Nli\ !,}\.:OL ;\butll 3(1 tu 40 per<.~t'llt of the anterior pituitary cells

~1rc somatotrupcs that S('crde growth hormone, and about :J.ll pc·n:elll arv UJrticot ropes that S('Cretc AC:TH. Each or the other cell types account~; for only 3 to 5 percent of the toLd; ncveniw\t.:ss. they secrete pmvcrful hormones for C011lrol!iug lhyr'<lid (unction, Sl'Xllal functit)tlS, ;-~nd milk \(\cn)tion by the breasts~

Specific Areas in the Hypothalamus Control Secretion of Specific Hypothalamic Releasing and Inhibitory Hormones. All or most of the hypothalamic horrnunes arc Sl'creted at nerve endings in the median ern i nence bdurc being transported to the anterior pituitary

gland. Electrical stimulation of this region excites these nerve endings ~mel, therefore, causes release of essentially all the hypothalarnic hormones. However, the neuronal cc~ll bodies that give rise to these median eminence nerve endings are located in other discrete areas of the hypo­thalamus or in closelv related areas of the basal brain.·

T:~ble 75-2 HyrothJlJnlic Relea5ing and Inhibitory Hormones That Control Secretion of the Anterior Pituitary Gland

Hormone

Thyrotropin-releasing hormone (TRH)

Gonadotropin-releasing hormone (GnRH)

Corticotropin--relea~ing hormone (CRH)

Growth hormone-releasing hormone (GHRH)

GrowTh hormone inhibitory hormone (somatostatin)

Prolactin-inhibiting hormone (PlH)

Structure

Peptide of 3 amino Jcids

Single chain of 10 amino acids

Single chain of 4'1 <1rr.ino acids

Single chain of 44 amino acids

Single chain of 14 amino acids

Dopamine (a catecholamine)

Primary Action on Anterior Pituitary ' ' ,.-~-~"'''?';.' ',

Stimulates secretion of TSH by thyrotropes

Stimulates secretion of FSH and LH by

gonadotropes

Stimulates secretion of ACTH by

corticotropes

Stimulates secretion of growth hormone by

somatotropes

Inhibits secretion of growth hormone by

somatotropes

Inhibits synthesis and secretion of prolactin by lactotrooes . ·':/r :

:,(TH, Jdrenocort icutropic hormone: r SH. follicl~:-~tirnuldting hormone: LH. luteinizing hormone; TSH, thyroid-stimulating hormone.

Fur most of the <lntcrior pituitary hormones, it is the releasing hormones that arc irnporl;mt. but for prolactin, a hypothalarnic ird:ibitnry honnonc prob~1bly exerts more control. ·

I

DNA

I;

HypotholomUI

/,-l,odion eminence

Pul5es __ J\f"J\ __ Releasing hormcnos

Transcription ~

•• 1, • . ' ~· •:

mRNA :·

Plasma membrane

*

FIGURE 39-3 The action of hypothalamic releasing or inhibiting hormones on anterior pituitary cells. Characteristically the neurohormones are released in pulses, bind to plasma membrane receptors, and act through calcium ions (Ca' +; and other second messengers. They regulate gene expression, posttranslational processes, and secretion of anterior pituitary tropic hor­mones. cAMP, Cyclic adenosine monophate; DNA, deoxyribonucleic acid; •mRNA, messenger ribonucleic acid.

·-'( -·············--······· ··- ···---··- -- ---- --· -------- --------.----------------------- ------ -- -. --~-- ·-~---~-- ~-' ........ --~ - -·-· -- ~-~~- ·-0- ~ -- -~

Vasopressin & Oxytocin . \

In most mammals, the hormones secreted by the pos-terior pituitary gland are arginine vasopressin (A VP) ar1d oxytocin. In hippopotami and most pigs, arginine· in the vasopressin molecule is replaced by lysine to form lysine vasopressin. The posterior pituitaries of some species of pigs and m.arsLlpials contain a mixture of argi­nir1e and. lysine vasopressin. The posterior lobe hor­mones are nonapeptides with a disulfide ring at one end

\ (Figure 14-1 0) ~ · J

Posterior lobe

I.;,

Optic chiasma

Anterior lobo

Fig. 28.7 1 The trncts from the hyporhnlnmus to the pituitary. The paravcntriculnr nucleus anJ the supra-optic nucleus are thought to be responsible for the elaboration of oxytocin and ADH respectively. The other tracts terminate in the capiJiary plexus shown in Figure 28.-i aml carry the hypothalamic hormones which control the release or the hormones of the anterior pituitary.. ,. ·'

;,;;;~L2 ... : • • •--··--- • n• 'n • • n• • 0

-"' E 0 ... 0' ~

500

400

1-30 :X: (.9

tu 3:

>-0 200 0 ID

~--

\ ;!"·- -- .... ,,.

f~ l .,

:~

I·

;.

