Hypothalamus produced, 1 postr put one joc "prostaglandins stil sustain uterine contraction Develop benign prostate Fyperplaia ‘Lact Mal: testosterone production [Both sox Might result In depression Ant-Diuretic Hormone= arginine Regulation TEWery, siress, organ fare ote -SIADH vasopressin (AVP). + Osmoreceptors @ hypothalamus {Cancer surgury. bacterial *Barorocoplors @ eafoid sis aortic ach __JOeantal Pineal Gland Parainyrad Glands Panereas parathyroid hormane (PTH) alum and phosphorous levls-bone development recognition Insulin, Glucagon ‘bleed glucose levels ‘.pjrect measurement of blood hormone level 4. Screening Free thyroxine level of newbom for {2g-Cushing syndrome congenital hypothyroidism {UGircacan hr comparison at roughdeak 2.24-houre urine res corsa (UFC) 3Saiva 2. Diagnosis + Hyper-o: hypo-secrton slates ‘dently orighn ofthe cisorde ‘cate the dseated ogan(s) *Coeato the eausatve tumours) Complete surgical removal of causative tumour 69. Inta-opeatve blood Parathyrod Hormone (PTH level determination Adoquacy of exogenous homars ralacamant therapy 19. Bod thyroxine level fe Faves disease patent after complete thucidaciomy, + General nypapiutarsm due o lular macroadenoma 2.Dyramic Function est 22 blood samples 4-Avaferent ime point of the day eg. moming and evening corto! “anpropriate RI 2. Under dierent Candons to assess the intogriy ofthe corre 9. High Talovel1"2"tet 2. Treatment Mentoring + Stimulation test ~ Suspected hormone Aotcioney 29, fcortsol for Addzon's + Suppression lest Suspected hormone 29, Jeortsl for Cushing mocha Me typotalamic. 99. Hypopittarsm-s "2° ititarcond organ axis Tp test Piutanrendorgn ex y"nguiminéuced hypoalesemia to og. Hyperpititrism stale) ‘Growth Hormone-Glucose loading est GH ACTH} Corto! 7549 antysrousghicose-S0minxs 207TRH—tProlacting TSH jou—iGHetmiut 3. YGnRH_sTeSH aL “tno supression- AcromegahiGigantism ‘Syr-actortost-ACTH stimulation Doxs-motha-sone™=ACTH suppression Sed TRH stimulation tos: sorum TSH ftom thyroid resistant voryrometabole dys hypothyroidism Investigation of Amenorrhoea Investigation of Hypogonadism in Male Differential Further " " - _ FoH| uM) E2 pre] Direct | ecemiration| |FSH|LH|PRL|TEST| Differential Diagnosis N |B] | ~ | Polycystic ovaries | ovarian scan -|-|B- Pituitary neoplasm tty - Se ccaas : BIB) - | | | Primary testicuiar damage Hypothalamic GGG | nse esetncton 5 BIN | - | N | sertotic cet dysfunction y vig t Hyperprolactinaemia 5 y 4y . y Hypothalamio ptutaryHypothalamus ‘Anterior Pituitary gland ‘Thyroid gland {Thyroxine binding globuln uring pregnancy Hypothalamus ‘Anterior Pituitary gland Liver, pancreas HPT axie_MetabolieméBiochem homeostasis Hartinjeye big boss ‘Thyrotrophin + Releasing Injury or tumour ofthe hypothalamus +Hypothyoidism.underactive thyroid gland Hormone-TRH Puitary-»Prolactn®RL + Rogulations ‘itutary benign tumour-»Prolactinoma lactation 4. Hypothalamus cure by drug mimic dopamine Regulate the immune system STRH(H)* Dopamine "Pregnancy, HypoThytoidsm, Medication reduce dopamine action 2. Posterior pituitary gland “milk overpraguction, amenorrheae =oestragenitestosterone defcioncy *Oxytocin(+) «Anti-iuretic hormone 3. Oestrogen(+) {Hypopitutariem-reduced immunity, insuficint mike Thyroid ‘Stimulate the release of prolactin Stimulating ‘Actas a neurotransmitter ormone-TSH ‘ SHyperpluitariem-excossive