Pituitary gland Adrenal gland
Endocrinology
Hypophysis
The pituitary is located under the brain in the sella turcica-hypophyseal fossa of the skull. It is protected by the sphenoid bone wich surrounds it laterally and inferiorly. It is covered
by the diafragma sellae
Is formed by two lobes producing a variety of vital hormones
Anterior lobe
Posterior lobe Neurohy pophy sis
IHAI AAACJS MYPOTHAIAMIC SULC
PAKS   Ii.«.'        i i S
PARS INTCRMCD1A
l»vlFur-Ai">iHi ii y\ft PKOCESS
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PARS DIS1 AUS
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TISSUC
(TRABECULA1
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HOS1ERIOR LOBE
AM IFRIOR IODC
Hypophysial portal circulatinon , Neurosecretion, Portal veins trasport
EMOTION/ INřlUENÍ
HYPOTH ETICA FOR   FSH AND STIMULATION
;XTEROCEPTI
-PARAVENTRICULAR
NUCLEUS
HYPOTHETICAL SITE FOR   STH STIMULATION
HYPOTHETICAL SITE FOR   LH STIMULATION
SUPRA—OPTIC NUCLEUS
HYPOTHETICAL SITE FOR   TSH STIMULATION
i
SUPERIOR HYPOPHYSIAL ARTERY
1
35
NEUROHYPOPHYSIS
-Y
-NEUROSECRETIONS   FROM HYPOTHALAMUS RELEASED    INTO   PRIMARY   PLEXUS OF HYPOPHYSIAL   PORTAL   CIRCULATION AFTER PASSING   DOWN   NERVE FIBERS
YPOPHYSIAL   PORTAL   VEINS CARRY NEUROSECRETIONS   TO ADENOHYPOPHYSIS
SPECIFIC SECRETORY CELLS OF ADENOHYPOPHYSIS
NFLUENCED   BY NEUROSECRETIONS FROM HYPOTHALAMUS
O
o o
I
I I
THYROID GLAND
THYROID HORMONES
CORTICAL HORMON ES
TESTOSTERONE     ESTROGEN PROGESTERONE
BONE, MUSCLE, ORGANS (GROWTH)
PANCREAS
UMPORAI   POlC  OP   BR AIM OP1K. CHIASM RIGHT   OPTIC TRACT PITUITARY GLAND OCULOMOTOR   NERVC (111) TUKFK   CI M CREVJAA MAMILLARY BODIES 1RCJCHILAR   NERVF <IV1 rRlGCMINAI   NERVC (V> AHIMJCCNS   NEWVF <VI> PONS
HYPOTHALAMIC SULCUS ANTERIOR COMMI5SURI-IAMINA  TEHMINA1 IS timer-:   ClNERELI AA
INTER VhNl RICULAR FORAMEN
FORNIX
CI IOHOIO PLEXUS OP 3rd VENTRICLE
Tl IALAMUS
PIWI-AL GLAND
MAMILLARY BODY CHIASMATIC CISTERN OPTIC CHIASM DIACHKAGMA SEILAI-HUUITARY GLAND
H
y p
o
p
h
y
si
INTERPtOUNCULAR CISTERN
NASOPHARYNX
PON I INF CISTERM
Visual Fields
Optic Nerve
Optic Tract
figure*— 29- The most ciommon visual field! defe<zt, bitemporal hemianopiii (black areas of visual fields) cs caused by compression of rhe? posterior aspect of the chiasm {A-y from below. VI suit I disturbances, resulting from com press Ton of the optic nerves, thiasnn, and rracts are Fisted Lit;low. The site of lesion is indicated by nurnber-
Adenohypophysis
anterior lobe is responsible for the production of:
1. STH ( GH) somatotropic or growth hormone
2. ACTH adrenocorticotropic hormone
3. TSH thyrotropic hormone
4. FSH follicle-stimulating
5. LH luteinaising hormone
6. PRL prolactin, luteotropic hormone or lactogenic hormone
Neurohypophysis
posterior lobe is responsible for the sekretion of:
1. ADH antidiuretic hormone, vasopresin
2. Oxytocin
The two hormones are realy built in the hypothalamus. In the neurohypophysis they are only stored and secreted into the blood stream
Adrenocorticotropic Hormone
(ACTH)
ACTH stimulates adrenal glands