100

\

G.-owth hortl'ol1e (GH), also ca\led somc:Jtotfopic hormo\'U CSH\ ot sowdtoVopin, is a ~J'f\all protein molecul~ Co'Otaioing 19f amit10 acids havinq a rnDl~c.~lat ~ei~ ht of 22

10D'5.

It Cat) SCI'S '}rowth oF ~ll tiso;ues of-the bod) fi1at 3rG

capable C>f 9t()\IJlJ"ICj. rt prarnotes boih lncreas.«i ~' 2"s and numbers of c~lls.

0~----~------~----~----~~----~----~ 0 100 200 300 400 500 600

DAYS

figure 75-4. Comparison of weight gain of a rat injected daily with growth hormone with that of a normal rat.

~ ~ /~

I I

Adipose tissue

;~tJ;,~~ftf!.k~~S~t~t-~0~~:::~~ : '~1:"f-G liJ'E<::lS;f':u··T6 ke i1i;YJi ~~'gy;~f~~~~~ r·-,J·:--~!.t.- __ ,.,,.."' __ -.:. ~-~~::~~F~ .. ~~~

y . .:..diposity

/ Bone, h.:art, lung

r~idncy PGncreos !;-,;e$!ine

Islets " ' 'd :-orult-1yrot s

Skin

Connective tissue ,'"t;,-.-~o • .c.o·,-.,_-'l,~,~~~··,:~ .. .,., .. ..,..,.,~-, -.. O ... "'F"·--.... --... ...... _r-_,_,..,

t Organ size

fOrgan function

HGH l · ~ .... ~ . _·. --1..,, :...:..~. ..... o<.-

Liver

: .;.. Lc.an body rr.a~s!

..... ""'

t Linear growth

E Fig. 48-21 Biological actions of GI-L The effects on linear growth, organ size, and lean body mass are mediated by somatomedin produced in the liver.

\ \

'.J

--····· ---:.:: ;~1~:7~!:~\,~':,:~:·::~~:, '-:-::~_. ~ .. :.::

.... . :~-1;: ... <. _.,,;;~~ EFFECT OF GH IN ENHk~CING FAT UTILISATION, FOR ENERGY:

1) INCREASESTHE RELEASE OF FATTY ACIDS FRON THE ADIPOSE TISSUE.

2) FATTY ACIDS CONCENTRATION INCREA:SES'IN BODY FLUIDS.

3) IT ENHANCES TI-IE CONVERSION OF FATTY ACIDS INTO ACETYL- C 0 A. ,

1viTH THE SUBSEQ.UENT UTILISATION FOR ENERGY.

lt) IN THIS CASE SPARE THE PROTEIN

5) UNDEH THE EFFECT OF GH THE HOBILISATION OF FAT REQ.UIRES

NTNlJTF.S TO HOURS, WHERE AS PROTEIN SYNTHESIS CAN BEGIN

IN f.liNUTES.

6) UNDER THE EXCESSIVE OF GH GREAT ANOUNT OF FAT HOBILISED,

THEREFORE A LOT OF ACETOACETIC ACIDS ARE FO'ffi.!ED BY THE

LJ;VER AND RELEASED INTO THE BODY FLUID~S, THUS CAUSING

(KETOSIS) o WHICH IS CALLED "KETOGENIC EFFECT'' OF GIL ----

- ~ 6 ..... ~ ~<--~- ~-; ~ ·.~~ . ·:~ '·'t·~~~:-~~;~ ~-· . ~-~-- ..... -·-··· -- . -~ ... -.. --·· ..

:: .· > .· =--:;l~it~~il . \~:£·.~'i0:;.,:~~jf£~i&f'~?~ ;i :i{ c .... . .. ,. '•.'· . -:"7~·-:·· . : · •. : ·:ft!~~-:'·;;~.:z::;~·-,..$3~~ . . . . ., _j~,_~).r..• .... ~.-,, . .,:?z...'..-.-:. • .::re-_,.:;...,J

\ .,j

-.

