You are on page 1of 10

PITUITARY HORMON ANTERIOR LOBE:       Growth hormon (GH) Prolactin (PRL) Adrenocorticotropic hormone (ACTH) Thyroid stimulating hormone (TSH

) Luteinizing hormon (LH) Follicle stimulating hormone (FSH)

POSTERIOR LOBE:   Arginine vasopressin (AVP)/ Antidiuretic hormone (ADH) Oxytocin

HYPOTHALAMUS HORMON        GHRH (GH Releasing factor) PIF (Prolactin inhibiting factor) ACTH RH (ACTH Releasing factor) TSHRH (TSH Releasing factor) LHRH (RH Releasing factor) FSHRH (FSH Releasing factor) MIF (MSH Inhibiting factor)

HYPOPITUITARISM    HYPOTHALAMIC OR PITUITARY DYSFUNCTION HORMON DEFICIENCY SINGLE OR MULTIPLE ETIOLOGY OF HYPOPITUITARISM

= Mass lesions  metastatic Ca, adenoma, granuloma, craniopharyngioma, meningioma, chondrosarcoma, germinoma, glioma, chordoma of the clivus, Rathke’s cleft cyst, apoplexy, Langerhans cell histiocytosis, MEN 1 (multiple endocrine neoplasia type 1/ pituitary & parathyroid & pancreas tumors) = Diseases  Sheehan’s syndrome, autoimmune hypophysitis, encephalitis eclampsia, sickle cell anaemia, African Tripanosoma = Genetic  Kallmann’s syndrome: isolated gonadotropin deficiency + unilateral agenesis renal + cryptorchidism, nystagmus, cleft lip, bilateral synkinesis, high arched palate

feet or gigantism if occur before epiphysis closed . lentigines. hemochromatosis. aneurysma subarachnoid hemorrhage GROWTH HORMON   EXCESSIVE GH SECRETION Disease : Acromegaly/Gigantism Essential marker Dx: .Excessive growth of internal organ . ca bronchial.GH not severe decreased after 1 hour OGTT AETHIOLOGY      Mostly macroadenoma May be associated MEN 1 Part of Mc Cune Albraight Syndrome Part of Carney syndrome (atrial myxoma. longterm intrathecal opioid. sweaty & soft handshake . loss of visual field. adrenal hypercortisolism) Ectopic secretion GHRH/GH by lymphoma.Excessive growth of external organ : jaw. mandibulae & skull enlarge. stroke. hoarseness. surgery. hypothalamic tumor. trauma. hand. methadone = Hypopituitarism without mass lesions  idiopathic. feet growth = Facial bone.Insulin like growth hormon (IGF-I) increased . sinus.Headache. pancreatic tumor CLINICAL SIGN Acromegaly : = Extremity enlargement growth developed after closer of epiphysis  finger widen. extreme prolonged exercise. sleep apnea . carpal tunnel syndrome. radiation. malnutrition. hypertrophy pharynx & larynx tissue  deep voice. CABG.= Physiologic isolated hypogonadotrophic hypogonadism  severe illness. teeth space wider =Macroglossia. obese DM type 2. amenorrhea. asthenia. acoustic neuroma.

free T4 decreased RADIOLOGY & IMAGING    X Ray finger & toes (tufting of terminal phalanges & foot (thickening hell pad). skull (enlarge sella & thickening skull) CT Scan. because of fibrous dysplasia of skull base Cabergoline drug Pegvisomant (GH block/GH receptor agonist) Octreotide injection SC Lanreotide injection SC GH DEFICIENCY    Central obesity mild to moderate Increased systolic BP Increased LDL-cholesterol . enlarge. colon polyps. muscle & fat & bone. DM. showed the pituitary tumor.optici suppressed can cause hemianopia = Hypertension LABORATORY         IGF-I Increased up to 5 x PRL/ prolactin mostly increase OGTT  IGT. DM SGOT/SGPT mostly increased Ureum & creatinine mostly increased Ca serum (hyperparathyroidism) Anorganic P increased TSH increased . vertebrae overgrowth & spinal stenosis. cardiomegaly & heart failure. hepatomegaly. skin papilloma. acanthosis nigricans = Supra sella tursica growth tumor : chronic & severe headacne. arthralgia. Chiasma n.=Enlargement of the internal organ & skin : goiter. more superior then CT Scan MANAGEMENT       Micro surgery operation : endoscopic transnasal transsphenoidal pituitary operation  Adenoma extirpation & removing Difficult technic for Mc Cune Albright syndrome. showed the pituitary tumor MRI. cystic acne. weight gain.