An exces of hormone causes Cushing's Deasese Luck of hormone causes Addison's Desease
Adrenal glands
Adrenal cortex
hydrocortison - vital corticosteroid regulate carbohydrates metabolism
aldosteroun - mineralocorticoid regulate mineral metabolism (salt, potassiem , and so water balnace , blood presure)
adrenal androgens - they are not vital steriods
Adrenal medulla part of sympathetic nervous system
adrenalin, nordrenalin acting as vasoconstrictors and cardiac stimulants
Thyroid Stimulating Hormone
• Thyreotropic hormone (TSH) regulates the functional activity of the thyroid gland, it induce thyroid hormon syntehsis and release
• TSH oversecretion induce leds to central hyperthyroidism , it is caused by very rare TSH producting pituitary tumors, it represent less than 1 % pituitary tumors
• Luck of TSH - Central hypothyroidism
Hypothyreosa
Thyreotoxicosis
Somatotropic Hormone
(STH,GH)
Is responsible for growth
Lack of GH in childhood causes Pituitary dwarfism or arrested grows
An excess of GH in childhood causess Gigantism
An excess of GH in adults causess Acromegaly
4.Folicle Stimulating Hormone
Control developement of ovarian follicles and spermatogenesis in the testes
5.Luteinizing Hormone (LH)
In conjunction with FSH induces the secretion of oestrogens, ovulation and corpus luteium production in females and that of testosterone in males.
6.Prolactine (PRL)
• Luteotropic hormone is lactogenic hormone - induces the secretion of milk in the fully developed mammary gland
An excess of PRL - hyperprolactinemia caused by prolactinoma
Prolactinom
galactorea,amenorhea, menstrual irregularitis, decrease or loss of libido- sexual dysfunction, it is causess by prolactin secreting adenomas Prolactinoma
• Galactorea - 50% women, 35% man
• Mikro and makroadenomas ( 10mm)
Prolactinoma - Treatment
Medical management - DOPAMIN AGONIST
normalization PRL level and reversal tumor mass
• tergurid - Mysalfon, dopamin agonist
• bromocryptine -Parlodel, semisynthetic ergot alkaloid, it is dopamin agonist
• quinagolide - Norprolac, nonergot dopamin agonist
• cabergolin - Dostinex 0,5mg tbo , dopamin agonist, has longer duration of action (administrated twice weekly)
Prolactinoma - Treatment
• Radiotion Therapy - linear accelerator radiotherapy is effective in controlling or reducting the size of prolactinomas , but it takes years to achive maximal efekt
Side efekt, pituitary faillure, brain atrophy
• Stereotactic Radiosurgery non-surgical
precisely-targeted radiation small tumors, preserve healthy tissue
• Surgery no very efektiv , relapsing
Cushing's desease - central
hypercortisolism
Adrenal overstimulation by ACTH due to a pituitatry adenoma induced adrenal steroidogenesis of Cortisol, and although aldosteron and androgens
Cushing's syndrome is a collection of signs and symptoms due to prolonged exposure to Cortisol, -excessive cortisol-like medication such as prednison or tumor production of Cortisol
566     THE ADRENAL CORTEX	
TABLE 12—15. Signs and Symptoms of Cushing's Syndrome	
Sign or Symptom	Reported Incidence
Centripetal obesity	79-97