.· .... ... ·~.:.

·\

··- .. :..~---------·-· ~-'..~ ...... ._L.;:.:....:....---"":""...-<'--,.... .. ',,;;~

~ DIABETOGENIC EFFECT OF GH.

1) \vE HAVE ALREADY NENTIONED THAT GH INCREASES BLOOD GLUCOSE

CONCENTRATION.

2) IN ADDITION GH !v£AY HAVE A DIRECT EFFECT ON BETA-CELLS.

3) IN THESE CASES P.ANCHEAS OVER STIHULATED AND THE ::ELLS

FINALLY, BURN OUT.

4) w1-IEN THIS OCCURS THE PERSON DEVELOPS DIABETES HELLITUS.

5) THEREFORE IS SAID GH HAS DIABETOGENIC EFFECT.

.:· :·. . ' . . . . " . :.~ . . .... :· ~-· .

'-~~:;..o· ....... ylt';,,,,, .. # _ _._ •• ·-""'..'.~--- ... =--~----~---=---------····~-~-- 0 ,,, •·•·--"-=----~-·-·· A-- Oo''" -- 0 ,oo O oo •••~•··~--·-... ------·---;..:. __ .. ,.....! .. , .... ___ -~-: ~,.~: •';: ••• ,:,; :.,· ... -:_..... ... 0 0 ' '

Diabetoge11ic Effects of Otl1e1· A11te1·io1· Pituitaly-.. :·-~.~-~~--:~:--:~·-;. .. ·<-::<:t~···: -->- __ . I-I Ol'111011es. Growtl1 l1orn1011e is not tl1e only anterior.-:~~-<·_:--.··.-.· -:· ·· ~ · pitt1itary hor1none that increases the blood glucose ~on--<:'~-.\ ... _:.-· · _. -/ · ce11trati"on. At least tl1ree otl1ers can do tl1e same: ad-:·.-:.:~.--. · · rcnocorLicoLropin, thyroid-stin1ulating l1ormone, and >i)--:>rs--,.·~ . prolaclin. Espcciall,y irnportant is adrenocorticotropin,·:~)~ PJLJ~J:::_.

I . l · l f · 1 · b l AcTH \V 11 c 1 Increases t 1e rate o cort1so secretton y t 1e . · ~ . udrenul cortex. C~orLisol Lhen increases the blood glucose· · c~JJ,·s~

_r;onclm Lra_Lio_!l by_ increasing the rule of_gl uconeogcncsis. · +-' ~-•o,.w.,,; L~!h~.~ \~fJc~ct, quanlilatively,. iH probably equally us diu·~ · . u · ·

betogenic as the effect of growtl1 l1or111one. . . . . ~~~--::::·-----. ........ ~- ~-·.-··" .,. .. ~ ..

. . . ·

;-~\ ..

(lro\vth honnune is Sl~uetcd m <1 ptds;lLtlc p;.ttLClll,

incr~asing and decreasing The precis(~ nwchanisms ·

that control secretion oC growth hormone arc not fully understood, b~tt :;everal facloi·s related to a person's state C)f nutritio·n or· .stress arc known to stimulate sccrctimi:

30 Sleep

(j) c­o co E E 20

Strenuous exercise

'- en 0 co .!:0. ,... -

;:::; E ~a, 10 .... c (j.._;

04----.----.---.---~----r---,

8 am 12 4 pm 8 pm 12 4 am 8 am Noon r'l1idnight

Figure 75-6 Typical variations in growth hormone secretion throughout the day, demonstrating the especially powerful effect of strenuous exercise and also the high rate of growth hormone secretion that occurs during the first few hours of deep sleep.

