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Page 1: msg2018.weebly.commsg2018.weebly.com/uploads/1/6/1/0/16101502/6-4-2014.pdf · 2019-08-03 · 2) fatty acids concentration increxsesin body fluids. 3) it enhances the conversion of
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Paraventricular nucleus

Neurosecretory cell

Hypothalamus

Tubero-hypophyseal tract

Infundibulum

( post.trior pituito.r NEUROH

Figure 18-8 Tortora/ Anagnostakos: Principles ol Anatomy am! Physiology, 5/e Copyright@) t9e7 hy !1nrpor & flow, Publl~h!Jr~. lrrc. 1\11 rlyhts '"~orvod.

r ior pitu itcu y ADENOHYPOPHYSIS •

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• • • • •

Capillary of pituitary portal system

-t·--- Antorior pituitnry coli

Fig. 28.5 R~lutiouship bet ween hypothalamic ncuroncs and an­terior piwitary cells. (l;rvm H .. Guillcmin & H.. Durgus ( 1972) Sciefllijic A11writ:on 227 (5) 2/1-33.)

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--:.:..-.. --~~-~-~Pf~-:7'~7~:.:-'? _ _;:~~:0-~-~~p--::-:r..-.·~:·:-;:-.~:-y~:~::-;:::.:T.:~·~::::-.:~:·:;:~"::·::~·::;.;M::;3:-~~-~.::.._~.--:-=::-;-;:-:-;:~?:f'?7~ :~:70."·~:~7-'"7'"".".~~:~-~:~:~ :---~~ ---. '"~·.-· -.- •. -7.- ... - _..,-. --- ~---, -··- ··- - ... ·.:.~~-

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Axon of hypothalamo· -----hypophyseal tract

Posterior pituitary cell (storage cell)

Fig. 2B.H Hole of the ,-)()stcrior pilllitnry cells in the storage of the hormones oxytodn nnd t\ D [I claborntctl by hypothalamic ncuroncs (Ft·vm It Guillemin & H. llurgus ( IY72) Scientific AmericatJ 227 (5) 2t1-33).

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Superior hypophyseal

~ artery

Anterior lobe

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 magnocellular 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.

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. I • Somatotroph A r-Most cells that prod!ce W gro~-t~ h_q,rr:n.g_ne

1 ~ngJ · ·. Lactotr..,ph

prolactin are separate cells. : j However, some ·norm1al !

Corlicotipotrcph .

and tum·N cells · t are single cells that Growth

1\ produce both '

_gr_owth hormone

and prolactin."!

( . -

-

Prolaclin (PAL) .·

Stimulates Initiates Stimulates Increases Stimulates ;:me:::! milk . adrenal skin lhvroid

body production cortex pigmenlalion gland to 1 growth by mammary to secrete secrete its

Melanocyte­stimulating hormone (MSH)

Stimulates sperm

production in testes

Thyrotroph

l Thyroid­

stimulaling hormone

(TSH)

Stimulates egg

production in ovaries

' ;

<:: - -........

Gonadotroph

Follicle­stimulating hormone

(FSH)

-~

':- ..

and luteinizing hormone. However,· a fe~ separate cells may exi~ --r ·som_e pro~ucing follicle- ·

LuteiniL!ng st1mulattng hormone and hormone sam::. producing

(LH) '"'

\ luteinizing ho.r~ne.

1f --

-

.

Prepares uterus for

implantation of a ferlilized

ovum

Stimulates secretion of testosterone

by testes

i J,t:~:~:~... glands il.s ~~~r~~-~~s- hormon_e~-- .. _ . _ . . .

: . FIG·c·~E 19-6 Cells o~h~ .. ~-d~-~ohypophysis as re~~~led :by- special strai~s.l . -- ·-·-·--------- -------·-··- -

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.Anterior : Pituita!'; Gland Contains . Several ·Different Cell Types That Syntliesi?:e and ·secrete Hormones . . Usually, there is one cell type for each major hormone formed in rhe ·anterior pituitary gland. With special stains attached to high-affinity antibodies that bind with the distinctive hormones, at least five cell types can be differentiated •.

Tabie 75.-1 Cells and Hormones of the Anterior Pituitary Gland-and Their Physiologrcal Functions

· Somatotropes

...... ~~ Ccirti~6tropes >··~. :·,- ' . . .

)Thyrotropes .. ::·

Gonadotropes

· Laci:otropes .' ~ammotropes

···: :;.•

.:;~:},\(~~~·~;;i~J~~l1f~emi~try .. ··. Hormone .· ... :; .. ,

Growth hormone (GH; somatotropin)

Adrenocorticotropic hormone (ACTH; corticotropin)

Thyroid-stimulating hormone (TSH; thyrotropin)

Follicle-stimulating hormone (FSH)

Luteinizing hormone (LH)

Prolactin (PRL)

Single chain of 191 amino acids

Single chain of 39 amino acids

Glycoprotein of two subunits, a. (89 amino acids) and p (112 amino acids)

Glycoprotein of two subunits, a. (89 amino acids) and p (112 amino acids) Glycoprotein of two subunits, a. (89 amino acids) and p ( 115 amino acids)

Single chain of 198 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 cortex

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

Stimulates deve~opment of ovarian follicles; regulates spermatogenesis in the testis Causes ovulation and formation of the corpus luteum in the ovary; stimulates production of estrogen and progesterone by the ovary; stimulates testosterone production by the testis

Stimulates milk secretion and production

IGF, insulin-like growth factor. About 30 to 40 percent of the anterior pituitary cells

are somatotropes that secrete growth hormone, and about 20 percent are corticotropes that secrete ACTH. Each of the other cell types accounts for only 3 to 5 percent of the total; nevertheless, they secrete powerful. hormones for controlling thyroid function, sexual functions, and milk

secretion by the breasts .

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-·~· · ....... ~ ..

Specific Areas in the Hypothalamus Control Secretion of Specific Hypothalamic Releasing and Inhibitory Hormones. All or most of the hypothalamic hormones are secreted at nerve endings in the median eminence before being transported to the anterior pituitary

'. ··----~- ··~ --.---·-·--·- .... ' .... ·•.--•..-::•: ~._..,._w,•..:;·~.·-- ·..--, •- • , ,.,,,.._,

gland. Electrical stimulation of this region excites these nerve endings and, therefore, causes release of essentially all the hypothalamic hormones. However, the neuronal cell 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. ·

Table 75-2 Hypothalamic Releasing and Inhibitory Hormones That Control Secretion of the Anterior Pituitary Gland

11.0.rmo~~£: ··_, ::.:;:i1~tl~·~~dJ~1~·J:: ·,:~ ··;::;::::iJ~t~i~~~~~~~ r: :-··:·~ Thyrotropin-releasing hormone (TRH)

Gonadotropin-releasing hormone (GnRH)

Corticotropin-releasing hormone (CRH)

Growth hormone-releasing hormone {GHRH)

Growth hormone inhibitory hormone (somatostatin)

Prolactin-inhibiting hormone (PIH)

Peptide of 3 amino acids

Single chain of 10 amino acids

Single chain of 41 amino acids

Single chain of 44 amino acids

Single chain of 14 amino acids

Dopamine (a catecholamine) ·

. · · ."; , . · .. .-···, . . '~··_\ ~:;:~~~1-;{~r: · .

Primary Action on Anterior: Pituitary::. ' . . .... : . ~ Jo::.·.. =7.-~:;~~11-~'-lt•.!,- ...

Stimulates secretion ofTSH 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 secretion19f.wolactin by lactotropes · '· >::~~~};)~:· · ·.

ACTH, adrenocorticotropic hormone; FSH, follicle-stimulating hormone; LH, luteinizing hormone; TSH, thyroid-stimulating hormone.

For most of the anterior pituitary hormones, it is the releasing hormones that are important, but for prolactin, a hypothalamic inhibitory hormone probably exerts more control. ·

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DNA

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•' i ' I ' I ~ I ~ . : • .. , \ . ." '' ·:.' ... _-., ._, Hypothalamus - ~ ;-. .,-._ ·:. :" l. '•.' •. :. ; :l •. ;•• ;~ . ; • : ~ . ·.

Median eminence

Pulses __ NV\ __ Releasing hormones

Transcription

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. _;•,.1·,· 'j

: '! ... ,· .·

, . . .. :· ~ .

Plasma membrane

·;. 1 '· · , ,. .

* ·: :,.. · .· . . . '·

--- Pa<kaglog ; e.· c:>l . . > Re ease v1a

c_J •; ®":;"''' ,: · ·:/-;:: ·, Secretory ' .. :

· · ,_· granules .· ·. ·,. ';,

; . ·.·

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.

.... . .. ::''

.. ::+ ,\:)~;~,~~fr,;.l . ·~· ' • ~ •• ' , • : 111 .' ,.

