Hypoparathyroidism, Hypocalcemia, and Osteomalacia PDF

# Hypoparathyroidism Hypocalcemia (Tetany) - **Definition:** Increased neuromuscular irritability due to decreased ionized Ca or Mg. - **Etiology:** - **Hypocalcemia (Quantitative defect):** - **Diminished Ca intake:** starvation, dysphagia. - **Diminished Ca absorption:** - **Hypop...

# Hypoparathyroidism Hypocalcemia (Tetany) - **Definition:** Increased neuromuscular irritability due to decreased ionized Ca or Mg. - **Etiology:** - **Hypocalcemia (Quantitative defect):** - **Diminished Ca intake:** starvation, dysphagia. - **Diminished Ca absorption:** - **Hypoparathyroidism:** - Surgical removal, - Autoimmune destruction, - Goiter: with diversion of blood supply from parathyroid to the enlarged thyroid gland. - **Deficiency of Vit D:** rickets or Osteomalacia. - **Myxoedema, Panhypopitutarism, Cushing.** - **Gastrectomy, atrophic gastritis, and gastric carcinoma.** - **Malabsorption syndrome.** - **Increased Ca loss in urine:** - Loop diuretics - **Increased Ca precipitation in tissues:** - In acute pancreatitis - **Alkalosis:** - **Respiratory:** hysterical - **Metabolic:** vomiting, Conn's syndrome, diuretics. - **Mg deficiency.** # Clinical Picture - **Latent tetany:** (serum Ca 7-9 mg%): - There are no spontaneous manifestations but it can be induced (provocative tests): - **Chovestek's test:** Tapping of facial nerve in front of the ear causes facial muscle contraction. - **Trousseau's sign:** Sphygmomanometer inflation around the arm above systolic pressure for 5 minutes →carpal spasm. - **Erb's sign:** current < 4mA causes muscle contraction (normally at least 8 mA is needed). - **Manifest tetany (Ca < 7 mg%):** - **Muscle spasm in the form of:** - Spasm of the facial muscle. - Spasm of Jaw (trismus) - Spasm of larynx (Laryngismus stridulous) - Spasm of the diaphragm (hiccough) - Spasm of the back muscles. - Carpopedal spasm, muscle twitches & convulsions. - **Effect on ectodermal structures:** - **Nails:** Loss of luster & brittle - **Teeth:** Hypoplastic, transverse furrows and punctuate holes if the condition develops before formation of permanent teeth. - **GIT:** Malabsorption. - **Skin:** desquamation, atrophy, roughness, alopecia, and candida infection. - **Hair:** Premature loss of hair. # Oral manifestations if hyperparathyroidism occurs before age 6: - Delayed eruption of the teeth - Wide pulp chambers - Enamel hypoplasia - Short roots - Apical foramine remain open. - Multiple impacted teeth. # Treatment - **In acute attacks:** Ca gluconate 10 ml of 10 mg% solution SLOWLY over 10 minutes. - **Treatment of the cause:** - In hypocalcemia: Oral Ca lactate 2 gm T.D.S. - Active Vit D (1-25 DHCC, or 1-alpha HCC) 1 ug daily, - Thiazide diuretics to decrease Ca excretion in urine. - In Alkalosis: treatment of the cause. - In hypomagnesaemia: oral Mg # Osteomalacia - Osteomalacia is characterized by defective bone mineralization, bone pain, muscle weakness and pathological fractures. - There is failure to replace the turnover of Ca and P in bone matrix so, bone becomes demineralised and the bony substance becomes replaced by soft osteoid tissue so it is mainly a qualitative bone defect. # Causes of Osteomalacia - **Vit D deficiency.** - Dietary - Lack of synthesis in skin.- ↓absorption. - Defective metabolism - Anticonvulsants - CRF - **Low P with normal Vit. D.