Table 75-3 Factors That Stimulate or Inhibit Secretion of Growth Hormone

Stimulate Growth Hormone Secretion

Decreased blood glucose Decreased blood free fatty acids Increased blood amino acids

(arginine) Starvation or fasting, protein

deficiency Trauma, stress. excitement Exercise Testosterone, estrogen Deep sleep (stages II and IV) Growth hormone-releasing ~hormone ~ t;hrelin

Inhibit Growth Hormone Secretion

Increased blood glucose Increased blood free fatty

acids Aging Obesity Grovvth hormone inhibitory

hormone (somatostatin) Growth hormone

(exogenous) Somatomedins (insulin-like

growth factors)

• ghrelin, a hormone secreted by the stomach before meats.,

\ \

\!y!nthalarnus

Stomach

Pancreas

Large intestine Small intestine

Figure 71-1 Feedback mechanisms for control of food intake. Stretch receptors in the stomach activate sensory afferent path­ways in the vagus nerve and inhibit food intake. Peptide YY (PYY), cholecystokinin (CCK), and insulin are gastrointestinal hormones that are released by the ingestion of food and suppress further feed­ing. Ghrelin is released by the stomach, especially during fasting, and stimulates appetite. Leptin is a hormone produced in increasing amounts by fat cells as they increase in sile; it inhibits food intake. ,..

·----"" Ghrelin-a Gastrointestinal Hormone-Increases Feeding. Gl11·elin is a hormone released mainly by the oxyntic cells of the ston1ach but also, to a much less extent, by the intestine. Blood levels of ghrelin rise during fasting, peak just before eating, and then fall rapidly after a meal, suggesting a possible role in stimulating feeding. Also, administration of ghrelin increases food intake in experimentaL animals, further supporting the possibility that it may be anorexigenic hormone. However, its physi­ol!Jgic role in humans is still uncertain.

~

'· ~

I I

Birth Childhood Puberty .Adult life Senescence

I Fig. 48-19 Lifetim~ pattern of growth hormone (GHl s~crction. GH le\·ds are higher m children thJn Jdults with a ~ak period during pubcny. GH secretion declines with Jging.

/\ /'

(

Sleep ! i

Somatostatin GHRH--

Growth hormone

Stimulate ., Inhibit --if---

• Fig. 48-20 Regulation of growth hormone (GH) secre­tion. The hypothalamic peptide (GHRH) stimulates gro'.•'th hormone release, whereas the hypothalamic pep~ide so­matostatin inhi.bits it. Negative feedback is by the peripheral mediator of HGH action: somatomedin~Negative feedback occurs both via somatomedin inhibition of GHRH ·action and by somatomedin sti~ulation of somatosratiG release. HGH in­hibits its own secretion by short-loop feedback. In addition GHRl-I inhibits its OWi1- release via ultra :;bort-Ioop feedbacL In both of these cases the negative feedback is, probably via increasing somatostatin rctr~asc.

! :) S!imulolo

cj {:::!) lnhiLif

Scrt"X1~o~futin GliHJ I !___ ------·

/1,,,;,,, r-_ _._ _____ _.\

O<ids L-.-------, l'ilvilury

Gil

Sotnafontodilr Somulomodin

fltlUHE 39·10 llc~:ulr~lion of Ull !if'<:tetioll. Nutn btlllt n tlitm:t !ltiJHllloloty ami n direclluhlbitocy iulhll111l:c from tim liyl'ollullatnlln. iJt~!Jilfivn ((wdlmch lly llw JlPiip!Jnl!ll protlact is exerted nt the llypll\ halnHiic 111111 llw pil11ihu y lovl!l. U 1/H/1, U1 ow lit IHHllltiiH! ·1 ulw•silqJ huflliVItU; FF/1, hcu lnll y ncidr;,

·:~···--~~~~~,'

'.' .. :·::"'~<', ' . . '. ~ ' . '

' i ·' I

~;~;f~~t ....... . .,

2~,:wg . > ·· ·· . . . . : .;, .. ::i,~ . . . . . : . . . .. . . . . . . . . 1: 'i ~: EFFEC~~Yf,~~f,;·~YI'JP~YSECTOMY. Severa{ notable mor- I .. ' • ·- ¢,. .. ' "'.~-,~:~ •.. t~,: ·,-t. ':~- ¥· ••• ; •""··h ,.. • • ;. • •

f · . :· · · 'phologi_C.~af:'.~pd fu~·cq~nal alterations result from total hy-~:- _· pophys.ecfonl.y in the young anin1ai. These are as follo\vs: t

. . . ' . . . ·. ;. . . I·' .. . . . .. ···~·. ·:_,:: .. ~- ·. .

f -· . 1-.. Failu'i·e· of the gonads to !nature, with resultant infantile f . sexual developn1~nt and sterility because of lack of LH l an~f FSI-l . •

2. Atrophy of the thyroid gland and the characteristics of thyi·oid insufficiency because of lack of TSH. :

3. Atrophy of the adrenal cortex and signs of hypoadrenal­isn1 without salt loss because of ACTH deficiency.

4. Cessation of growth. failure to attain an adult stature, a decided tendency lo\vard hypoglycernia, hypersensitiv­ity to insulin,,:and a loss of body nitrogen accon1panied

f __ j __ by diminished fat catabolism because of lack of STH_:__ }

-\

ANTIDIUREiiC P.ORt_.I.ONE DEfiCIENT

/

GGN,b.DOTROPINS DEFiCIENT

/ / /

y-1

\ ~ . . .