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-~ Vasopres~in &-o~;~~d~------ .... --- --. --------···-·--··-- ------ t

0

• \ .f. In most mammals, the hormones secreted by the pos~ r:·

terior pituitary gland are arginine vasopressin (A VP) and 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 marsupials contain a mixture of argi-

. nine and lysine vasopressin. The posterior lobe hor-.. ·in ones are nonapeptides with a disulfide ring at one_ end \(Figure 14-10)~ · J

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~ ~ -

r

rl! ~. · ~ ..

·~ ~ ~ ~ ~ ~

. I p

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.. ,. -·~, ...... ---· -4-PIIMI • ..,$2.0'"U""'Wi,..,. __ ,...,., .. ~""""ft"'ft..........,.,.. • ............ fAW;"""' .. ..,. • .,., __ d .,, ________ ,...~ 'P~r(~'l-•..,....

). , . ,/ · .. ·. · Paraventricular . ·. · J

nucleus( 0 x 'jt.oci?1)1

r: ~

Supm-optic , . :.) nucleus ('fi DH:_

'' '

Posterior lobe

·~ ,.. ,.

.• , r I . ; ~

Anterior lobo

Fig. 28.7 1 The trncts from the hypothalamus t~ the pituitary. The paraventricular nucleus and the supra-optic nucleus are thought to be responsible for the elaboration of oxytocin and ADH respectively. The other tracts terminate in the capillary plexus shown in Figure 28.'1 and carry the hypothalamic hormones which control the release of the hormones of the anterior pituitary. . , .. •

#-

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G.-owth hofmone (GH), also ca\led somc:Jtotropic hormoYJt CSH) or So7»dfoVopin, is tt SJ'I\all protein moltcule containing 19C amit10 acids haviflq a mc;l(!c.ulaf wei,ht of22,005'. It CatA~q~ 9rowlh of aU ti5SU~s of. thf bod) fhat arG .

capable t>f 9r6Winq. It prornDles hoih Increased ~' 2"S and numbers of C9ll s .

0~----~------~----~----~~----~----~ 0 tOO 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.

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r Hr . , r / .. . . .. . _ ... .'.:( __ ..:...:..:.~ .. .. - .. -

Adipose tissue

+.Adiposity

Kidney Pancreas l;,testine

Islets Parathyroids

Skin Connective tissue

+Organ size

+Organ function

·'

: .;. Lean body ma~s!

t Linear growth

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

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~c-- ·::~1!':;'\f~~;-,~ ·_. :: . ··-·-.... -.. ~\fl§i: ... ~> .;_·.· -.-! .:,-'~/ ;;~J; I

EFFECT OF GH IN ENHk~CING FAT UTILISATION, FOR ENERGY:

1) INCREASESTHE RELEASE OF FAITY ACIDS FROJ.-1 THE ADIPOSE TISSUE.

2) FATTY ACIDS CONCENTRATION INCREXSESIN BODY FLUIDS.

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

WITH THE SUBSEQUENT UTILISATION FOR ENERGY.

q) IN THIS CASE SPARE THE PROTEIN

5) UNDER THE EFFECT OF GH THE MOBILISATION OF FAT ~EQUIRES

MIN~TF.S TO HOURS, WHERE AS PROTEIN SYNTHESIS CAN BEGIN

IN 1-1INUTES ..

6) UNDER THE EXC~SSIVE OF GH GREAT ANOUNT OF FAT NOBILISED,

THEREFORE A LOT OF ACETOACETIC ACIDS ARE FO~IED BY THE

LIVER AND RELEASED INTO THE BODY FLUID?, THUS CAUSING

(KETOSIS)o WHICH IS CALLED "KETOGENIC EFFECTtt OF GH.

:,-;.:·: ::;·~~~~~i{fiJ!l~i:j-;~i-~,{;, ~ ; . T' :.{~'; -..

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DIABETOGENIC EFFECT OF GH.

1) lvE HAVE ALREADY NENTIONED THAT GH INCREASES BLOOD GLUCOSE

CONCENTRATION.

2) IN ADDITION GH ~~y HAY£A DIRECT EFFECT ON BETA-CELLS.

3) IN THESE CASES PAi~CREAS OVER STI1--iULATED AND THE ::ELLS

FINALLY, BURN OUT.

4) WHEN THIS OCCURS THE PERSON DEVELOPS DIABETES MELLITUS.

5) THEREFORE IS SAID GH HAS DIABETOGENIC EFFECT.

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Growth hormone is secreted in a pulsatile pattern, increasing and decreasing. The precise mechanism~· ·· · that control secretion of growth hormone a.re not fully . understood, bl}t ~everal fac~ors related to a person's state of m~tritio~ or-stress are known to stimulate secretion: .. •. . .

30 Sleep

Q) c­om E E 20

Strenuous exercise

... (/)

0~ .ca. .c-

~.g,10 ... c (!J-

0~---,----.----.----.----.---.

8 am 12 4 pm 8 pm 12 4 am 8 am Noon Midnight

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

Stirriulate 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 -Chrelin

Inhibit Growth Hormone Secretio~ , · · : _~: . . > .. : ... .

.: :: . _ _:::

Increased blood glucose Increased blood free fatty

acids Aging Obesity Growth hormone inhibitory

hormone (somatostatin) Growth hormone

(exogenous) Somatomedins (insulin-like

growth factors)

• ghrelin, a hormone secreted by the stomach before meals. !

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.J::----·~-~-----· ···--- -··

Hypothalamus

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 f

that are released by the ingestion of food and suppress further feed- . ing. 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 size; it inhibits food intake. _.

-7 Ghrelin-a . Gastrointestinal H~-r~~~e-lncreases

Feeding. Ghrelin is a hormone released mainly by the oxyntic cells of the stomach 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 physi­ologic role in humans is still uncertain. _.......... -

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~

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............. '--- .

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Birth Childhood Senescence Puberty Adult life

I Fig . .tS-19 Lifetimt! pattern of growth honnone (GH) secretion. GH le\"els are higher in children than adults with a peak period during puberty. GH secretion declines with aging.

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(_

( Sleep

Somatostatin G H R H ___ ____.

Growth hormone

-Somatomedin ~.- Somatomedin

Stimulate ,... Inhibit~~

• Fig. 48-20 Regulation of growth hormone (GH) secre­tion. The hypothalamic peptide (GHRH) stimulates grov .. th hormone release, whereas the hypothalan1ic peptide so­matostatin inh~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 stirrulation of somatostatir. release. HGH in­hibits its own secretion by short-loop feedback. In addition · GHRH inhibits its ow a-release .via ultra short-loop feedbacL In both of these cases the negative feedback is1 probably via '·

increasing somatostatin re!r,ase. __/

.. \

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' ' ' ; s··oYi1fC111tr

· :: 0d"pl1rnluo a·Adre-nlfrgy ~

S'iros's Sleop ~

~ Hypoohalamo•

. \ So~tost"U"

Amino ..--..L------1\ acids 1....-.--------·

Sornaloruodin

Piluilary

GH

c:=) Stimulolo

C/ t=)lnhiuit

Somolomodin

FH1Ul\E 39-IU Hnuuln lion o[ Clll sec1 etiun . N utn both n tlil Hcl s timulalory and a directluhibilory inlluolll!!1 lto111 Urn hypolhnlaJIIIII'l. NoHntivr. (nP.dllnt:lt hy Llro pnr iphmnl product is exerted at the hypothnlnt11ic nud llw pituitary lovel. Ulllll/, U1owllr hoiiiHrrw··IUlonsill!J hunuuuo; FFI\, Irco fully ncidH.

1:

j

f

I I

! I

.. :: .. ·--~;:.:: ::t~i~:?/ ·. : :··,\ . ..

..

·r I r

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·J

~

I ~

I *1-~

~ i ~ j

~

' ~ , ~ ;·.· .. '~·~., ~

~

~

I I

~<; .;

·:·-- ... ··-;;,:·

.:,

. /:·: · ·: _ ·. L. Faiflire:.:of the gonads t'o ;'ffiature~· with-resulfant infantile -, 0'- ": ':. ·~~:_.:~':~~ ... ~~,~~:::• 0 ,·N-·o- :: "~ .. 0r •', .._ 0 ,' •o', '.\~,,.., • •

0 .'•

_ -_ .. __ . se~)J:·at\I¢~vel6p.lhent and sterility because of lack' of LH . -- ... ·:. :::. a~-ct~'f''s:H:~- .. · -. '· . :·:::'. ·_ ..... ,, - .... <: '.- : .. :- .'-'":.· :~: .. -~. ;: '•' ·,···

. . 2. At~~p.l;~· -~r the thyr~·id gland ahd the · ~haracteri~tics. ·of . · :.. thyFoia-·"tr~s·unicicl1.2y bcc~use of lack of TSH. ,· 3. Atr~pl1:,~:, of the adre~al cortex a~d .signs of hyp:~adrenal­

isn1 without sal~ loss because of ACTH deficiency. 4. Cessation of growth, failure to attain an adult stature, a

decided . ter1uc~1cy ·toward hypoglycemia, hypersensitiv­ity tcr ~~1sulin/_;1~1d a loss of body nitrogen accompanied

'\ - . ------~ -·-· ·-by diminished fat catabolism because of lack of STH~ J

. ' ' ~-

···-·-··-· ---· .. . ···-· ... ·-·· ·-·

., _ ____ ;;i.;''~izJ;;-~;;;;;~i~r:: :, _ 0 ~~~:~:r;~:l,:-:&~t{~i.¥~-~:; _

. ... .