Hydrocortisone tablet . infiltration to sella tursica for example : adenoma chromophob/acidophile. craniopharyngioma.DHEA (dehydroepiandrosterone) .MRI supra seller mass/sol/tumor etc MANAGEMENT a. LH. cerebrovascular bleeding. Sheehan’s syndrome. Hormon substitution therapy .Estrogen tablet/cap – Etc. TBC/fungal meningeal spreading to pituitary. DE. Deficiency : GH. others SOL (Space occupying lesion) in supra seller . Transsphenoidal operation : removing pituitary tumor b. TSH. FSH.carotis interna. amenorrea     ACTH deficiency  cortisol/adrenal hormon deficiency  symptom & sign like Addison’s diseases TSH deficiency  hypothyroidism symptom & sign  cretin.rhGH injection . LH deficiency  androgen & estrogen deficiency  lack of libido. mixoedem PRL deficiency  lactation disorder MSH deficiency  look pale RADIOLOGY .   Small heart and reduction cardiac output Asthenia May occur combine pituitary hormon deficiency  Panhypopituitarism PANHYPOPITUITARISM Several pituitary hormon deficiency Developed due to PROP 1 gene mutation. aneurisma a.Levothyroxine tablet .CT Scan hypophysis tumor. . ACTH Clinical sign depend on the pituitary hormon deficiency  GH deficiency syndrome Gonadotropin deficiency  FSH.

CORTEX : -CORTISOL -ALDOSTERONE -ANDROGEN B. MEDULLA : -EPINEPHRINE -NOREPINEPHRINE GLUCOCORTICOID PHYSIOLOGIC EFFECT  Stimulate gluconeogenesis & decrease cellular glucose use  Mobilize amino acid & fatty acids  Inhibit the effects of insulin  Give rise to ketone bodies in metabolism (ketogenesis)  Elevated RBC & platelet level  Exhibit anti inflamatory effects e. Pai due to steroid withdrawal much more.INTRODUCTION Insufficiency adrenal produced  Deficiency adrenal hormon  Primary (adrenal gland) Secondary (pituitary gland) Tertiary (hypothalamus) INCIDENCE & PREVALENCE   Estimate incidence in the developed world 0. depletion eosinophils & lymphocytes. inhibit IL2.g. stimulate PMN. 2007)  ADRENAL HORMON A.000 population (Stewart. 2003) Incidence Primary adrenocortical insufficiency (Pai) UA western population nearly 50 cases per 1 million. vascular response to vasoconstrictor.8 cases per 100.2007) Pai has multiple etiologies. reduction circulating lymphocytes (>T cell) . however 80% caused by autoimmune adrenal destruction in USA (kevin K. occur approximately 6 million in the USA (Kevin k. increases capillary permeability.000 & prevalence 4-8 cases 100. reduction adherence of macrophage to endothelium.

gut. fungal. CMV. IDDM. hypothyroidisme. mucocutaneus candidiasis. eosinophilic granulomas)  Secondary tumor (breast. secretion K & H ion Aldosterone excess : retension Na. dental enamel hypoplasia. sarcoid. BILATERAL ADRENECTOMY B. alopecia. salivary & sweat gland Kidney : stimulate reabsorption Na. Autoimmune polyendocrine syndrome II (APS II): Addison’s. ADRENAL HEMORRHAGE (Waterhouse Friderichsen syndrome)  meningococcus septicemia 7. hemochromatosis 6. ADRENOLEUCODYSTROPHIES 8. gonadal failure) 2. vitiligo.MINERALOCORTICOID PHYSIOLOGIC EFFECT     Primary action aldosteron : to renal. bronchus)  Sheehan’s syndrome  Pituitary irradiation  Idiopathic . hyper K & acidosis ADRENAL ANDROGEN HORMON   ANDROSTENADIONE DEHYDROEPIANDROSTERONE (DHEA) ETIOLOGY INSUFFICIENCY ADRENAL A. INFILTRATION: Amyloid. HIV 4. hypogonadism. PRIMARY: ADDISON’S DISEASE 1. craniopharyngiomas  Pituitary apoplexy  Granulomatous diseases (Tbc. Autoimmune polyendocrine syndrome I (APS I) (Addison’s. METASTASIS TUMOR 5. CONGENITAL ADRENAL HYPOPLASIA 9. SECONDARY ETIOLOGY  Exogenous glucocorticoic therapy  Hypopituitarism  Removal ACTH secreting pituitary adenoma  Pituitary tumor surgery. ACTH RESISTANCE SYNDROME 10. INFECTIONS: tbc. hypo K & alkalosis Aldosteron deficiency : increase Na loss. pernicious anaemia 3.