MALE ADULT

En CE~iCE\!T

8 (USUALLY CRANIOPHARYNGIOMA) :>- { EXTENSIVE TUMOR

..... POSTSURGICAL Q · OCCASIONAllY GRANULOMA ~

w OR TRAUMA

................ .........

" --\ ' -' ....... _ \ ' --

\ ' -....... -.. ,\CTH M,SH STH

G'!. ,. ~N~p~ ~I 9t :J.-c· ·1: ~ /~·

I :s CJ BA

DE::'ICIE~T DEi'iClENT DEr!CIENT ~-.....

\ '....., ' \ ' \ \ _X. \

~

Y~

'

! I l

f DKREASED

fEMALE ADULT

DECREASED liBIDO, AMENORRHEA

HYPOTHYROIDIS.~ ADRENAL CORTICAL !NSUFFIOENCY

PAllOR DWARASM, MUSClE LOSS AND MICRO­SPLANCHNIA, TENDENCY TO HYPO­GLYCEJv\IA

DIABETES INSIPIDUS (LA. TENT UNLESS ,\DRENAl CORTICAL HORMONES ARE PRESENT

USIDO, ASPERNdA, LOSS OF SOME FACIAL AND BODY HAIR

CHILD

DELAYED PUBERTY

OR ADMINISTERED) (DErKIENT GROWTH PRECLUDES.. EUNUCHOID HABITUSj

- --···----------~

\ ...... _.~ ') -"

GONADOTROPINS DEFiCIENT .//,

/{ . 1/' •

-.;· ~ ' ....

~ ~ ~

MALE ADULT

DECREASED LJSID01 ~MIA, LNS Of SOME FACIAL AND BODY HAIR

FS-\\Al.E ADULT

DECREASED LIBIDO, . tVAENORRHEA

CHILD

DELAYED PUBERTY

iS:-i DE:'ICiENT

I I

I

HYPOTHYROIDISM

(DEFICIENT GROWTH PRKLUDES EUNUCHOID HABITUS)

.................

... ACTH DE:'iClENT

\

\

~\ '

........

>-0 0 ~

0 ~

EXTENSIVE DESTRUG!VE TUMOR (USUAllY Qlli.Q_MP2_l::!.QB.E._l.J)".:!QMb OR OANIOPHARYNGlOMAl

POSTPARTUM NECROSIS. OCCASIONAllY GRANULOMA

OR TRAUMA· POSTSURGICAl

' ...... ' ........

........ '.....

MSH DEriCIENT

STH OEF!CIENT ... ......_,

' " ~ ' \ \ J I I

t ADRENAL CORTICAL INSUFFICIENCY

PALLOR DWARFISM, MUSCLE tOSS AND MICRO­SPLANCHNIA,

TENDENCY TO HYPo­GLYCEMIA

-

?

"""

-~-·.

-~--~·-·-··-• •' '-(---~.--~-.:-~-.:~·.:-~7;"• "H ~- ••··~----~;~:;:.: ••;~- --·~---·--~ ··-' --------~:. ~--;~I~Tf~~;:i:~lt:;:f::~K~t~~t~~!?JE

---· .. .:.:.:_ .. ::;--.·--·-·::_·-~--~~-~(..: ....... ···--~~·~·---~· ,.• -------- _.., -····--·--- .... ~-~-:...---~-----,~---~--

~ ~

. ,..,; __ , ----"' =-~.-aa.n.-.. ~&E~~.-.-u. .. w.~.m--.-~~-~--~:~=-~~==~-~~-·--~~~~--·-~--~~~~~--~,~~~~--~:~:-~,Q~~=:~,~,~~~--~--··~:-,~--.u--.... ~ .... .caa .. ~----~-. ...................... ..

G {POSTPARTUM NECROSIS

GONADOTi<O?INS D!:FICi~NT

~~"' /{

/ /

_.,:·.<t::;"":\ \..