' . ·.,·• .....

·.: ··•··. -. ~· ...... .

:.'

·- ·-- ·· ••.. .:_. •. _.h.

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-\ '-.J

(.

.,·,,

ANTIDIURETIC HORMONE ,- GONADOTROPINS DEFICIENT DEFiCIENT

/ / / /

y/f

II \ MAlE ADUlT

~ ~

I

T~H

DEi'iC:ENT

__ . .;..-;

8 (USUAllY CRANIOPHARYNGIOMA) >- { EXTENSIVE TUMOR

_. POSTSURGICAL g · OCCASIONALlY GRANULOMA w OR TRAUMA

... ' ..... ,_ ' ·-\ ........ -........ --\ ........ --\ ......... , -. ......

~ ..-'

f.~~ Jli CJ BA

AOH MSH STH DEfiCIENT DEriCIENT DEFICIENT .. ....._

\ ............. " \ ........ ~ \ \ ~ \

y~ I I I

t DECREASED

FEMAlE ADUlT

DECREASED LIBIDO, AMENORRHEA

HYPOTHYROIDISM - ~

ADRENAL CORTICAL INSUFFIOENCY

PAllOR DWARFlSM, MUSCLE lOSS AND MICRO­SPlANCHNIA, TENDENCY TO HYPO­GLYCEMIA

DIABETES INSIPIDUS (lATENT UNLESS ADRENAl CORTICAl HORMONES ARE PRESENT

liBIDO, ASPERMIA, lOSS OF SOME FACIAl AND BODY HAIR

CHILD

DELAYED PUBERTY

OR ADMINISTERED) {DEFICIENT GROWTH PRECL!,JDES.. EUNUCHOID HABITUS)

-··--··---~

C: . ..

~. i: m ~: . .

.[~> f\•

l~ f I rt t ..

. r,~• ~-:;.; · i}:·

! I W:--

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\

... , ·: ~ ~i

-~~-1-<~.

,/I 7 /' ...,

GONADOTROPINS DEFICIENT

. .#'/'

/I

. ' ' .•... ~-~'. ~ • • -· !": • • •

,_ . . ~.· -: .

FEMALE ADULT

iSi-i DEFICiENT

I I

I

MALE ADULT

DECREASED DECREASED HYPOTHYROIDISM UBIDO, ASPERMIA, LNS Of SOME FACIAL AND BODY. HAIR

LIBIDO, . A.M..ENORRHEA

CHILD

DELAYED PUBERTY

{DEFICI~T GROWTH PRECLUDES EUNUOiOID HABITUS)

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

\ .

>­(.') 0 0 i= w

EXTENSIVE DESTRUOIVE TUMOR (USUALLY QillOMOPHOBE ADENOMA OR CRANIOPHARYNGIOMA)

POSTPARTUM NECROSIS. OCCASIONALLY GRANULOMA

OR TRAUMA· POSTSURGICAl

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

AGH DEFiCIENT

MSH DEfiCIENT

STH. OEF!CIENT..,

\

\

~' ~ &.'.

ADRENAl CORTICAL INSUFFICIENCY

' ' ~

PALLOR

' ' ' \ \ I I I

t DWARFISM, MUSCLE _LOSS AND MICRO­SPLANCHNIA,

TEN-DENCY TO HYPo­GlYCEMIA

l

·--·::

-----.-;-··----. ··-.. -- ... - ~o.·,~~f:'~:•:;~:o\1~·-~~~ft~f.~:~~~~

I • , ~ ~

~ ~ w ~

r· !· i t­l

F I" ·.•. "

l~ ~ l\_ ~;

t L ~ r·: 1-·v r ~ ~

K

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iij,Jlii'''~''~"'"'"i%"'' '' .,, ' . ·_. ~-.. ~--~'~·· . . ..... ;;;,,. '""'·'-- . . ....... ----·---·· ) .. ~ ·-.--·-·· ~ .. .

/ /

GONADOTROPINS DEFICIENT

/ /

.,/" /{

a \·.-. ) ~~ '!. ~

MALE ADULT

DECREASED \iBIDO, ASPERMIA, LOSS Of SOME

FEMALE ADULT

DECREASED LIBIDO, AM:NORRH::A

' ~FACIAl AND BODY HAIR

',

CHILD -:.;DELAYED PUBERTY

OVERGROWTH OF LONG BONES (EUNUCHOID HABITUS)

' '

HYPOTHYROIDISM (SOME GRO\VTH IMPAIRMENT MAY RESULT FROM THIS)

G {POSTPARTUM NECROSIS 0 CHROMOPHOBE ADENOMA 0 CRANIOPHARYNGIOMA 5 GRANUlOMA

MSH - STH PARTIAllY NORMAl DEFICIENT

ADRENAl CORTICAl INSUFFICIENCY BROUGHT ON ONlY BY STRESS (IllNESS OR. OPERATION)

' SOME DEGREE OF PALLOR MAY BE PRESENT

~

).~$ hers.~

NORMAL GROWTH AND DEVELOPMeNT EXCEPT FOR EFFECTS OF GONADOTROPIN DEFICIENCY AND HYPOTHYROIDISM

i-·.

\ ... ·· .. .-

i I I.

L ~,::

r ,. 1·:

[i::

f.'

;::

:::::_:·

i ( .. , ...

It r::: ~

[

w ~ .. r l ·· ~

~

~ ( ... ~

~

k ~ , ;·. K

L ~ r ~ ~ ~

~

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-.tJ~I~h~~~i~~-,~.:~~~, f: -· - - · ---- ·-· ...... ,_,_, __ · ~·-·· ." ·- · .. :.:;.~.'_...::..; - :·c:..; .. · ·-----

~~-,~·v/

,"" GONADOTROPINS DEFICIENT

/ .,..r _/{

,.,

N,AlE ADULT

DECREASED LlB100, ASPERMIA, LOSS OF SOME :rACIAl AND BODY HAIR

CHILD -

\

FEMALE ADULT

DECREASED LIBIDO, AMENORRHEA

DELAYED ?UBERTY

.. :-

, OVERGROWTH OF LONG BONES (EUNUCHOID HABITUS)

THYROID FUNCiiON NORMAL

POSTPARTUM NECROSIS CHROMOPHOBE ADENOMAT­CRANIOPHARYNGIOMA ..,... -CONGENITAl lACK Of DaTA CEll~ ("GONADOTROPHS")

ACTH NORMAL

GRANULOMA

STH NORMAl

MSH NORMAL'-...

\;::s;:::: --.-·'"'~-.,..w: .. ..,...~.,._::; ..:;... ~. ~~- .. -.. . '=:\"·· •. --~ ..=.....:-:· -~::--.... . ;~. ; ~W ... ! ... . '{' ~~;-,..:.;~'"?"~

\' .. ~~ ~ .._ . '-<'!';.:-;;. I

\ '~'"' ~ ~ --:~ \ .. '" « - <>~~..._;-.

l r ~~-e.~:: :.;...-:r:

. /

t:f..-: .;,,.; ~,...

ADRE::..JAL CORTICAL FUNCTION NORMAL

NORMAl PIGMENTATION

NORMAL GROWTH AND DEVELOPMENT EXCEPT FOR EFFECTS OF · GONADOTROPII'-­DEFICIENCY

~,. ·.~·· . ·.·•. i . '

· .. ·: :/ f;: f. I· r~:

l:r '· r . , ... ,. ~{:·

~~ .. '; r,/

r ,, I I

0 ,., I f• ~ ~ < ..

t b ~

1'~. ~ r ( r· t ~

I' (

J L p

0 R ( ~ r " 0 ~ ·0

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.. . -I

'

. .

G ~~\Ci~~~" ._ r ~ G ,, o/l. • . . ' . . ) ' - () . . rt. J 0 ~~·

cellA {~w~~- oc:~ bejo.A..t aJJ~~c--c_e_l df '

b~~~ L5su_v.r w;lJ cy{ovJlv-f4 ~~J ·

H.-e. b (7Vc8/Ji b e c~ M-e. ~ p~JW <>-{-< ~ .1</>'y b <fi--.0" ~ "'v-e. /l"--0 i --o ~ VJ i-14 k le_ ~ J '

r-7~ ~:; '2>- 1 -Jed ~- r,e_e. ~f ~t/.(_ ~;?#'1.~(~"'/(o r,

bvJ of J;_,d d 0 ~eft; .fy.uf. _ · -

: _ f ~ ~~ ;Ya,--vh~ vvi-l"-·..;( 1A£-~~ wikf d.Q.vdof roWl- ~- ''

. . ' I

.· IJi s.? I> "'RJ-<.II . ff P. ;

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f .. '/ • ~ \ I

PITUITARY GIANT CONTRASTED WITH NORMAl MAN (ACROMEGAlY AND SIGNS OF SECONDARY INSUFFICIENCY MAY OR MAY . NOT . . BE ·PRESENn ..