secretin of hyrod hormone T + HypoThyradism / Underactvethyrod gland due to necclent secretion of thyroid hormones BME-vet> ‘Somatostatin + Genetic conditions {+Hypoptutarism- nsuficent TH THypertyrodism / Overactive tiyroldgland-excossive TH secretion inactive Thyroxine (4) Control Metabolsm, Muscle, Brain, Bone, Heart ‘AMhyrotoxicosis] -Goitre sR RMD Primary causes + Graves’ diseasc32IR “Titiodo-thyronin (T3) + Benign tumourfintammation ofthe thyroid Direct secret20% or iverBkidney _-—-Steandary cause: conversion *Hyperpiuitarsm 4 Hypothyroidism 4+/Autoonmune diseases 0.9. Hashimoto's thyroicitis, Congenital Hypothyrodisum HPG* axis_slop, food intake, stress, exercise and memory CGroweh hormone 1 Hypothalamic or Ectopic (FR) releasing tumours hormone 4 ‘Somatostatin Excercise **Somatostatin=Growth hormone FoRH r . Inhibitory hormone (GHIN) {cr 41s Growth Ez Hormone Promote child growth Maintain adults normal body structure and metabolism. e.g, Blood Gla + Piutary adenoma ~Criren GiantsmiAdul Acromegaly 4 Genetic mutation or pituitary gland injury sDwarism insulltke growth factor 1 ( F Somatastaint Diadotes metus Gallstones fat intolerance and diarrhoea?Hypothalamus Coeotopin| Releasing Hormone “Circadian rythm Dileront Reference ‘Highest a= 8 am. * Lowest midnight ‘Anterior Pituitary gland Arena tropic Hormone both Sterol onmons—+ CGucocorteoid corsa! Mineral corbcoid *Aicestrene ‘kcadian rhythm ‘Stimulated by svesses 1 relay adenoma 1 sCushing’s disoase-iyporiulaism | Eelope ACTH tumour-Smat cl ng cancer (SCLC) 1 -Congental adronal hyperplasia (CAH}-Genetic Gisordor wih inadequate production of cares, 1 -Aiddson’s dlsease-Adional isutciency + Contra boos sugar levels + Regulate motabelgry {Reduce inflammation + Asst memory formulation * Conta boos pressure via equating sa and water * Support the developing fetus curing pregnancy 8p Contoed by RAASystem{Renin Angiotensin Algostrone Increase potassium excretion in urinereatscrption of Nadvater 16s ‘Androgen(sex hormones)-estarone ‘Acranal Glands (Mecuta) "Non soos hormone ‘Adrenaline! spineptrine "Nog feedback ‘mechanism mesales by presynaptic ‘renaceptore (or)ecrenatina! spinephnine| Newrtranemiter chemical mediators Fagrignt “Aes sressllstuaton-oNerve Tigers adeonating “Crronle-+1ACTH-+toortscltmetanolsmiblood Gly Addison's ease: ‘SHypopsutrien/Sie effect of puatary surgery or radation therapy Cushing syndrome Adrenal sumeur i male [Cushing Syndrome 4 Stross ~Thiggr @ combination ofhormones & nerves signals 2rkcaion Side Effects Mimic potentate cortisol ‘tec 43:1-Adrenal Glas Tumours - excessive carta! 42°Phutary Ghnds ~ excessive ACTH ityperpitutatsm {Benign puter adenomastRm * Cancorousputaryturours Hypotension, Hyperkalaoia Lethargy/soopy 5S ypoatdosteonism Rare 2 Primary ~ Damaged advenal lands resulted in ‘Addison's Disease tAceenal tumours ma Produced and released continuously and mainly rom nerve endings of sympathetic nervous system + Mawiaia@ eontnuous low level af acvty of he sympathete nerwous system {Siero therapy = prolonged / excessive Polenaly Wfebvoatoning i not voalod promptly Critical hvponatrasmia adrenocortal decency + Damages aarena lancs resus in Addison's Disease dusto atommunty oT "acute adrenal eutcency Adrenal enzyme defects ~ Deficiency of: *rrexhydronjage* Mi ehysronylase * Z1-ahydronyase»CAH