~ " . ) :4/~-~~-~ ~~~7:=-~s~ ~:.:. ''$,':!~¥JJ \~~,~~"' ... ~w~ ... _""·~~ .... !"Y"

.·-1~~- ~.:: ,;JUl T rcMA~E ADULT

:::CR:AS:u D:CREASED ~~3;'J8, ! .. S?ERt,l~lA, U5tDOr ~OSS Or SOM:: .AM:-NORP.HS-\

.. r t~.CL-'\L r'\ND 3CC':' ~AIR

CHilD

--s::L.W::D ?USEP.TY OVi:RGROWTH Or LONG 30N:S

(:O::JNUC~OJD H,.\S!T JS)

TSH

HYPOTHYROIDISM (SOME GRO\-\'iH IMP AIRM'ENT MAY RESULT fROM TH!S)

g CHROMOPHOBE ADENOMA 0 CRANIOPHARYNGIOMA ~ GRANULONv\

ACTH PARTIAllY DEFICIENT

MSH - STH PARTIAllY NORMAl DEFlCIENT

~\ \_\~~~-~ --~~ / ;·.r·

I j-:·

/ ·'i.r : ., . ., .... ~ .~

c~ ;-~-"-~·;.

ADRENAL CORTICAL INSUFFICIENCY BROUGHT ON ONLY BY STRESS {ILLNeSS OR_ OPERATION)

' SOME DEGREE OF PALLOR MAY Be PRESENT

~

).~~ he! B.-\

NORMAL GROWTH AND DEVELOPM::NT EXCEPT FOR EFFECTS OF GONADOTROPIN DEFICIENCY AND HYPOTHYROIDISM

1--1 ' I . I-.

~:~::~::::,.:.::..:__~-·-··---·-·

" ~~~~- /.- .

./

,..,... GONADSITRO?I ~S J!:FIC!ENT

/,;'

,r'~ ;/ {

---,..-·- \ • "• •. :-t .:~ -,

' h'/"' '· .. -''·(· -"-"~· ·''-'"'"· ~· ·~-~~-·--':' ; -~ -·~.f: ~~·"'··.i.;_.:-:~~-.f·_~ ·-:..- ;.:';_;:;. > ' .•. -~ y'

sV,AL2 .4DULT

:-.::cR::l .... SED U Blf)::J, AS?ERli\!A, ~oss Of so,v,: ~ACl.t..l AND SODY HAIR

:::tv.ALE ADULT

DE:CR::ASED LIBIDO, AM:NORRHEA

CHILD

D::V-.. YE:> ?LJG::RTY , OVt:RGRO\VTH Of LONG BONES

\:UNUCHOiD HA!:>!TUS)

THYROID FUNGlON NORN,Al

ACTH MSH NOR!AAL NORMAl

POSTPARTUM NECROSIS CHROMOPHOBE ADENOMA+"' CRANIO?HARYNGIOIY\A .,_ . CONGENITAL LACK Of DElTA aLL~ ("GONADOTROPH S") GRANULOMA

STH NORMAL

~\ "' :·---~· ......... ~ \)--.'~·-*~# \. ;~ ~~;r1•' ~/ ··r~ ... ,~

)?.Y " !

-

-,~~-- . 8)i,..r ADR~i~AL CORTICAl FUNCTION NORMAL

;;:,~~~::~ ~-~·-!·-~~;~: .. ·~· ' ---~- ----44.~"·~~ ... A ~.:!=,: ..... ")~~ .. -~ :.:f'2",.o_~--... ~ 6~~ ~-- '(. '2~ :;'--,;--:: ...... "'--:t::r..·i··-._;;.~~-:~~:::. ~

NORMAl PIGMENTATION

NORMAL GROWTH AND DEVELOPMENT EXCEPT FOR EfFECTS OF GONADOTROP!l'­DEFICIENCY

'-.I

I I

PITUITARY GIANT CONTRASTED WITH NORMAl MAN !AOOMEGAl'f AND SIGNS Of S(CONDAR'f INSUffiCIENCY MAY OR MAY.NOT. &E PR£S[Nl} ..

~ .

J.~~ ~CIDA

... \ ... · ~ .

· .. ,· ',•

':

. '. :': ·,. ;·· .. · •.••.. ·~ ; :! ·•. ; ~· .. :. • . ' ..•

';''. . . •·.. ,. ' .-.·: ... :: ..... -::.· .