.,·.·

~ · .. · .. • ~' : I

-~· ! , \I ,. ·· "-·:--·. . ., . .

. · . ........ ~

..... · ..

. . ·

.

:···:;·,· ... :·:::,· __ .:'-!,·:···:···.·_:_~_:_.:·.·.·:··_:.·:;_· .. · .. ·;.:_:_·_:_::_;.~.:;_:_ •• _; ___ ;~ . .:_·_'·:.::,,.·_·:···,·····:_.·:.:•.·:··._: _ ... :······:: .. ·:··,···:::·-···._·.:_.·;~.·.· .. :.:: .. ·::_:·; .. -,::·:. ::::?.~-.:~f;;~i-.~i .. :: .. · · · . •'i>~·[Ni

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~ C}Lo/M~r}J~- [ -6 f.A-0rlowL o~wu 4;{-.v,_ . ~IL 1 UJL-.- c,e_ I ~.(A tfL<- f ~ a-{ {.f.:t _j CH-c_; . .

t

b""'0· ]~<- pv.-.s~ ~~ ~ov.l tdfvr.1 .

bJ fi-R_ s...f-A +~ru.v.r c.a.vt c_0>1!f~ '}1-o wt~., a-v...d 1: ~ Gc/V\-vi eM'/ 'YL0 '""' ~ 4 f...J.c.J.,.....<.JJ . ,_ f ....... .e aA.-1)-/1-Y<-~ ~ i-n ..(.l....e_ ~ ba...v.J· ~.,fL.~~"-. -/td a-.ddJo -(:~ ~I ~$k I IJ v /o..Lk.J / ~Aa D.Jv(;_ja/

>v:.J. ~) -1. ~.....<. .-f o .Neil. "'S 6tN b-.0 a-vJ. ,fk<_ p o-U;,.,

o.{ ~L..e vtde bl\P..~ . . J _ (•-~".l("" . ~ S~-f ,((55 vetA· o/L olt.{}a.w-

-·---~; . .

);,h. }_; vu, t. ,;,F1 W-.~ ~ ~c~~ ~-{~ ~~·

.· _ , :.

·-·::";:7· •.:·"?-':F7f:¢:::"707HS'7:~'''1'%'X~;'{$B?n:~':'7?::::::~c;;:,;r%!Sc:'::y:'S~0":~7:~-;~:'Z:'•~~,,~,:;'~;:~;~;.\?t>"\;~:g~~:;~t?'i~r.':~m~:0B~~S4:•i;''->"·'"-~7'': ·· .: ··· -- -·· .

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I ,j.

/

v

/· I

lHORACIC VERlEnRA IN ACROMEGALY• HYPEROSTOSIS, ESPECIAllY MARKED ON ANTERIOR ASPECT

TUI'liNG OF PHALANGES IN HANDS AND NARROWING OF PHALANGES IN FEET

•:

. . .-:-:·:·;.··! .·t~: :~· .-:t:, . . . . :

.. :~:i{

· : .. ·· .•· . . , .

.'\· •' .. ·.· , .. .

.....

. ·~

:•' ..

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Dopamine

Stimulate

Inhibit

Prolactin

----~

--(/ )Ia

TRH

• Fig. 52-25. Regulation of prolactin secretion. The predom­inant n1ode of hypothalamic regulation is tonic inhibition viu dopamine. Although TRH stimulates prolactin release, its physiological role is uncertain, and evidence suggests another hypothalmnic peptide may be more physiologically important. Prolactin exerts short-loop feedback on its own secretion by stiinulating production of the hypothalamic inhibitor, dopa-

0

111111C .

I

: ·. •.·

l \

~ \': I

1

i ' i

i i I ' l

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v

/ ( 0 V"'f. to~' .-t \ J./<H\ M.L> n) Paraventricular " • .1 I o

nucleus

Neurosecretory cell

Supra-optlco-hypophyseal r-:--__ _

tract __,...__.

Tubero-hypophyseal tract

NEUROHYPOPHYSIS Figure 10·8 Tortora/Anagnostakos: Prlnclplos of Anatomy and Physiology, 5/o Copyright (i) 1987 by Harper & Row, Publishers, Inc. All rlgll!s reserved.

Supraoptic nucleus

(ADH) 1"'

·. ~oJ'.T)

ADENOHYPOPHYSIS

•,

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I

/'I / i : . ... l/

----

Doleclod by Deloclod by .. .... ........ ·-·-·-· ---·:-· Osmorocoplors ...,..,__ _____ _

/\IJII r.nt:rnlod 111

IIXtlll lrlllllllllll!l Ill I lOlii ul!ypupl!ysi:J

/' (

",.. _,.

Slirnulnlo\ socrclio::

ol ADH

,.,/'

I I 1 Inhibit 1 s::crolion I ol ADH I

Neurosocrolory cell synthesizes ADH

Hypothalamus

FIGURE ·to-·10 Regulation of the secretion of antidiuretic hormone (ADH).

.· ,

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·{.I · l Vasopressin & Oxytocin ··._. ·:·· \ .~ In most ~ammals, the hormones secreted by the pos-~! · terior pituitary gland are arginine vasopressin (A VP) I and oxytocin. In hippopotami and most pigs, arginine· ~ . in the vasopressin molecule is replaced by lysine to form 1 lysi~e vas~pressin. The posterior .Pituit~ries of so~e 1 species of pigs and marsupials con tam a mixture of argi-J ·>I ~~

I %1 , .. ;~

iti~ -~ ''f.~

:%1 ' I

gl· :~

' ''] i uo_.,. _________ .,,,~-·-•"•••'•--•-•- ... •-·•-••·""' ••'••-'•'•• •'•''•'·' ,,.,,,,, .. ,.,, •'- ••-••·/•••,.· •• ,,,,, ..

-

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------ - -·- - ·--·--·-·--------'--------------------------(~-~===--- -~---~--=-~ ... ~ .. ~ ... =·-=-.. =--~ .. ~~~~~~~.~--~~~-~---=----~--=--~--~- -=·-=-.. -=.-~-=-=---=-=- ~-=-~---~-.. =---~·-=--=--=--~-.. =-~--~

8 ~ olcohol

Roloosa sllmulolod by: I, II\CI''U:•III\1 phl'oll\11 ll!ollllll\lllly ld\lhydrulhuol dui••L iud l1y hypolhulumlc osmorcCI.lplur~

2. Reduced blood pressure deleclcd by carolid sinus bororcccplors

3. Reduced blood volume delcclcd by rcccplors lri 'loll olrlum

4. Hoemorrhogc

5. low oxygen, high carbon dioxldo In I he blood

6. CNS slimulollon caused by poln, slrcss, lraumo, anxiely

7. Endocrine sl imulallon adrenaline, cortisol, sex steroids

i. . .

(-)

blood'"~'' ~

rnulnlulns IJiood prcs~uro to specially impor1onl during haemorrhage)

't vasocanslrlcllon

ADH . , glycogenolysis

oool-:~-..---~ ' .:

Increases ·' · ;:.{;~---+- walcr roabsorpllon __.,

.In ~-o~~-~lln,D duels ...... i • ·•·· !.! I

decreases plasma a_smola1'1y ·0 sllmulolor'y orlccl

Q lnhlbllory erlccl water nol reabsorbed Is excrelcd In I he urine N[l High plasma osmolollly = low conccnlrollon In blood I.e. dchydrollon

. I Fig. 7.5 Th~ control of ADH s~cr~lion and ils actions on the 1-;ic.Jnuy, liver, and blood vcss~ls .

I '

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{~ ''-3 ~.;I ~~:

' ·1,

;~ ·;:; . . :·,, :·~:

/i:

1 1 ~ .~ ~

t

~/., ~ w ~

~

~ ~

1 ~ l

~ ·\_

. .!

j .l I . \

r"rg. 30-4. Factors that regulate the sccreton of .illH by the hy­

pothalamone!.lrohypophyse.:ll system (li".'S). + = stimulation and = inhibition.

Emotional s<ates · ·-·

~

! . . I ~aCI Pe:-iphc:-al +

Q) or c~e::norece;::tors ...

I H.,O T - ! -- 1+. , . . I+ 0 ' ' •W -···

l t -\r'e":,; PO

l ECF + • .. •• c. 2

Arte:-ial pH ® OSliiOb.Jiry or

t Aneriai PC02 .

+ .. ,~,

Central + ' osmoreceprors

I

(j)

Pain I I+ ' ,.

c::-.;s

+

, H::-.;s -~+

ADH

t

I Stre!i,<; I I

1-

..--·

t Ce:1tral ve:1ou,<; :?::" pres.~ure

I+ ., 1._ef't atrial ,·olume re::eptors

I....--.

t 1

t Caro aner: press

id .• r.(

ure

t+ Carotid: nd c. ode barorece ptors

+

T I

I - Diencephalon ··

l

C Kid~e~·-] )lo H20 reabsorption

' . "

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.•

-~---···-·-···-·-·· · -,· I • . . . . ,. . ; -~ ·.