Facial plethora	50-94
Glucose intolerance	39-90
Weakness, proximal myopathy	29-90
Hypertension	74-87
Psychological changes	3 1 -86
Easy bruisability	23 84
Hirsutism	64 81
Oligomenorrhea or amenorrhea	55-80
Im potence	S5-80
Acne, oily skin	26-80
Abdominal striae	51-71
Ankle edema	28-60
Backache, vertebral collapse, fracture	40-50
Polydipsia, polyuria	25-44
Renal calculi	15-19
Hyperpigmentation	4-1 6
Headache	0-47
Exopht ha 1 mos	0 33
Tinea versicolor fnfection	0 30
Abdominal pain	O 21
Adapted from a tabJe in Howlell TA, Rens 1 H,	Hesser CM. Cubhing's syndrome. Cfin
Endocrinol MeLab 1985; 14:911-y 45. CopyriyhL T985,	The Endocrine Society. Drttrh wmma-
rized from Gushing1-4*3 PloLi et al.,1-'-" Ross et aJ.,1MJl	Gold,'1*" Inffcoate et al.^-" Cuhen,LI-7
Liddle,1M;! tJrhanic and Georger1Hllh and Ross ^ind Linch	
Cushing's syndrome
Acne
Facial hirsutism Supraclavicular fat pad
Evidence of bronchial tumour or asth ma treated \A/ith steroids
Polyuria and n octu ría
Renal calculi
Striae
Evidence of rh e u ma to i d arthritis treated with steroids
Loss of st alp hair Plethoric face Moon face
Pigmentation
Ischaemic heart disease or cardiomegaly
Hypertension Pigmentation of scars
— Spinal osteopetrosis Bru ising Thin skin Amenorrhoea
Proximal muscle wasting and weakness
Venous thrombosis
Leg ulceration
.Oedema
Short stature, cessation of growth in children
http://img.medscapexom/pi/emed/ckb/endocrinology/l 16364-
138556-117365-138806.
570 THE
ADRENAL CORTEX
Figure 12-38. Hypothalamic-pituitary-adrenal function in normal individuals (A) and the pathophysiologic aberrations in pituitary ACTH-dependent Cushing's disease (B), primary adrenocortical disease (i.e., Cortisol-secreting adrenal tumor, bilateral micronodular dysplasia, and bilateral ACTH-independent macronodular hyperplasia) CO, ectopic ACTH syndrome (D), ectopic CRH syndrome (E), and iatrogenic Cushing's syndrome caused by pharmacologic dosage of glucocorticoids (F).
CLINICAL DIAGNOSIS Oř CUSHING'S SYNDROME
2 OR 3 24-H URWE COLLECTIONS FOR CORTISOL AND CREATININE
NO CUSHNG'S SYNDROME
CUSHING'S SYNDROME
I
POSSIBLE PSEUDO-CUSHING'S SYNDROME
I
MIDNIGHT PLASMA CORTISOL
CUSHNG'S SYNDROME
I
POSSIBLE PSEUDO-CUSHING'S SYNDROME _I_
"I
NO CUSHING'S SYNDROME
LOW-DOSE DEX SUPPRESSION, CRM-DEX / NALOXONE TESTS
I
CUSHING'S SYNDROME _■ I I
MAJOR DEPRESSIVE DISORDER
2 OR 3 LATE AFTERNOON / MIDNIGHT PLASMA ACTH & CORTISOL MEASUREMENTS
I
HO CUSHING'S SYNDROME
ACTH - DEPENDENT CUSHING'S SYNDROME
HIGH-DOSE DEXAMETHASONE SUPPRESSION TEST
T
ACTH - INDEPENDENT CUSHING'S SYNDROME _I_
ADRENAL CT / MR IMAGING
CUSHING'S DISEASE
I
I
CUSHING'S DISEASE VS. ECTOPIC ACTH SYNDROME
I
SURGERY
0 1 ^-OCTREOTIDE, CT & MR IMAGING. METYRAPONE / CRH TESTS
CUSHING'S DISEASE
CUSHING'S DISEASE VS. ECTOPIC ACTH SYNDROME
I
OPERABLE TUMOR I
SURGERY
INFERIOR PETROSAL SINUS SAMPLING
I-
CUSHING'S DISEASE
ECTOPIC ACTH SYNDROME
PITUITARY CT / MR IMAGING -■-
ABDOMINAL CT / MR IMAGING
T
SURGERY
SURGERY
Figure 12-45. A diagnostic laboratory approach to confirming the existence of Cushing's syndrome and determining its cause.