eosinophilia Hyperpigmentation or vitiligo Other autoimmune endocrine deficiency LABORATORY FINDING IN PRIMARY ADRENAL INSUFFICIENCY     ANEMIA EOSINOPHILIA AZOTEMIA HYPONATREMIA 40% 17% 55% 88% . vomiting. hyper K. TIREDNESS. azotemia. hyper Ca. history weight loss & anorexia Acute abdomen/pain Unexplain hypoglicemia Hypo Na. hypotension or shock Nausea.   Lymphocytic hyphophysitis POMC processing defects POMC gene mutation PRIMARY ADRENAL INSUFFICIENCY SYMPTOM            WEAKNESS. FATIGUE ANOREXIA GASTROINTESTINAL SYMPTOM Vomiting Nausea Constipation Abdominal pain Diarrhea SALT CRAVING Postural dizziness Muscle & joint pain 100% 100% 92% 86% 75% 31% 31% 16% 16% 12% 6-13% CLINICAL SIGN      Weight loss Hyperpigmentation Hypotension (<110mm Hg systolic) Vitiligo Auricular calcification 100% 94% 88-94% 10-20% 5% CLINICAL & LABORATORY ADRENAL CRISIS        Dehydration.

Treatment with dexamethasone allows ACTH stimulation testing without affecting or interfering with the measurement of serum cortisol levels.) Low dose ACTH stimulation test Overnight metyrapone test CRH test Auto AB-21 hydroxylase THORN Test Insuline tolerance test Glucose tolerance test RADIOLOGY    COMPUTED TOMOGRAPHY SCANS MAGNETIC RESONANCE IMAGING ULTRASONOGRAPHY Other Tests  Adrenocorticotropic hormone stimulation test  Note: Inemergent situations.  Repeat cortisol levels every 30 minutes (some authors recommend 60 min) and 6 hours after ACTH administration  Normal response is indicated when the cortisol level doubles in response to ACTH stimulation  In adrenal insufficiency. do not delay treatment of presumed adrenal insufficiency during diagnostic testing.  Obtain baseline serum cortisol and ACTH levels  Administer 0.   HYPERKALEMIA HYPERCALCEMIA HYPOGLICEMIA 64% 6% <3% LABORATORY TEST (PRIMARY ADRENAL INSUFFICIENCY)           Basal plasma & urine cortisol low ACTH stimulation test (tetracosactrin iv/im) Prolonged ACTH Stimulation test (differ primary & secondary adrenal insuff. serum cortisol levels fail to rise after ACTH administration Electrocardiograph (ECG): Elevated peaked T waves may indicate hyperkalemia 24-hour urinary cortisol: Use only in nonemergent situations   .25 mg (250 mcg) of cosyntropin (synthetic ACTH) IV/IM.

dexamethasone (4 mg IV) can be used instead of hydrocortisone to avoid interference with testing of cortisol levels Administer fludrocortisone acetate (mineralocorticoid) 0.2 mg/day replacement mineralocorticoid .TREATMENT : ACUTE ADRENAL INSUFFICIENCY  CRISIS SHOULD NOT BE DELAYED WHILE WAITING FOR DEFINITIVE PROOF OF DIAGNOSIS  BASED ON CLINICAL & LABORATORY FEATURE OF AN ADRENAL CRISIS Emergency Department Care (KevinM Klauer. Ohio UC Osteopa. breathing and circulation Employ coma protocol (ie. thiamine.m.1 mg qd Always treat the underlying problem that precipitated the crisis     Imaging Studies   Chest radiograph CT scan  A CT scan of the abdomen may slow hemorrhage in the adrenals.hydrocortison 12. a head CT scan may show destruction of the pituitary (ie. During ACTH stimulation testing. calcification of the adrenals (seen with TB). or metastasis  In cases of secondary adrenal insufficiency.5 mg/2 – 3x/day -deoxycorticosterone trimethylacetate 1 cc im every week -DOCA (Deoxycorticosterone acetate) 25 mg/mouth -Fludrocortison 0. glucose.05 0. empty sella syndrome) or a pituitary mass lesion TREATMENT: CHRONIC ADRENOCORTICAL INSUFFICIENCY  SUBSTITUTION TREATMENT . 2007)     Maintain airway. naloxone) Use aggressive volume replacement therapy (dextrose 5% in normal saline solution [D5NS]) Correct electrolyte abnormalities as follows:  Hypoglycemia (67%)  Hyponatremia (88%)  Hyperkalemia (64%)  Hypercalcemia (6-33%) Use dextrose 40% as needed for hypoglycemia Administer hydrocortisone 100 mg IVP q6h.

Consultations  Endocrine consultation following admission is beneficial. Emergency management should be implemented in the ED prior to consultation when sufficient clinical suspicion for this diagnosis exists  ICU admission is necessary fo most patients with acute adrenal insufficiency and adrenal crisis CONCLUSION  Incidence Primary adrenocortical insufficiency (Pai) 50 per 1 million. otherwise we are loosing a golden periode of treatment   . secondary: steroid withdrawl approximately 6 million in USA Pai has multiple etiologies.000 (Western). a general internist can manage the process. prevalence 4 to 11 cases per 100. If no endocrinologist is available. however 80% cases are caused by auto immune adrenal destruction Awarenss to clinical & laboratory Pai & secondary adrenocortical insufficiency is very important.