TABLE 9-G. Factors Affecting ADH ·· sccrction • •. .r ,' I ' I 1 .

Stlrnulatory Factors · 1111~~ p~ ~~ryi, f~<;~.9.r.:> ,:, ·~.:,..: .. :i. , ~ I • • • • . , '

' t ~ "':' .•

Increased serurn osrnolarity •:· ,'. Decreased scrun1 osinolarity :~;[ ·: Decreased ECF volun1c Ethanol · · · · ~- (·: · '. ··<·· . · ·' '

Pain Nausea Hypoglycen1ia Nicotine Opiates . An tinco.!?las tic drugs

a-Adrenergic agonlsts Atrial natriuretic peptide (AN?) . . . , •

· : : i i . : ~ :I :·j ! ~ :· I . 1 ! ·~ i _ .... j • : ,

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Endocrine system

These are the systems of the body:

The nervous system, skeletal, cardiovascular, respiratory, digestive, urinary, endocrine, reproductive, lymphatic, and immune. These systems form the body of the humans and mammals. From these systems just two systems control the human body: nervous system and endocrine

system, one for immediate action and the second for delayed action. Endocrine system for immediate action and sometimes for delayed action like the release of

adrenaline from the adrenal medulla, Nervous system for immediate action. Now we compare these two systems:

Characteristic Nervous System Endocrine system

Mechanism of control Neurotransmitters release in response to nerve impulse, from neuron to neuron, from neuron to muscle cell, from neuron to gland cells.

Hormones are delivered usually directly in the blood to tissues.

Cells affected Nerves, muscles, gland cells. Almost all the cells of the body.

Types of actions Neuron to neuron: action potential in the second nerve. Neuron to muscle: muscle contraction. Neuron to glandular cells: secretions of enzymes or hormones.

Changing in metabolism either anabolism or catabolism.

Time to onset of action Usually immediate Usually delayed sometimes immediate

Duration of action Generally brief Generally longer

The types of hormones or glands : Exocrine glands their secretions are released into a duct open either inside the body into a lumen

such as the intestine or outside the body such as sweat glands.

Endocrine glands, there are two types of endocrine glands (ductless glands) classic endocrine glands and other endocrine glands:

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Classic endocrine glands are group of cells synthesis and secrete chemical substances called hormones, directly into the blood, and through the blood the hormones reach their target cell, these are classic endocrine glands, and the hormones also are classic hormones.

Other endocrine glands do not release their hormone directly into the blood, but these are minor glands: Autocrine glands: hormones synthesized in endocrine cells and sometimes released into the

interstitial spaces, bind to specific receptor on the cell of origin. Paracrine glands: hormones synthesized in endocrine cells and sometimes released into the

interstitial spaces, bind to specific receptor of nearby cells affecting their function.

Neuroendocrine: two subtypes; the first subtype is hormone produce by neurons and release directly into the blood, example: posterior pituitary. The second subtype is hormone produce by neurons and release into the cleft affecting the post synaptic neurons, so these hormones are neurohormones either release into the bold or into the synaptic cleft, example: Adrenalin from the sympathetic nervous system.

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Pheromones: are volatile hormones released into the environment act on olfactory cells of

another individual, so they are substance produced by an animal usually that act at distance to produce hormonal, behavioral, or other physiologic changes in another animal of the same species :

o In animals the deers produce the musk it affect the other deers and it is produced by the males not the females, also the amber produced by whales.

o And these pheromones might be present in human beings, people getting attracted to each other by these pheromones.

Some important points about the endocrine system : A single endocrine gland may produce many hormones such as anterior pituitary, pancreas.

Some hormones have multiple actions in their target tissues called tropic hormones or effects, this phenomenon occur when single hormone regulates several functions in the target tissue, example: in skeletal muscles insulin stimulates glucose uptake, glycolysis, glycogenesis, inhibit glycogenolysis, stimulates amino acids uptake, stimulates protein synthesis and inhibit protein degradation. The same for insulin in the liver or adipose tissue.

Single hormone may be secreted by more than one endocrine gland such as somatostatin secreted by the hypothalamus and the pancreas.

Some hormones are known to have several effect in several different target cells, example the testosterone, the male sex steroid hormone, for normal sperm formulation in the testes, stimulates growth of accessory sex organs or glands such the prostate and the seminal vesicle and promotes the developmental of several secondary sex characteristics such as beard growth and deepening of the voice.

There is also multiplicity of regulation in the endocrine system the input of information from several sources allows highly integrated response to many stimuli which is of ultimate benefit to the whole animal, for example: several different hormones insulin, glucagon, epinephrine, thyroid hormones, adrenal glucocorticoids may regulate liver glycogen metabolism, they produce simply the normal plasma glucose level all these hormones together.

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Single target cell may be influence by more than one hormone, some cells contain many types of receptors responding in different ways to different hormone, to illustrate: insulin promotes the conversion of glucose into glycogen within the liver cells by stimulating one particular hepatic enzyme, where as another hormone which is ''Glucagon'' enhance the degradation of liver glycogen, so the insulin increases the glucose level in the blood and the glucagon decreases the glucose level in the blood, because the same cells in the liver they have different receptors, some receptors for insulin and some others for the glucagon.

The same chemical messenger may be either a hormone or neurotransmitter, such as somatostatin either neurotransmitter produced by the hypothalamus or hormone produced by the pancreas.

Some glands in the body they produce just hormones, but there are other organs In the body they produce hormones in addition to other functions such as intestine (produce hormones as well as enzymes or other secretions), ovaries ( produce hormones as well as producing ova) , testes (produce hormones as well as sperms) . In this figure you see the only endocrine glands, also you see the mixed organs; they have

nonendocrine function in addition to secretion of hormones such as stomach, pancreas, ovaries, lungs, heart, kidney, intestine etc…(refer to slides)

The general functions of the hormones: Metabolism: hormones regulate the metabolism either anabolism or catabolism. Reproduction: there is no reproduction without hormones, no sperms without testosterone and

other androgens or estrogen (because the estrogen also it has role in the production of the sperms), no ova without estrogen and progesterone.

Digestion: digestive system does not function without hormones; it needs hormones to function properly.

Blood circulation: cardiac output, blood pressure, vasoconstriction, vasodilatation and control the blood volume and consequently the body fluid volume, all these are controlled by hormones, and any wrong especially in some specific hormones all previous mentioned things are disturbed.

Transport of substances to tissues: many substances are transported by hormones or increased or decreased its concentration in the blood.

Defense against pathogens: immune system responses are regulated by hormones, such as inflammation, antibody production and fever.

Growth: it is does not occur properly without growth hormones, deficiency in GH lead to dwarfism as well as cretinism.

Stress response: regulate the body’s response to stresses. Behavior: hormones affect the behavior; the behaving of the females is different from the

behaving of the males because of hormones, females shy and cannot fight because of the estrogen, males fight because of testosterone.

Done by: Hala Makahleh

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*Remember that:

-Posterior pituitary hormones :- ADH (Ant diuretic Hormone) & Oxytocin

-Anterior pituitary hormones :- GH, ACTH, TSH, FSH, LH & Prolactin

*First, we'll discuss the GH ,because ALL the cells of the body are considered as target cells for this hormone.

*Referring to the figure above, there're two curves ,the lower one represents the normal growth of a rat while the upper one represents the growth of the same rat injected with the GH. This indicates the effect of the GH.

-Again, GH causes the growth of ALL tissues of the body ,that are capable of growing.

-It increases the sizes & numbers of cells.

*Growth process is affected by many hormones, which function synergistically "they synergize with each other"

*These hormones, beside the GH, insulin ,insulin-like growth factors 1&2,thyroid hormones, cortisol ,estrogen , androgen.

-All these hormones "the previous 7 hormones" function together "they complement each other"

-They cause the growth.

-The most important in a normal post uterine life "after born" is the:

1)GH 2)Insulin-like growth factor 1

*It doesn't mean that the others are not important , If they're deficient, it'll cause serious problems.

*Especially, GH & insulin synergize with each other and there's a relationship between these two hormones ,so as to cause growth.

*If we've a rat ,without pancreas & pituitary gland, injected with GH, the result will be :little increase in the growth.

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-the same result will be observed if the rat was injected ONLY with insulin "there'll be a little increase in the growth".

-But if the rat was injected with both, GH & insulin, there'll be faster increase in the growth. "remember that these two hormones function synergistically".

*GH affects the cells of the body in two ways:

1)Directly 2)Indirectly

-Directly by affecting the adipose tissue ,liver & muscle cells.

-When the GH affects the liver ,it'll produce proteins ,which are hormones called ((somatomedin)) OR ((Insulin-like growth factors)).

-Somatomedin are many hormones "about 6 hormones" that have a similarity in their structure ,also in their function ,but the vary in their potencies.

GH

Adipose tissue Liver Muscle

( decrease adipocity ) ( increase the body lean mass )

Somatomedin

Chondrocytes

-Somatomedin are the indirect effects produced by GH.