** - Familial hypophosphatemic rickets. - Renal tubular disease. # CIP (Osteomalacia in the adult counterpart of rickets). - Skeletal discomfort (from bone and muscle pain). - Bone tenderness. - Tetany may be manifested. - Muscular weakness with marked proximal myopathy with waddling gait. # Investigations - S. Ca↓, S. PJ. - Alkaline phosphatase ↑, parathyroid hormone ↑, ↓vitamin D level. - **X ray→** bone rarefaction with translucent band (pseudofraction or looser's zones) i.e. linear areas of low density surrounded by sclerotic borders. # Treatment - Treatment of the cause. - Vit. D, Ca supplements. - Diet e.g. milk, cheese or yoghurt - Alfa-calcidol especially in cases of renal failure. # Osteoporosis - It is defined as a decrease in the absolute amount of bone mass leading to enhanced bone fragility with increased risk of pathological fractures. - Unlike Osteomalacia, the defect in osteoporosis is that the bone that is present is normally mineralized but is deficient in quantity, quality and structural integrity. # Risk factors: - Female, Family history, early menopause. - ↓ Ca intake, reduced activity, smoking, alcohol, antacid, excessive caffeine, corticosteroids therapy and genetic factors. # Causes and types - **Post menopausal osteoporosis.** - **Secondary osteoporosis:** - Cushing's syndrome.. - Hyperthyroidism. - Acromegaly, D.M. - Rheumatoid disease. - Chronic renal failure - Chronic liver disease. - Rheumatoid arthritis. - Immobilization. - Drugs e.g. corticosteroids. # C/P: - Boney aches, back pain, Pathological fractures. - Loss of height due to thoracic kyphosis and collapsed vertebrae. - The most common sites of pathological fractures are the forearm (colles' fracture), spine (vertebral fracture) and femur (hip fracture). # Investigations: - Plasma chemistry is normal (normal serum ca, P and alkaline P). - Alkaline phosphates may be ↑ following a recent fracture. - X ray→ ↓bone density (rarefaction or osteopenia). - DEXA scan to measure bone density by dual-energy x ray absorption scanning (DEXA), it may show osteopenia (low bone mass), osteoporosis or severe osteoporosis. # Prevention of osteoporosis - Exercise. - Calcium supplements 1000-1500 mg/day; also dairy products are recommended e.g. Milk, cheese and Yogurt. - Restriction of caffeine intake. - Stop smoking and alcohol intake. - Estrogen replacement therapy in early menopause. # Definite treatment of osteoporosis - Bisphosphonates, they are osteoclasts antagonist e.g. Alendronate 10mg/day (osteomax or fosamax) orally at morning, it can be given 70 mg one dose/week. Bisphosphonates should be used with caution in patient with renal impairment. - Calcitonin 100 I.U every other day by S.C or IM injection. It can be given by nasal spray 200u/day. - Calcium 1000-1500 mg/d orally. - Vitamin D 400-800 IU/d orally. # Chapter4 Thyroid Gland ## Anatomy - The gland is formed of two lobes connected to each other by an isthmus. - The gland is closely attached to the thyroid cartilage and to the upper end of the trachea, and thus moves on swallowing. # PRIMARY THYROTOXICOSIS "Grave's Disease" - **Etiology:** It's autoimmune disorder - **Clinical Picture:** - Female-to male ratio is 8:1 - Occur in middle age (30-50 y) - **Neurological manifestations:** - **Psychic:** restlessness, anxiety, insomnia & rarely mania occur. - **Organic:** - Fine tremors of outstretched hands & unsupported tongue. - **Ophthalmopathy:** exopthalmos producing substance "EPS ". It results from infiltration with myxomatous tissue in retrobulbar space, extraoccular muscle & lacrimal gland. - **Exophthalmos:** uni or bilateral. - **Swelling of eye lids & lacrimal glands.** - **Lack of corrugation of forehead on looking upwards.