Endocrinology PDF Study Notes

Endocrinology Dr. Mohamed Roshdi ,MD Assistant Prof. Internal medicine  Learning Objectives Knowledge Relate pathophysiological basics and etiology of thyroid, parathyroid, pituitary and adrenal gland disorders Describe epidemiology, manifestations, complications and management of thyroi...

Endocrinology Dr. Mohamed Roshdi ,MD Assistant Prof. Internal medicine  Learning Objectives Knowledge Relate pathophysiological basics and etiology of thyroid, parathyroid, pituitary and adrenal gland disorders Describe epidemiology, manifestations, complications and management of thyroid, parathyroid, pituitary and adrenal gland disorders Skills Interpret clinical manifestations and investigations of thyroid, parathyroid, pituitary and adrenal gland disorders to formulate reasonable diagnosis. Apply evidence-based management plan for thyroid, parathyroid, pituitary and adrenal gland disorders Distinguish patients in emergency situations to formulate a comprehensive management plan; ensuring keeping patients in normal homeostasis The Thyroid Gland and Thyroid Hormones Anatomy of the Thyroid Gland  The thyroid gland function: is to secrete a sufficient amount of thyroid hormones & the parafollicular cells secrete calcitonin (an important factor for Ca.homeostasis). Follicles: the Functional Units of the Thyroid Gland  The Thyroid Produces and Secretes 2 Metabolic Hormones Two principal hormones – Thyroxine (T4 ) and triiodothyronine (T3) Required for homeostasis of all cells Influence cell differentiation, growth, and metabolism Considered the major metabolic hormones because they target virtually every tissue  Iodine Sources Available through certain foods (eg, seafood, bread, dairy products), iodized salt, or dietary supplements, as a trace mineral The recommended minimum intake is 150 g/day  Production of T4 and T3 T4 is the primary secretory product of the thyroid gland, which is the only source of T4 T3 is derived from 2 processes – About 80% of circulating T3 comes from deiodination of T4 in peripheral tissues – About 20% comes from direct thyroid secretion  Carriers for Circulating Thyroid Hormones More than 99% of circulating T4 and T3 is bound to plasma carrier proteins – Thyroxine-binding globulin (TBG)75% – Transthyretin (TTR), also called thyroxine-binding prealbumin (TBPA) 10%-15% – Albumin binds about 7% Carrier proteins can be affected by physiologic changes, drugs, and disease Only unbound (free) hormone has metabolic activity and physiologic effects – Free hormone is a tiny percentage of total hormone in plasma (about 0.03% T4; 0.3% T3) Thyroid Hormone Action  Effects of Thyroid Hormone Fetal brain and skeletal maturation Increase in basal metabolic rate Inotropic and chronotropic effects on heart Increases sensitivity to catecholamines Stimulates gut motility Increase bone turnover Increase in serum glucose, decrease in serum cholesterol Thyroid Hormone is Critical for Normal Bone Growth and Development T3 is an important regulator of skeletal maturation at the growth plate – T3 regulates the expression of factors and other contributors to linear growth directly in the growth plate – T3 also may participate in osteoblast differentiation and proliferation, and chondrocyte maturation leading to bone ossification  Control of thyroid function ▪ Hypothalamic- pit- thyr. Axis Hypothalamus  TRH.  ant. Pituitary  TSH.  thyroid hormone secretion. Thyroid-Stimulating Hormone (TSH) Regulates thyroid hormone production, secretion, and growth Is regulated by the negative feedback action of T4 and T3  Abnormalities The major abnormalities in the function of the gland are hypo- and hyperthyroidism. They occur when the hormone secretion is disturbed. Thyrotoxicosis & Hyperthyroidism Thyrotoxicosis: a clinical syndrome resulting when tissues are exposed to high levels of circulating thyroid