.; ~ :~ .-. . ;:r·'·.

. ·~:~·.·~_·· .. -~·:.::t~~:.~_-.· .. : .... <:.-~·· ... ~' ·. . ' . ·, .·><:'· ·, ,:·:.)

. ~ : . .. '

/! ""' l ,_J!LO :!_"'~R.j/:_~- ! {) '{:,w;rro u/L 0 CCJv'&{ "-l{~ tLrtljJ.J~U! ~Vl {~.,_ J ~c-yl o-{f~ _jo-<'J

b ""'0 . 1 }i._.,_ p vt. 5 OVJ C!.L:<M ~ 'Yl o w fJ M 1

bJ f,f,.,R_ s~ ,t~ru.v? CJwl c_CNl-1~ ~io w,:.,_,:J

tVv<-J 1 ~ G OV'-vf {! tVYI r o'-" ~ 4 [.._ ,Lc.JAA.UJ .

,_ r: ,..... 2. aA--;)/}<><.w ~~ h -~: £....._ ~ bo..<.v.;'

~ )L... ~ ~"- /u.J ~.Joo ~k(_ ~I ~s..c-! /; iJ/1/-h.J 1 ~/La DA-t.ifal

;-;_ol~) .\ \.....<.. --€. o vJt/1. J 6<N b~ ~ ,f~ p oM~ o.{ {ke v~e.bJ\P..~ ..

J- r4/ ~ S~f {~'55v..M 0/l. Ofi.{}a.<4

);.kt )_; <J lA' t crY'~ I ~~ b e.c"""' .e.

~-~~ ~~·

____________ .._ __________________________ _

1!10RA(i( YlRTEDRA IN AC~OMtGAlY• HYrtROSTOSIS, L5P£CIA~l Y MARKED ON ANlERIOR. ASPECT

I I l

j··.

J II . I

!/:f.~: , . .• ,l-<\,•l

'""'NG OF fHAIANG.S IN H >NOS AND• •. ·:-'! r_,_ ~ :·'·. NARROWING OF PHALANGES IN FEfT ·. . . ~

;.' ... '

Dopamine

Stimulate

Inhibit

Prolactin

----~

--(/ ..

TRH

• Fig. 52-25. Regulation of prolactin secretion. The predom­inant n1odc of hypothalamic regulation is tonic inhibition viu dopatninc. Although TRH stimulates prolactin release, its physiological role is uncertain, and evidence suggests another hypothalamic peptide may be more physiologically imponanl. Prolactin exerts short-loop feedback on its own secretion by stin1ulating production of the hypothalamic inhibitor, Jopa­nlme.

dj" \I

) i :..,; :'

. I I,

I

I I < ;_

f) aravontricu1ar nucleus

Neurosecretory cell

Supra-optico­hypophyseal

tract

Hypothalamus

Tu bero-hypophyseal tract

NEUROHYPOPHYSIS Figure 11l·8 Tortora/Anagnostakos: Princlploa of Anatomy and Physiology, 5/o Copyrloht (iJ 1907 by Harpor & Row, Publishers, Inc. All riQhts rosorvod.

Supruoptic nucleus

((-4DH)

" ~o(J)

ADENOHYPOPHYSIS

' . • 0

I

I

----

/\lH I :.nt:tn!nd "~ n .. q:Jt ~I!IIU1Pnl~l ill 1 'CUI uhypopilysi:J

/ (

(

' /

Uc!0ciod lJy

i,~'ourosucrotory

cell synltloslzes ADH

FIGURE 10·10 Rouulalion of tho secralion of antidiuretic hormone {ADH).

. '

J VasoPr.;ssi~&.-O~Yio~in . . \

In most mammals, the hormones secreted by the pos-terior pituitary gland are arginine vasopressin (A VP) and oxytocin. In hippopotami and most pigs, arginir1e. in the vasopressin molecule is replaced by lysine to form lysine vasopressin. The posterior pituitaries of some

. species of pigs and marsupials contain a mixtLlre of argi~ nine a11d lysine vasopressin. The posterior lobe hor­

. mone? are nonapeptides with a disulfide ring at one end \ (Figure 14-1 O) ~ J

.-- ··-- •••·--• A--··~·-···~·-------­~- ·--··--.. ---a •• I '-· I r ,....------- ··-·--·-·· ...... ----·----! r .