** - **Cardiovascular system:** - Palpitation is the commonest symptom due to - Tachycardia (sleeping pulse > 100 / min). - Arrhythmia - **Respiratory:** Tachypnea. - **GIT:** - Increased appetite with loss of weight. - Diarrhea & even steatorrhoea. - **Genitals:** menstrual disturbance, infertility. - **Skeletal:** osteoporosis. - **Cutaneous:** - Warm flushed skin (salmon pink). - Pretibial myxoedema. - **Metabolic:** Hyperglycemia up to DM due to insulin antagonism. # Oral Manifestations: - Normal growth of the Jaw. - Early shedding of deciduous teeth. - Early eruption of permanent teeth. # Precaution should be taken with thyrotoxic patients: - Local anesthesia should be free from adrenaline. Because of the sensitization of the myocardium and potentiate chest pain and tachycardia. Pilocaine containing octapressin is an alternative - GA should be done by anesthetist. - Antithyroid drug induce agranulocytosis which may cause oral and oropharyngeal ulceration. - Avoid stress by prescribing tranquilizers. - Acute infection should be managed immediately. # Investigations for Hormone Level: - Total T4 & T3: increased. Free T3 & T4: increased. - TSH: decreased. - Thyroid scan, Ultrasonography and needle aspiration biopsy. # Thyroid Crisis - **Definition:** it's exaggerated manifestation of hyperthyroidism. # Precipitating factors: it's precipitated by - Stress - Infection - Surgery # Clinical picture: - Nausea & Vomiting. - Profuse sweating. - Tremors. - Tachycardia. - Fever may reatch≥40C. - Finally, heart failure and death, # How to manage thyroid crisis? - Hydrocortisone 200 mg intravenous - Ice pack, wet pack, fans. - Antipyretics (Acetaminophens not aspirins) - Antithyroid drugs: Carbimazole 15-25mg/6h P.O (or via NGT if needed)after 4h give Lugol's solution 0.3ml/L/8h for 1wk to block thyroid. - B- Blockers if no contraindication. - Chloropromazine 50mg p.o/IM as a sedative. - Na+ or K+ 500 mg every 8 hrs as infusion. Digoxin and diuretics in heart failure. # Hypothyroidism ## Cretinism : - It is hypothyroidism in childhood. # Causes - Congenital absence of thyroid gland. - Congenital enzymatic defect in synthesis of T4. - 12 deficiency (endemic cretinism). - Excess antithyroid drugs during pregnancy. # Clinical Picture - **CNS:** mental retardation, slow speaking. - **General features:** - **Face:** puffy eye lids, depressed nose, big lips, protruded tongue, delayed dentition, Malocculsion, anterior open bite. - **Hands:** square-shaped, with short fingers - **Disproportionate dwarfism:** height > span - **Delayed walking & waddling gait** - **Hypothermia** - **CVS:** bradycardia. - **Skin:** dry, cold, scaly, with SC myxoedematous tissue deposition in hands, face & supraclavicular region. - **Muscle:** weakness, constipation, pot - belly abdomen # Investigations - Low T3 T4. - TSH level: high "characteristic" - Serum cholesterol: high - X-ray carpal bones: delayed appearance of ossification centers & epiphyseal dysgenesis # Myxoedema: - It's Hypothyroidism in adults - **Clinical Picture common in female 30-50 years** - **General:** - Intolerance to cold & hypothermia - Tiredness, weakness & weight gain - **Face** - Expressionless. - Puffy eye lids & loss of outer 1/3 of eye brows. - Malar flush. - Red glazed tongue. - May be cataract. - **Skin** - Dry, cold, non sweaty, pale. - Non pitting edema: due to SC mucinous material. - **Nails are thick; body hair is sparse & brittle.** - **Colour:** yellowish due to carotinemia (lack of conversion of carotene to Vit A in liver due to absence of T4). - **CNS:** - **Slow cerebration, apathy, poor memory - Rarely myxoedema madness** - **Speech:** slurred speech (mucinous material in tongue) with hoarseness of voice. - **Nerve deafness.** - **Peripheral neuritis, carpal tunnel syndrome.** - **Suspended jerks:** delayed relaxation of tendon jerk. - **Myxoedema coma.