hormones. In most cases, thyrotoxicrisis is due to hyperactivity of thyroid gland. i.e. hyperthyroidism. HYPERTHY Von Graefe'ssign ·The upper eye lid lags the eyeball asthe patient is asked to look downwards. Joffroy'ssign Absence of wrinkling on the fore head when the patient looks upwards with the face inclined downwards H Y P CJ U -V 1 PEl R 11Vl IR O l D 11SM " J l'WlctilD llSM D RY HAIR H A I R LO S S P U FFY FA C E BULGING EYES S L O W H E A R T B E AT S W E AT I N G W E I GH T GAIN R A P I D H E A R T B E AT C O N S T I PAT I O N \II/EIGHT L O SS BRITTLE NAI LS REGULAR GAS A R T H R I T IS S O F T N A IL S C O L D I N TO L E R E A N C E S L E E P I N G D I F F l C U LT I E S DEPRESSION H E AT IN T O L E R A N C E D R Y S KJ N I N F E R T I LI T Y FAT I G U E I R R I TAB I L I T Y M E M O RY LOSS MUSCLE WEAKNESS H E AV Y M E N S T R U A L N E RV O U S N E S S PERJOOS SC AN T M ENSTRUAL MUS CLE A CH E S PERJOD S Hv1othvroidismvs. Hv1erthvroidism No Energy No Libido Cold sensitivity o Sleep Weight Gain bertarian Mental Fog Hot stuff Depression Rake thin Dry skin and hair Mental Fire Goitre Anxiety (Menstrual changes) Heart racing & tremor Light periods Evaluation of thyroid function: 1.Measurement of : [by RIA]. Total T4 ( normal : 4 -12 ug/ dl ). Total T3 ( normol : 80-120 ng/ all). 2. Measurement of free T3,T4 ( 0.4 ng /dl, 1.6 ng/ dl respectively). 3.Radio - active iodine uptake (R.A.I.U): I131 or I123 ‘preferable’ Normal uptake (24 hours after giving the isotope) → 5 - 30 % of the administered dose. Useful in the diagnosis of hyperthyroidism. 4. Serum TSH 5. thyroid ultrasound 6. fine needle aspiration biopsy Pituitary Gland  Growth Hormone Physiology - Increase Blood glucose - Increase Protein synthesis. - Increase Free fatty acids ' FFA'  ACROM EGALY Excessive growth caused by over secretion of GH. Benign p ituitary tum or (adenoma) Clinical picture: Coarse facial features. Exaggerated supraorbital ridges. Enlarged soft t issue Nose, Lips. Tongue enlarge and become more furrowed. Ma n d ib le (separation of teeth) Overgrowth of the jaw bone prognathism). The hands and feet enlarge: - Larger rings, gloves and shoes. - Spade like hands. Coarse body hair increases as the skin t h ickens frequently darkens. Mou rice 1ll t ISwedi1h Angel c e c s h od siie1 wit h Mor. 8 c  The sebaceous and sweat glands in the skin enrarge, producing excessive sweating. Voice deep and husky {Cartilage in the larynx may thicken). Joint pain is common Cardiomegaly, Hypertension and Hepatomegaly Compress ion of t he nerves: Sensory disturbance and weakness in the arms and legs. The pitu itary tumor may also cause severe headaches Irregular menstrual cycles. ADRENAL GLAND DISORDERS  secretes The adrenal gl:and Cortisol, m ineralocorticoid, and the renal androgens from cortex while the adrenal medulla secretes the adrenaline (epinephrine). Functions of the adrenocortical hormones : The very complex processing and ut i lization of many nutrients, including sugars (carbohydrates}, fats, and proteins The normal funct ioning of the circulatory system.and the heart The functioning of muscles Production of blood cells The norma l processes involved in maintaining the skeletal system Proper functioning of the brain and nerves The norma l responses of the immune system. Excess hor mone (most ly cortisol) circulating in t he blood strea m. Cushing synd rome Etiologies: Iatrogenic: Steroid therapy (most common cause) Pituitary adenoma (ACTH) adrenal cortex (hyperplasia) Adrenal Cause ( Cortisol) - Adrenal Adenoma. - Adrenal Hyperplasia. - Adrenal Malignancy Ectopic Source {ACTH) : (Small Cell Carcinoma of the lung) Symptoms: Mood changes (depression and euphoria). Easy bruising. Weakness. Weight gain. Amenorrhea. Back pain. Signs: Weight gain, and an abnorma l accumulation of fatty pads in the face "moon face", in the t runk "truncal obesity", upper back and the back of the neck (1'buffalo hump") Stria rubra Purple and pink stretch marks High blood pressure. Weak, th inning bones (osteoporosis). Weak muscles. Thin, fragile skin, with a tendency towa rd both bruising and slow healing.  