Cushing's sy therapy
Pituitary dependent ( central)cushing's sy
• Transphenoidal surgery
• Transcranial surgery
• Radiotherapy ( not recomended as a primary treatment)
• Stereotactic Radiosurgery non-surgical precisely-targeted radiation small tumors, preserve healthy tissue
• Medical treatment - metyrapon, aminogluthetimid, ketoconazol/kabergolin, mitotan (adrenolitic agent), pasireotide somatostatin analog5-Signifor
Acromegaly
Gowth hormon exces acting
Acromegaly
Sears of previous pituitary surgery
Field defects
Large nose
Th ick frps, separation of teeth
Skim papillomas
Galaclorrhoea
Hepatomegaly
Carpal tunnel synd rome
Testicular atrophy
vlay be tall stature
."Thick skin folds Prominent supraorbital ridges Ocular palsies Acne
Large tongue
Goitre
Increased sweating
Card iomegaly Hypertension
Lumbar spondylosis
"Thick skin
Increased size of hands {broad)
Osteoa rth r itis
Large, broad feet
Acromegaly
Acromegaly
Acromegaly
Acromegaly
Acromegaly Therapy
• Surgical management -transpenoidal,transcranial
• Stereotactic pituitary tumor ablation by Gama knife
• Radiation - is higly idnividual choise depending on the experience
• Dopamin agonists (Bromocriptin, Cabergolin)
• Somatostatin analogs somatostatin release inhibiting factor receptor ( Octreotid , Lanreotid)
• Growth hormone receptor antagonist
(Pegvisomat)
Neurohypophysis
posterior lobe is responsible for the sekretion of:
1. ADH antidiuretic hormone, vasopresin
2. Oxytocin
The two hormones are realy built in the hypothalamus. In the neurohypophysis they are only stored and secreted into the blood stream
NC'CLEUS
HVHOIHALAMiC ARCA
4
HOS1ERIOR LOBE
AM fFRIOR IODC
Hypophysial portal circulatinon , Neurosecretion, Portal veins trasport
EMOTION/ INřlUENÍ
HYPOTHETIC-A FOR   FSH AMD STIMULATION
ÍXTEROCEPTI
if
-PARAVENTRICULAR
NUCLEUS
HYPOTHETICAL SITE FOR   STH STIMULATION
HYPOTHETICAL SITE FOR   LH STIMULATION
SUPRA—OPTIC NUCLEUS
HYPOTHETICAL SITE FOR   TSH STIMULATION
i
SUPERIOR HYPOPHYSIAL ARTERY
1
35
NEUROHYPOPHYSIS
-Y
-NEUROSECRETIONS   FROM HYPOTHALAMUS RELEASED    INTO   PRIMARY   PLEXUS OF HYPOPHYSIAL   PORTAL   CIRCULATION AFTER PASSING   DOWN   NERVE FIBERS
YPOPHYSIAL   PORTAL   VEINS CARRY NEUROSECRETIONS   TO ADENOHYPOPHYSIS
SPECIFIC SECRETORY CELLS OF ADENOHYPOPHYSIS
NFLUENCED   BY NEUROSECRETIONS FROM HYPOTHALAMUS
O
o
o o
I I
I
THYROID GLAND
THYROID HORMONES
CORTICAL HORMON ES
TESTOSTERONE     ESTROGEN PROGESTERONE
BONE, MUSCLE, ORGANS (GROWTH)
PANCREAS
Antidiuretic hormone (ADH)
ADH preventing excessive loss of water in the urine, thus causes water to be retained by the kidneys
• Luck of ADH causes Diabetes insipidus
It has aditional property of causing the blood presure to rise. So it has alternative name Vasopresin
Oxytocin
Oxytocin acts on the smooth muscle of the uterus at the end of pregnancy.