I I I I I I

I: I

I I

I i

I.

Eolna>a llimulalad Gy: I, :m·a,·n~.ln~J phi'•H1tltJ',t\tuhllny

lduhydrl1H~u\) dul\•\h.td ll"l bypuihulu:t\IC O~lllOft:CCplur,

2. Rcd•Jccd blood pressure dciectcd b•( corolid sinu~ bororcc~pJors

l. ~cducd ll!cod velum a ueretlcu ty receptor: lnlcfl olrium

4. Hocmc.rrhogc

5. Low o,;ygcri, hl!Jh cor !Jon tJioxldu In ll>l) blood

b. CNS ~1imulollo:1 cou~ccJ by pain, ~lrc;s, lieu mo. cro><iCI'(

7. (ndoolnc ~llrnvlolion odrcnolinc, corli~ol, ~ex $lcrc:ds

) I

g_,

walcr no I reabsorbed I~ cx<1clcd In Jhc vrino

·-· ............ -···-··-··-· __ , .... --···---~ ... - ...... _ ... ____ .,. ___ ·-·--·0· ...

t11olntull1:. hlooJ prcs~ur0 tospcdoilt' impcr1onl during hocmcrrhogel

t vosocan~lrltllcn

dccrcmes plcsmo osmolo''ly

8

0 st:mulo:ort oUccl , , (-) lnhlbllor; cilctt

N[} High plasma osmo!ollly = low conccn:;aUon in blood I.e. dchydrallon

. ( Fig. 7.5 lhc conlrol of ADH seem lion ond ils oclions on lhc kitlnuy, liver, and blood vessels . ......_

·'

j J I

~

- \

., ·-rrg . .3<J.-.4. Factors th.at re-.,'l.Jl.;Jtc the S.."'C"eton oi ADH b:; the hy­potlui.amone~ohypophy~I 5y~LC.'11 !lE'iS). + = stimulation and (j)

= inhibition. _____ \ ___ _

t ~aCI CD or

I E-,0 T

L--·-·

1-r l

4 ECF

[ os;-;-;cl~li1y

~+ Central osmorecepiors

--

I r I T

J. 1 I

Emotional s<ate:>

Pe:-iphc~al

c;;.::nor ~(;eiJr ors

! j+

..\r:e;:a: PO,

Ar\e:-i2i pH cr ® Allc::iai PC02

+

r· P::in I I+

~ f , +

-7"

c;-;s

+

l H~S

t+ ADH

I v

--.... -

,- .- .. ,,,, I .) t i ·~ _ ..

..1. . C:::lt ;u.JI I v··n"''l" -;.

p;~<~:m:-~ I I+ l

L~(t ;:url2.f 'ciu:••c: rc~~;;tors

t

'

!r I C"·_ ,,.;<' - l .A. <..:..1 ;.),,_

I /·· ! . ., __ , _,", I i G, ~-..... • ~' ~

I pr<SSJtc J I+ '(

Czroc~d o.r:C ::or :ic t-ar ere::~.:;:: c r s

l L__ w•_.

v r l Dienccpha!on l

j KidneJ"] > 1!,0 reJ.bsorption ,_ --·--------~-- ··--·

TABLE 9-G. Factot·s A.ffccting ADI-! Secretion

Stirnulatory Factors

Increased serum osrnolarity; Decreased ECF volUinc Pain Nausea Hypoglyccn1ia Nicol inc Opiates Antinco_!?laslic clrugs

· Decreased scrun1 osinolarity (;\ ~ Ethanol · a-Ad rcncrgic agon ls ts At rial no.t ri urct ~c P<?P lidc (AN,P)

' ~ :, I I / ...

·~~------------------~-------------------------------------

';:

.Jt~kl: IIOiJ t\NL!

OXYTOCII-l rJCI(tD UP ny CAPILLARIES or- I'OSTERtOfl tO[lE

AffERENT IMPULSES fRQt..', G:!VICAL D:LAT A TIO~l OR VAGINAl STIM.VliiTiOI t

OXY"iOCIN P:CKED UP BY PRIMARY PLEXUS OF PORTAL SYSTEM ."-NO CAARI(D BY PORTAL V£lNS TO ADENOHYPOPHYSIS

OXYTOCJN STI.\\UV..iES OUTPUT OF PROlACTIN

' ... . . •