*So, the GH exerts its effect either directly, which is the Main way for the GH, or indirectly.

Glucose uptake

Lipolysis

RNA synthesis

Protein synthesis

Gluconeogenesis

Somatomedin

Glucose uptake

Amino acid uptake

Protein synthesis

Affect: Bone ,heart ,lungs, kidney, pancreas, intestine ,islets ,skin parathyroid ,connective tissue.

Amino acid

Protein synthesis

RNA & DNA synthesis

Collagen & Chondroitin sulfate

Cell size & Number

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*From the functions of the GH, the metabolic ones are important because they're essential for the human beings minute by minute and hour by hour.

U*Metabolic Effects of GH :-

1)Increased rate of protein synthesis ( increase rates of GH is probably resulted by increased rate of protein synthesis )

2)Increased mobilization of fatty acids or energy.

3)decreased rate of glucose utilization.

-GH enhances the body protein, uses up "utilizes" the free fatty acids for energy & conserves carbohydrate.

(It spares the glucose to be available at any minute for energy, because Uglucose Uis for UFast Uenergy)

U*Hypersecretion of GH :-

(There's an excess "NOT normal" in the secretion of GH)

A)Diabetogenic effect of GH

-GH increases blood glucose concentration.

-It may affect the Beta-cells of pancreas directly , causing over exhaustion of beta cells

-Finally, the result is a diabetes mellitus.

*Direct & indirect effects by production of insulin as well as affecting Beta-cells.

B)Ketogenic effect of GH

U*Effects of GH in enhancing fat utilization, for energy:-

Increases the release of fatty acids from the adipose tissue. 1)

Fatty acids concentration increases in body fluids. 2)

3) It enhances the conversion of fatty acids into Acetyl-CoA, with the subsequent utilization for energy.

4) In this case spare the protein.

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5) Under the effect of GH ,the mobilization of fat requires minutes to hours, where as protein synthesis can being in minutes, because protein synthesis is performed by many hormones NOT only GH.

6) Under the excessive of GH ,great amount of fat mobilized, therefore a lot of Uacetoacetic acidsU are formed by the liver, causing Ketogenic effect.

U*Diabetogenic effects of other anterior pituitary hormones:-

1)TSH 2)Prolactin 3)ACTH

*The most important hormones ,which are functioning together, are GH &Insulin in:-

1)Protein intake

2)Carbohydrate intake

3)Fasting

-In protein intake--->Both GH & Insulin increase including somatomedin

-In carbohydrates intake---> JUST insulin increases ,because it leads to the entering of glucose into the cells, but GH is NOT needed in this condition.

-In fasting---> JUST GH increases ,here we don't need insulin, we need glucose from non-carbohydrate sources.

*The secretion of the GH shows a diurnal rhythm as well as pulses or oscillation rhythms & developmental rhythm.

*The level of GH during the 24 hrs.. the highest at 12 noon and at 12 midnight

the probable explanation of high GH at midnight is the escape of the cells which secrete GH from their control by nerves ,so body becomes out of control of the nerves ,so death is mostly at 3-5 a.m

U*Factors that stimulate or inhibit secretion of GH :-

-The most important in stimulating GH is the metabolic, especially the UGlucose U.

-Also, the UGhrelinU, which is a hormone produced by the stomach as well as in the intestines .

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"They're saying now that it might be produced by the pancreas"

-Ghrelin can stimulate the appetite.

-The most important factors that inhibit GH secretion are: UObesity U, UAging & somatomedin.U Others are increased blood glucose and free fatty acids ,GH inhibitory hormone (somatostatin) and Somatomedins

-Stretch receptors in the stomach, as well as hormones along with these receptors, inhibit food intake.

-Peptide YY(PYY), cholecystokinin(CCK)& insulin are gastrointestinal hormones ,that are released by the ingestion of food & suppress further food intake

-Obese individuals have large stomach, stretch receptors are away from the food, so they take a lot of food in order to touch the receptors. Therefore, they've to accommodate gradually to decrease their food, so the stretch receptors to become closer to the food.

U*The level of GH during the life:-

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-From birth till death."Developmental rhythm".

-There's NO significant difference between adult & childhood."Little bit higher in the childhood".

*ALL types of stresses can lead to increase the secretion of GH.

* UThe pituitary gland deficiency:

The hyposecretion of the pituitary gland is NOT a pathologic, it's a physiologic case. The results of deficiency of pituitary hormones(both post. & ant. pituitary hormones):-

A)Panhypopituitarism *“pan = all “ ,the deficiency of ALL pituitary hormones *Oxytocin is NOT mentioned here, meaning that it's NOT so important. "its deficiency is NOT very serious".

1)UADH deficiencyU: water is NOT reabsorbed probably back into blood, it's excreted ,so there'll be a lot of urination (about 20 liter per a day). If the patient is not treated ,then he'll die. This disease is called ((Diabetes insipidus)).

2)UGonadotropin deficiency: U (LH & FSH) In male: Decreased lipido (There's NO testosterone), asperemia (NO sperms),loss of some facial and body hair. *note : LH affects leydig cells leading to testosterone synthesis In female: Also decreased lipido & amenorrhea(NO menstrual cycle).

3)UTSH deficiency: UHypothyroidism.

4)UACTH deficiency: U"adrenal cortex hormones are affected"

5)UMSH deficiency:U pallor color.

6)UGH deficiency: Ucauses dwarfism but mentally is normal.

B)Severe anterior pituitary deficiency

*It's similar to Panhypopituitarism except those of the post. pituitary hormones are normal.

C)Moderate anterior pituitary deficiency

*Gonadotropins& TSH are deficient, ACTH & MSH are partially deficient, GH is normal.

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D)Mild anterior pituitary deficiency

*JUST Gonadotropins are deficient ,the others are normal.

**we can notice that in ALL conditions "A-->D" Gonadotropins are deficient**

Hypersecretion of GH: -

Ua) Giantism or gigantismU

*If the over-secretion occurs before being adult(during the childhood),almost all the organs will be affected & become larger than normal. *These individuals will: -Be 8-9 feet height. -The giants have hyperglycemia,10% develop diabetes mellitus. -If the giants remain without treatment ,they'll develop panhypopituitarism. *All parts of the body develop in appropriate proportion. -Also the organs will be enlarged .

b)U Acromegaly

*If the over-secretion occurs after being adult, after the fusion of the long bones ,the person cannot grow taller (bones cannot grow) ,but the soft tissues can continue growing and the bones can grow in thickness.

*These individuals will : -Suffer from enlargement of the small bones of hands ,feet, cranium ,nose ,forehead ,supraorbital ridges , the lower jaw bone and portions of the vertebrae. -Many soft tissues or organs like : liver ,tongue ,kidneys are enlarged. "also the heart but it's a little bit enlargement". *There's NO appropriate proportion in the development.

Done by: Jenan Al-Hamed

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THE ADRENAL (SUPRARENAL) GLANDS

They are two glands, present above the kidneys. One adrenal gland is sufficient for human beings/mammals (example: we also have two kidneys but one is sufficient).

The Adrenal glands receive their blood supply from the aorta directly and hence they are essential for life, if we remove these glands from the embryo it will not survive. Their total weight is 6-10 g.

Each Adrenal gland is made up of two parts -two distinct organs- which differ in their histology, embryology, and functions (physiology):

1- Adrenal Cortex - 80% 2- Adrenal Medulla - 20%

The adrenal cortex is essential for life (since it controls Na, K and water metabolism) and not the adrenal medulla (since its hormones e.g. adrenaline can be produced by other organs like the sympathetic nervous system.)

In physiology of the endocrine system we will only discuss the adrenal cortex (we'll take the adrenal medulla later when we take the autonomic nervous system.)

҉ Adrenal cortex secretes 3 main hormones:

1- Glucocorticoids (Cortisol - the main target for ACTH) 2- Mineralocorticoids (Aldosterone) - ACTH has a minor effect on them 3- Androgens (Sex hormones) - ACTH has a minor effect on them

҉ Control of adrenal cortex secretion:

The Anterior pituitary gland secretes ACTH which regulates the growth of adrenal cortex cells in addition to the synthesis and secretion of its hormones. Fetal ACTH synthesis and secretion by the anterior pituitary gland begins just before the development of the adrenal cortex. The adrenal cortex is essential even for the development of the fetus. The extra-adrenal actions of ACTH include lipolysis and MSH-like actions.

Regulation of ACTH is among the most complicated of all the pituitary hormones. The following regulate the secretion/synthesis of ACTH (Adrenocorticotropic hormone):

1- CRH (corticotropin-releasing hormone) – most important, it is a hypothalamic hormone. 2- ADH : exhibits the same action as CRH 3- Neurotransmitters 4- Anxiety 5- Depression 6- All kinds of stress (infection, trauma, anesthesia, surgery…)

ACTH secretion responds most strikingly to stressful stimuli: a response that is critical to survival.

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• Extra note: - Cortisol provides negative feedback to the hypothalamus to

inhibit CRH secretion and to the anterior pituitary gland to inhibit ACTH directly. - ACTH provides negative feedback to the hypothalamus to inhibit CRH secretion.