It initiates labour and promotes lactation
The sellar patology
Nonsecretory adenoma Nonpituitary sellar mass
Craniopharingioma, Menngeioma, Granulomatosis lymf ,Sarkoidosis
Hypophysitis Empty sella
Pituitary apoplexy (Shihan's sy) Nelson's syndrom
Pituitary
failure picture
PANHYPOPITUITARISM
•ANTIDIURETIC
HORMONE
Dľí-ICIENT
>- f EXTENSIVE TUMOR
S I   (USUALLY CRANIOPHARYNGIOMA)
~< POSTSURGICAL
y    OCCASIONALLY GRANULOMA
m [  OR TRAUMA
GONADOTROPINS DEFICIENT
TSH
DEFICIENT
■MSH
DESCENT
'S"
DIABETES INSIPIDUS (LATENT UNLESS ADRENAL CORTICAL HORMONES ARE PRESENT OR ADMINISTERED)
FEMALE ADULT
DECREASED DECREASED LIBIDO, ASPERMIA, LIBIDO, LOSS OF SOME AMENORRHEA FACIAL AND BODY HAIR
w
IBA
Tg"
STI-I
DEFICIENT
\
HYPOTHYROIDISM
ADRENAL CORTICAL INSUFFICIENCY
PALLOR
CHILD
DELAYED PUBERTY (DEFICIENT GROWTH PRECLUDES EUNUCHOID HABITUS)
DWARFISM, MUSCLE LOSS AND MICRO-SPLANCHNIA, TENDENCY TO HYPOGLYCEMIA
Adrenal failure
Addison's
Easy to diagnose and treat -- if you think of it.
Di
normal adrenal
Addison's frojrjTB
autoimmune Addison's
iron overload
	
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ACTH stimulation test
hypotension hyperkalemia
sudden death
weight
loss
Normal Adrenal
insufficiency
Repeat: Improvement suggests pituitary disease ("secondary Addison's"); no improvement indicates primary adrenal disease.
Pituitary failure
5><r_:ar of previous -pituitary surgery
Optic atrophy,' I ompo rci I í i < • l<i defecrt
Fine scafp hair
( ~>cular palsies Wrinkling sfon
Galactorrhoea _ Pailor of nippJe; Hypotension _
Evidence of previous a c: rom ega ly or Cushtng's syndrome
Loss of body hair
Plump with_ fema le distribution of bodv fat
Skin dry, pale, fin
Atrophy of testes
Loss of muscie bulíc.
Ji
<_ i rowt h :
Increased if gonadotrophii failure alone, decreased if g;rowtb hormone fsiifurc
APS l.,2.- hyperpigmentace, addisonova choroba
APS l.,2.- grafitové skvrny
o
DOIA
(c) University Erlangen, Department of Dermatology Phone: (+49) 9131 - 85 - 2727
APS 1., 2.-addisonova choroba
APS L,2. - addisonova choroba
APS l.,2. - hyperpigmentace
DOIA
(cj University Erlangen, Department of Dermatology Phone: [+49) 9131 - 85 - 2727
Primary hyperaldosteronism
• Adrenal cortex adednoma producting aldosteron
Terapie: Spironolakton
Surgery - adrenalectomia
Primary aldosteronism
Papilloedema (very rare)
Po s it ive
Chvostek's sign
Oedema (rare)
F<ZC_. changes, hypokafaem fa
Hypertension
Polyuria, _
glycosu ria
_ Adrenal tumour,
very rarefy palpabJ
rvluscle weakness or paralysis
Ji
Pheochromocytoma
Adrenal medulla tumor producting adrenalin, noradrenalin acting as
vasoconstrictors and cardiac stimulants
Terapie Adrenalectomia
Alfal-adrenoreceptor block
Doxazosinum ( Zoxon tbl) ,Prazosinum ( Deprazolin tbl)
Phaeochromocytoma («ancJ associated conditions)
Hypertensive changes i n fti rid i
Facial haemangioma Café au lait spots -
Sweat! r t-g _ Epiloia
and neurofibromata
fvAed u I lary carcinoma of thyroid
"Tachycardia and palpitations
Hype rtension
Adrenal tumour
Thank You