Congenital adronal hyperplasia (Rare inverted autosomal recessive iorcer) 2° Hypopititarsm - Release insuteiant aroun of ACTH “ortay- Hypothalamus disorder |CRH-»ACTH 1 Hyporaldosteronism_-Hypervoliomi, Hypertension, Hypokalasria Primary alfosteroriam=Conn's syndrome + idopathic bilateral adrenal hyperplasat 22078 LMR “Excessively secreted by acral gi “Low rans levela due to negative fascback od “adverse group of seeders characterized by physiologic actin of the RAA systor + Usual elated to auc ronal blood flow 0.9, blockage or narowing of ‘he unalarien.Hypothalamus. Gonadotropin sean Posterior Folia Piuiary gland Stintating rane Formene Letonisng Hormones ovary Simanoroea in female “te of sperm production in mak "Ptr adeno “Overproducien a tsiesterone or cesvogen Male: spematoganesis by Sora cols of Fomale: Stimulates te growth of ovarian Incrasos ssstadslE (ossrasn) Male: Stmulates Ley cls nthe testes production, generals malo a2 sxual haractreiee Female: *-20k 162 ‘surge ovulation (may eriieaton Tosierone Esvogon gp of E132 ik Folcaar phase Progesteronolt LH SugeSovatton-scopus teu" Lata pao! {Hypotalamus vaumal {iefiann'® syndrome in male: Los ofthe davelapment of GoRH producing nerve call *Quatan hyperstimulation sydrome-Rare pur contons “Zhtaring ote ovaries “ Botenaly dangerous accumulation of Mud inthe abdomen leads to pain inthe pelvic area “primary satan or testeula alu Hypergonadotrophic hypogonadism(aonads 5%) | Wale-Kinetaters syndrome OY) + Femal-Turmer syndrome (60) _Kaliman's syndrome-co- Hypegenadtrophis hypogonadism’ |GrRH ‘Klieflter's syndrome XY/Turner syndrome (XO) 1 Premature vain fare ‘ Polyeystic ovary syndrome (PCOS;-male sono hormone | Male: Kallman’ syndrome {Pemel: Secondary vata falure Phar gland or Hypobwlamus pb + Produce by (ys cls Functions uring fost development tates the development ot ‘rao siral rd excema rope oan 2' Fer puna” sexval cara dovelopment 5. Estonia fr sperm production a make 4 Regulates the secotion of LK FSH 2 estodae tumour “androgen = Aaron tumour *Congental adrenal hyperplasia (CAM) Chien oth se + False growth spurt {Show sgns of ear puberty 5, Eraures that mussias and banes stay song ding and —~ Adults aes puberty Precocious puberty 6. Sra th body to make now blond calls “rity Female: ‘WVatraton and maintain te eproducive estan “Level netasued uring menstusin Tor ‘Ea maluzaton and then ovulation Greer f opener feo 2 Titkenng of te uta tng for mplantaton of ides Usps ec ‘eas {Poorly uncioned ovaries + Maina normal menstrual cycle 2 Maina tn ea sages of prognaney 4. Fetal development 4: Sangin pel wall muscles preparing orl + Cargo acon! byperpbia (CA) sason 1 etegul and Nea renal leeding 23. Dropin progesterone ering prognancy Nescarage or Ear lab Inadoquateproducon of cortsl inguffcont Aenaine Cushing hyperotutaram 17 testes mat + Tuma and blood supply intaruption fo the testes “Infant he tests (Otee AL) * Gaematherany of testicular carcor “etapa dorses o.9. Heemoctromatoae (can, ‘aon totes) Feyponitcinrien’ Dystuncton, Tumour “roeta devetoament Male characteristics may not completly dovtop SRleory.nonsbvlousinsticion 2" chara {Gincal resonations + Delay puberty development in gts “Inadaguata bone gow + Osteoporoes “erty fomate + Fatgue Mood sings tury agenoma-Hypoptatansn ‘cnt (excess 2ACTH (Excess 2 Growth Hormone (Excess ‘3 Coral xcoss