** # Myxedema Coma ## Precipitating factor: - Trauma, surgery, cold, narcotics, GA anesthesia, infections. - Hypothermia(cold) leads to muscle rigidity with both metabolic & resp. acidosis and multisystem depression (brain, heart, kidneys, liver). - Mortality is at least 50%. - Sedatives (diazepam), analgesic (codeine). The respiratory centre is hypersensitive to these drugs, they should be avoided or the dose must be reduced. - Mortality is at least 50%. # Manifestation: - Hypothermia. - Bradycardia. - Hypotension - Epileptic seizures # Myxoedema coma Treatment: - Gradual rewarming. - 02, ventilatory & CVS support. - Glucose IV for hypoglycemia. - Drugs: - An intravenous loading dose of 500-800 mcg of levothyroxine is followed by a daily intravenous dose of 50-100 mcg; the daily dose is administered until the patient is able to take medication by mouth. - Hydrocortisone100mgIV/6h. - Antibiotics for infection. # Chapter5 Diabetes Mellitus - **Definition:** It is a metabolic disorder of carbohydrate metabolism due to relative or absolute insulin deficiency leading to hyperglycemia + glucosuria with secondary disturbance of lipid and protein metabolism. - **Etiology:** - Primary (95%) - Secondary (5%) - Gestational DM - **Primary DM include 2 types:** - **Type I DM:** Juvenile-Insulin dependent DM. - **Type II DM:** Maturity onset-Non insulin dependent DM. - **Secondary DM** - **Pancreatic causes:** - Chronic pancreatitis - Pancreatectomy - Cystic fibrosis - Heamochromatosis - **Endocrinal causes:** - Pheochromocytoma. - Cushing. - Thyrotoxicosis. - Conn's syndrome. - Acromegaly. - **Others:** - Drugs: Thiazides, cortisol, diazoxide, C. Pills - **III-Gestational DM** - It develops in 3% of pregnancies especially in 3rd trimester. - The insulin reserve is not sufficient overcome the antagonists released in pregnancy - Glucose level return to normal few weeks after labor. - 30-50% develop DM after 10-15 years. # Comparative clinical features of type 1 & type 2 DM | Feature | Type 1 DM | Type 2 DM | | ------------------ | ---------- | ---------- | | Age of onset | < 40 yrs | > 40 yrs | | Duration of symptoms | Weeks | Weeks to months | | Body weight | Normal or wasted | Obese | | Plasma insulin | Low to absent | Normal to high | | Acute complications | Diabetic ketoacidosis | Hyper-osmolar coma | | Insulin therapy | Responsive | Responsive to resistant | | Oral therapy | Non-responsive | Responsive | | Auto-antibodies (Islet cell Ab) | Yes | No | | Associated with other autoimmune disease | Yes | No | | Ketouria | Yes | No | | Rapid death without ttt with insulin | Yes | No | | Family history of DM | No | Yes | | Diabetic complications at diagnosis | No | Yes | # Clinical Picture - Asymptomatic in 1/3 of cases and diagnosed accidentally during blood sugar testing for unrelated condition. - Polyuria: osmotic diuresis due to hyperglycemia (nocturnal enuresis in children). - Polyphagia with loss of body weight: defect in the satiety center or in Leptin. - Polydipsia. - Pain and parasthesia secondary to peripheral neuritis. - Premature loosening of teeth. - Blurred vision: due to osmotic swelling of lens. - Symptoms of complication. # Dental changes in D.M.: - Periodontitis. - Loss of connective tissue. - Loss of alveolar bone. - Pocket formation. - Gingivitis, gingival hypertrophy. - Salivary gland Xerostomia. - Sialadenosis (Parotid gland enlargement). - Atrophic glossitis. - Taste dysfunction. - Burning sensation of the tongue. - Oral candidiasis due to : - High sugar medium. - Immunological deficiency. - Decreased production of antibodies. - Peripheral neuropathy and poor. - peripheral circulation. # Investigations - **Blood sugar test;** - **Diagnostic criteria of DM:** - Classic symptoms of DM + Random plasma glucose ≥ 200 mg/dl (≥11.1mmol/l). (moles=mass / Mwt, Mwt glucose 180) - Fasting plasma glucose (FPG) ≥ 126 mg/dl(≥7mmol/l) and post prandial≥200mg/dl on2 separate occasions. - NB: Fasting: No calorie intake for at least 8 hrs. - Random plasma glucose ≥200mg/dl(glucose measured in plasma is10%greater than that of whole blood more than one occasions. - **Normal IFG IGT DM** - FPG <110 ≥ 110 & < 126 < 110 ≥ 126 - 2hr PPG <140 ≥ 140 & < 200 ≥ 200 - Random G ≥ 200 with symptoms - **NB; Impaired glucose tolerance(IGT): Fasting≤126mg/d 2hrs postprandial glucose ≥ 140 & < 200 mg/dl.