҉ The functions of the adrenal cortex - essential for life; include:

1- Controls Na+, K+, and H2O metabolism. 2- Controls carbohydrate, fat and protein metabolism and mobilization for energy. 3- Participates in the response to stresses of various kinds.

҉ The adrenal cortex is divided into three zones of cells:

• Zona Glomerulosa – 12% - Produces: Mineralocorticoids – represented by Aldosterone. Those control the metabolism of

minerals and water. • Zona Fasciculata - 65% - Produces: Glucocorticoids – represented by Cortisol as well as small amounts of Androgens.

Function: glucose metabolism. • Zona Reticularis - 23% - Produces: Androgens as well as small amounts of Cortisol. This zone doesn’t differentiate

fully until between 6 and 8 of years of age.

In adults, zona glomerulosa cells continuously migrate down to reticularis through fasciculata, they change their morphology, function and secretory pattern as they go.

҉ Now we will clarify the meaning of mineralocorticoid and glucocorticoid activity and the role of Aldosterone and Cortisol in each one:

♣Mineralocorticoid activity: measured in terms of the ability of the hormone to reduce the ratio of excretion of sodium to the ratio of excretion of potassium in urine. (In other words: the ability to retain Na+ and excrete K+.)

♣Glucocorticoid activity: measured as the ability of the hormone to increase glycogen concentration in the liver and increase glucose concentration in blood.

♣In terms of potency:

1- Aldosterone accounts for 90% of all meneralocorticoid activity while Cortisol has very slight mineralocorticoid activity.

2- Cortisol accounts for 95% of all glucocoticoid activity while Aldosterone has very slight glucocorticoid activity.

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♣In terms of actual participation: Cortisol's mineralocorticoid contribution is greater than aldosterone's glucocorticoid contribution. This is due to the secretion rate: the adrenal cortex produces more cortisol than aldosterone and this compensates for the weakness in its potency toward mineralocorticoid activity.

potency in meneralocorticoid activity

potency in glucocrticoid activity

rate of secretion

real participation in meneralocorticoid activity

real participation in glucocrticoid activity

aldosterone very potent weak less very potent weak Cortisol Weak very potent more potent very potent

҉ The change in ACTH concentration is parallel to change in Cortisol concentration: as ACTH increases Cortisol increases as well. ACTH release is greater in the early morning hours.

҉ Remember that steroid hormones are divided into: sex hormones and adrenal cortex hormones. Both are synthesized from cholesterol. The production of Steroid hormones involves many reactions and many steps and each reaction requires its own enzyme:

♣ As we know, the production of cortisol is mainly in the fasciculata. When cortisol production decreases or is blocked due to many factors (like enzyme deficiency), the concentration of Corticosterone hormone will increase. (The doctor didn’t say the reasons but I think it is due to the absence

of the main negative feedback inhibitor which is cortisol as we said previously.) In rats there is only corticosterone and no cortisol.

♣ Adrenal cortex hormones are released immediately upon synthesis and they are not stored. When there is an immediate need for new hormones new synthesis is required.

҉ 90% of cortisol binds to CBG “corticosteroid –binding protein” and 6% binds to albumin. The active form which is the free form of cortisol is 4%.

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҉ The main functions of Cortisol: it functions on almost all the organs. Those are the main ones.

1- Production of glucose from protein by gluconeogenesis. 2- Fat mobilization. 3- Supports the vascular response. 4- Modulates CNS functions.

Also:

- Acts on fat cells: increases lipolysis. - Skeletal muscles: Increases amino acid mobilization. - Immunosuppressive. - Stress response – Increased vascular response - Affects the liver:

♣ When there is a decrease in glycogen in the liver and there is a deficiency of cortisol the human will die of hypoglycemia (low blood glucose). Remember that cortisol is responsible for the synthesis of glucose from protein (gluconeogenesis). Cortisol is essential for life especially for fasting human beings and animals.

♣Cortisol doesn’t promote glycogenolysis. It facilitates the action of glucagon. This is called permissive hormone interaction.

♣Cortisol can bind very well to aldosterone receptors, but there is an enzyme called hydroxysteroid dehydrogenase which continuously inactivates cortisol and hence the actions of aldosterone and cortisol are not similar. In the absence of this enzyme their actions become similar the human being can’t survive because everything in the body will be degenerated.

҉ The Adrenal glands are unique during the fetal life especially after four months of pregnancy. They are unique in their size and function:

♣ Size: The size of adrenal glands in the fetus after 4 months of pregnancy is larger than the size of kidneys

♣ Function: Both parts -the adrenal cortex and medulla- function properly during the fetal life. Cortisol particularly has very important functions during the fetal life:

1- Production of surfactant from type 2 cells of the alveoli of the lung, a lack of surfactant which leads to the respiratory distress syndrome in newborns. If the newborn doesn’t breathe properly we give him cortisol and after a few minutes he will start breathing.

- It is called the magic drug: Cortisol diffuses into every cell in body with a nucleus. Cortisol treats and cures many diseases (Heart, skin, lung…etc). The strange thing is that sometimes it could cure one patient completely but have no effect on another, no one knows why, although some believe it could be due to a lack of receptor, a blood disease, or a genetic condition.

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2- Development of hypothalamic function and development of the thyroid-pituitary axis. 3- The sequential changes of the placental structure and in the ionic composition of amniotic

and allantoic fluids during development. 4- They are most important in the initiation of the endocrine changes of the fetus and mother

which are responsible for parturition. 5- The development of hepatic enzymes, including those involved in gluconeogenesis. 6- Induction of thymic involution.

҉ Natural and synthetic Glucocorticoids:

- Natural: • Cortisol • Corticosterone

- Synthetic: more potent

• Cortisone • Prednisone • Methylprednisone • Dexamethasone

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MSK system- 2nd yr medical students

Lab #1

Slide BB 179 : Osteomyelitis •Describe the microscopic findings in this picture. •What is the most common offending microorganism ? •What does the black arrow represent? •Name 3 complications of chronic osteomyelitis.

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Slide L131: Osteochondroma •Describe the histologic components of this lesion. Which one is truly neoplastic? •Is it a malignant tumor? •Name a genetic abnormality associated with this lesion?

Slide L208: Giant cell tumor • a common benign but locally aggressive bone tumor, belongs to the “Miscellaneous Bone Tumors “ • arise in the epiphysis and involve the metaphysis of long bones around the knee (distal femur & proximal tibia) •usually arise in 20s to 40s. •Prominent non-neoplastic multinucleate osteoclast-type giant cells.

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•Despite the name, molecular analyses have shown that it is the mononuclear cells in the tumor that are neoplastic. •Mononuclear cells express RANK ligand stimulate the development of surrounding non-neoplastic osteoclast-like cells. •Although considered benign, (½ of cases ) recur after surgery

Slide L208: Giant cell tumor

Slide L 213: Osteosarcoma •This is a microscopic picture of a femur tumor in a 21 year old male. What is your diagnosis? •What is the diagnostic histopathologic finding? •Describe the anaplastic features you see in the cells. •Name 2 genetic syndromes associated with this lesion.

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Please make sure to study the following jars from the pathology lab:

• 8/14 chondrosarcoma • 2/14 osteosarcoma (Codman’s triangle) • 5/15 sequestra (osteomyelitis)

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The Vertebral Column

Is composed of 33 vertebrae

5 sacral (fused to form the sacrum)

7 cervical

12 thoracic

5 lumbar

4 coccygeal (the lower 3 are commonly fused)

A typical vertebra consists of: 1-a rounded body anteriorly 2-a vertebral arch posteriorly. They enclose a space called

The vertebral foramen through which run the spinal cord

and its coverings

The vertebral arch gives rise to seven processes:

a-One spinous b-Two transverse c- Four articular

The spinous process is directed posteriorly from the junction of the two laminae.

The transverse processes are directed laterally from the junction of the laminae and the pedicles

The articular processes are vertically arranged and consist of: Two superior & Two inferior processes

They arise from the junction of the laminae and the pedicles .

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The pedicles are notched on their

upper and lower borders Forming

the superior and inferior vertebral notches.

These foramina, in an articulated skeleton, serve to

transmit the spinal nerves and blood vessels.

On each side the superior notch of one vertebra and the inferior

notch of an adjacent vertebra together form an

intervertebral foramen.

The transverse processes possess a foramen transversarium

for the passage of the vertebral artery and veins (note that the vertebral artery passes through the transverse processes C1 to 6 and not through C7).

Characteristics of a Typical Cervical Vertebra

The spines are small and bifid The vertebral foramen is large and triangular

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The first cervical vertebra

THE ATLAS

does not possess a body or a spinous process

It has an anterior and posterior arch

It has a lateral mass on each side with articular surfaces on its upper surface for articulation with

the occipital condyles (atlanto-occipital joints)

and articular surfaces on its lower surface for articulation with the axis

(atlantoaxial joints)

The first, second, and seventh cervical vertebrae are atypical.