occasional development of diabetes. Increased chance of infections. In women , Hirsut ism:abnormal hair growth (such as in the beard and mustache area), as well as loss of hair from the headi (receding hair line). N ormal ·C us h in g ' s  Hypofunction of the adrena l gland Etiology Seconda ry (Pit u ita ry insufficiency) Primary (Addison's Disease) (Primary ad renal fa ilure of adrenal glands} Hypoplasia or destruction by: Granulomatous d isease (e.g. Tuberculo sis, Fungus) Amylo idosis Hemochromatosi s Tumor Auto immune process Symptoms Wea kness, t iredness, dizziness. Fatigue or Lethargy. Nausea, Vom it ing, loss of we ight. Diarrhea , dehydrat ion. SaIt craving. Abdom inal pain Signs: Hyperpigmentation: - Skin darkness may seem like tan ning, on both sun exposed and unexposed areas. - Pigm:ented bucca l m ucosa. Hypotension Reduced Hair Growth Signs of dehydration 1'19..ire 2: tlyper;>igmontt'd m.. c d e $ ° " " ' ' lhe lowe< l p a n d I a n ! "e f a('l()t'Y, a Parathyroid gland  Parathyroid glands, four small glands located in the neck at the poster ior surface of the th yroid gland. · These glands secrete the parathormone (PTH), wh ich is responsible for keeping the constant level of calcium in the blood. Stimuli for PTH secretion : Hypoca lcemia ( Ca++level in the b lood), is the·main stim ullus. Physiological background on calcium regu lation:  Hyperpa rathyroid ism Sym ptoms M ajority of patients have no symptoms {50%). M ay have non-specific symptoms (weakness and easy fatigue) Primary hyper parathyroidism can cause symptoms due to hyperca lcemia - Anorexi a , nausea and vomiit i ng. - Dyspepsia - Constipation. Increase in incidence of Peptic u lcer and acute pancreatit is. lnterstial nephrit is: Ca deposition in the renal tubules leading t o inability t o concentrate urine leading to p o lyuria, p o lydypsia, nocturia lncre·ase suscept ibility t o renal stones ( Ca Oxalate and Ca phosphate stones), that can induce renal co lic and repeated UTI - Nephrocalcinosis due t o whole kidney calcification.  Impaired m entation, loss of memory for recent events. Emotional !ability, depression , Anosmia , drowsi ness, stupor &even coma. Weakness( proxima l muscles), artheralgia Severe prurit is ( calcification of the skin). Jo int pains. Very rarely pathologica'I fracture Calcification at the corneo-scleral juncti on. Keratit is and cornea l opacity. Solitary bone resorption causing - solitary cyst, brown tumor of the mandib le or - subperiosteal erosion of the phalanges). teitis fibro a cy tica Diagnosis Hypercalcemia: Norma I Ca = 9-llm g / IOOcc Hypophosphatemi a: Normal= 2.5-4 m g / IOOcc Increase alka line phosp hatase, Increase PTH level Urinalyses and kidney X-rays. Bone density test Treatment: Me d ical : treatment of hypercalcemia Surgical removal  HYPOPARATHVROl.DISM Failure of secretion of PTH due to : Surgical: after thyroidectomy, neck exploration , removal of neck malignancy. Transient after the remova l of a parathyroid adenoma. Idiopathic (autoimmune) Prolonged sever hypomag nesemia. Clinical picture: Asymptomati c or manifestations of hypocalcemia as: Neuromuscular activit y Numbness and t i ngling around the mouth and lips. Parenthesis in the hand and feet. Bronchospasm or laryngeal spasm (stridor) Carpopedal spasm (Spasmodic contra ctions in hands and feet), Diagnosis: Decrease in serum Ca. Increase in Phosphate in absence of Renal failure. PTH: If Low: diagnosis of hypoparathyroidism Summary References 1. Step-up to medicine 5th edition. ISBN-13: 978-1975103613 2. Davidson’s Principles & Practice of Medicine 23rd edition ISBN-13: 978-0702070280 Thank You