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tion with

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The second cervical vertebra

The AXIS has a odontoid process that projects from the superior surface of the body (representing the body of the atlas that has fused with the body of the axis).

or vertebra prominens is so named because it has the

longest spinous process, and the process is not bifid.

The transverse process is large, but the foramen transversarium is

small and transmits the vertebral vein

The seventh cervical vertebra

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Characteristics of a Typical Thoracic Vertebra

The body is heart shaped

The vertebral foramen is small and circular

The spines are long and inclined downward

Costal facets are present on the sides of the bodies for articulation with the heads of the ribs

Costal facets are present on the transverse processes for articulation with the tubercles of the ribs (T11 and 12 have no facets on the transverse processes)

The body is large and kidney shaped

The laminae are thick

The vertebral foramina are triangular.

The transverse processes are long and slender.

The spinous processes are short, flat, and quadrangular and project backward.

The articular surfaces of the superior

articular processes face medially, and those of the inferior articular processes face laterally.

Characteristics of a Typical Lumbar Vertebra

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The sacrum consists of five rudimentary vertebrae fused together Articulations 1-The upper border, or base, of the bone articulates with

the fifth lumbar vertebra 2-The narrow inferior border articulates with the coccyx.

3-Laterally, the sacrum articulates with the two iliac bones to form the sacroiliac joints

The anterior and upper margin of the first sacral vertebra bulges forward and is known as

the sacral promontory The sacral promontory in the female is of

considerable obstetric importance and is used when measuring the size of the pelvis. The laminae of the fifth sacral vertebra, and sometimes

those of the fourth also, fail to meet in the midline, forming THE SACRAL HIATUS

The anterior and posterior surfaces of the sacrum each have four foramina on each side for the passage of the anterior and posterior rami of the sacral nerves

COCCYX The coccyx consists of four vertebrae fused together to form a single, small triangular bone that articulates at its base with the lower end of the sacrum The first coccygeal vertebra is usually not fused or is incompletely fused with the second vertebra.

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Intervertebral Discs Their physical characteristics permit them to serve as

shock absorbers when the load on the vertebral column is suddenly increased, as when one is jumping

from a height. Their elasticity allows the rigid vertebrae to move one

on the other. Unfortunately, their resilience is gradually lost with

advancing age.

Each disc consists of a peripheral part, the

anulus fibrosus, and a central part, the

nucleus pulposus The anulus fibrosus is composed of FIBROCARTILAGE, in which the collagen fibers are arranged in concentric layers or sheets.

The nucleus pulposus in children and adolescents is an ovoid mass of gelatinous material containing a large amount of water, a small number of collagen

fibers, and a few cartilage cells. It is normally under pressure and situated slightly nearer to the posterior than to the

anterior margin of the disc.

The pressure developed in thenucleus pulposus may be great

enough to rupture the surrounding fibrocartilage

(annulus fibrosus). If this occurs, the nucleus pulposus may herniate (protrude) posteriorly

or into one of the adjacent vertebral bodies

This condition is called a herniated

(slipped) disc?!

The disc usually slips posteriorly toward the

spinal cord and spinal nerves.

This movement exerts pressure on the

spinal nerves, causing local weakness and acute

pain

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Curves in the Sagittal Plane In the fetus,

the vertebral column has one continuous anterior concavity

Curves of the Vertebral Column

Toward the end of the first year, when the child begins

to stand upright the lumbar part of the vertebral column

becomes concave posteriorly.

After birth, when the child becomes able to raise his or her

head and keep it poised on the vertebral column,

the cervical part of the vertebral column becomes concave posteriorly

r

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The development of these secondary curves is largely caused by modification in the shape of the

intervertebral discs. In the adult in the standing position the vertebral column therefore exhibits in the sagittal plane the following regional curves:

CERVICAL, posterior concavity THORACIC, posterior convexity

LUMBAR, posterior concavity SACRAL, posterior convexity

.

Abnormal Curves of the Vertebral Column

Kyphosis is an exaggeration in the sagittal curvature present in the thoracic part of the vertebral column.

It can be caused by muscular weakness or by structural changes in the vertebral bodies or by intervertebral discs.

Scoliosis is a lateral deviation of the vertebral column. This is most commonly found in the thoracic region and may be

caused by muscular or vertebral defects

Lordosis is an exaggeration in the sagittal curvature present in the lumbar region.

Lordosis may be caused by an increase in the weight of the abdominal contents, as with the gravid uterus or a large ovarian tumor

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Various conditions may exaggerate the normal curves of the vertebral column, or the column may acquire a lateral bend, resulting in abnormal curves of the vertebral column.

Abnormal Curves of the Vertebral Column

Scoliosis : the most common of the

abnormal curves is a lateral bending of the vertebral column ,usually in the

thoracic region

Kyphosis :(hump) Is an increase in the thoracic curve of the

vertebral column

Lordosis :bent backward

is an increase in the lumbar curve of the vertebral column

Atlanto-Occipital Joints The atlanto-occipital joints are synovial joints that are formed between the occipital condyles, above the facets on the superior surfaces of the lateral masses of the atlas. They are enclosed by a capsule.

Joints of the Vertebral Column

Ligaments Anterior atlanto-occipital membrane Posterior atlanto-occipital membrane

Movements Flexion, extension, and lateral flexion. No rotation is possible

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Atlantoaxial Joints The atlantoaxial joints are three synovial joints: one is between the odontoid processand the anterior arch of the atlas the other two are between the lateral masses of the bones The joints are enclosed by capsules. Ligaments Apical ligament: connects the apex of the odontoid process to the anterior margin of the foramen magnum. Alar ligaments: Cruciate ligament: This ligament consists of a transverse part and a vertical part. Membrana tectoria: This is an upward continuation of the posterior longitudinal ligament. Movements There can be extensive rotation of the atlas and thus of the head on the axis.

The upper and lower surfaces of the bodies of adjacent vertebrae are covered by thin plates of hyaline cartilage. Sandwiched between the plates of hyaline cartilage is an intervertebral disc of fibrocartilage The collagen fibers of the disc strongly unite the bodies of the two vertebrae.

Joints Between Two Vertebral Bodies

Ligaments The anterior and posterior longitudinal

ligaments run as continuous bands down the anterior and posterior surfaces of the vertebral column from the skull to the sacrum The anterior ligament is wide and is strongly attached to the front and sides of the vertebral bodies and to the intervertebral discs. The posterior ligament is weak and narrow and is attached to the posterior borders of the discs. These ligaments hold the vertebrae firmly together but at the same time permit a small amount of movement to take place between them.

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Ligaments

1-Supraspinous ligament: This runs between the tips of adjacent spines. 2-Interspinous ligament: This connects adjacent spines. 3-Intertransverse ligaments: These run between adjacent transverse processes. 5-Ligamentum flavum: This connects the laminae of adjacent vertebrae. In the cervical region, the supraspinous and interspinous ligaments are greatly thickened to form the strong ligamentum nuchae. The latter extends from the spine of the seventh cervical vertebra to the external occipital protuberance of the skull

Joints Between Two Vertebral ArchesThe joints between two vertebral arches consist of synovial joints between the superior and inferior articular processes of adjacent vertebrae The articular facets are covered with hyaline cartilage, and the joints are surrounded by a capsular ligament.

The joints between the vertebral bodies are innervated by the small meningeal branches of each spinal

nerve The nerve arises from the spinal nerve as it exits from the intervertebral foramen. It then re-enters the vertebral canal through the intervertebral foramen and supplies the meninges, ligaments, and intervertebral discs. The joints between the articular processes are innervated by branches from the posterior rami of the spinal nerves

Nerve Supply of Vertebral Joints

naal

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Muscles of the Back The muscles of the back may be divided into three groups: 1-The superficial muscles: connected with the shoulder girdle. 2-The intermediate muscles: involved with movements of the thoracic cage. 3-The deep muscles or postvertebral muscles belonging to the vertebral column

Deep Muscles of the Back (Postvertebral Muscles) In the standing position,

the line of gravity passes through the odontoid process of the axis, behind the centers of the hip joints,

and in front of the knee and ankle joints thus, greater part of the body weight falls

in front of the vertebral column. It is, therefore, not surprising to find that the postvertebral muscles of the back are well developed in humans.

The postural tone of these muscles is the major factor responsible for the maintenance of the normal curves of the vertebral

column.

Superficial Vertically Running Muscles

Erector spinae muscleIliocostalis Longissimus spinalis

Intermediate Oblique Running Muscles Transversospinalis: SEMISPINALIS MULTIFUDUS ROTATORS

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Flexion is a forward movement Extension is a backwardmovement

Both are extensive in the cervical and lumbar regions but restricted in the thoracic region.

Lateral flexion is the bending of the body to one or the other side. It is extensive in the cervical and lumbar regions but restricted in the thoracic region.

Rotation is a twisting of the vertebral column. This is least extensive in the lumbar

region.

Circumduction is a combination of all these movements.

The following movements are

possible: flexion, extension, lateral

flexion, rotation, and circumduction.

VERTEBRAL COLUMN MOVEMENT