** - **Impaired fasting glucose (IFG): FPG ≥ 110 & < 126 mg/dl.** - **Glucose tolerance test:** - Patient should be fasting (overnight) - Fasting blood sugar is done. Bladder is emptied - The patient is fed 75 gm glucose orally, and blood sugar level testing for glucose is performed every 2 hr for 2 hrs. - **Three criteria for a normal curve:** - Fasting less than126mg/dl reaches maximum in one hour and must be below the renal threshold. Returns to normal after one to one and half hour. - An increased fasting blood glucose above 140-150mg/dl. After one h an increased peak value above 200mgldl and or a delayed return to normal after 2hours sample are characteristic of diabetes. - **Urine analysis:** - Glucosuria: occurs when glucose serum level exceeds 160 mg%, but it is not a good indicator for DM diagnosis or assessment of treatment (Clinistix strips or Glucotest) is a method to detect glucosuria by the patient. - Ketonuria: for diagnosis of diabetic ketoacidosis (Glucostrips K) - **NB causes of glucosuria:** - Renal glucosuria: hereditary low renal threshold. - Lag storage curve (alimentary glycosuria): thyrotoxicosis. - Stress hyperglycemia. - Reducing substances in urine e.g. salicylates & Vit C. - **Home blood glucose monitoring:** - Capillary blood glucose is measured by the patients (Accu check active, one touch strips or Dextrostix strips). Blood is taken from the side of a finger not from the tip which is densely innervated. - Used in patients with tight glycemic control - **Plasma insulin level:** (N=20 U/ml). - **Hormone end product:** C- peptide level correlates with insulin serum level. - **Investigation to assess treatment efficacy:** - Glycosalated hemoglobin (HbA1c): - Hb Alc is synthesized over the life of RBCs in proportion to the degree of glycemia prevailing, and thus gives an index of the average blood glucose over the life of Hb molecule (2-3 months). Normally it is less than 6% of total Hb, and if > 12% Poor glycemic control in the past 3 months. # Management of Diabetes. - Diet Control and exercise. - Oral Anti diabetic Drugs: - Sulfonyl Urea (Glibenclamide(Daonil)) - Gliclazide (Diamicron). - Glimepiride(Amaryl) - Repaglinide (Novonorm). - Glipizide. - Biguanides: Metformine(glucophage) - Glucosidase inhibitors:Acarbose(glucobay) - Pioglitazone - **New Drugs:** Galvus, Galvus met (Vidagliptin/Metformin). - Insulin - **Source of insulin** - Animal origin: porcine - bovine - Human insulin by genetic engineering (recombinant DNA technique) - **Administration** - Insulin is given SC in different places of skin. - Insulin pump. - Insulin pens. # Preoperative management ## Type 1 diabetes mellitus - The uncontrolled patient should be referred to the physician before any dental procedure. - It is usually best to admit patients 2-3 days before elective surgery, particularly if outpatient adjustments are difficult. - Ensure good preoperative control usually with short-acting insulin (or a mixture of short- and intermediate-acting insulin) twice daily. Extra short-acting insulin can be added if necessary. - Monitor blood glucose throughout the day. - On the day of surgery starve from midnight and do not give the first dose of insulin. - Operation should be as early as possible (ie put the diabetic patient first on the list). - Check glucose and electrolytes early on the day of surgery (defer if glucose >13 mmol/L or if there is significant electrolyte disturbance). Start intravenous (IV) infusions of dextrose (500 ml 10% dextrose plus 10 units of soluble insulin plus 10 mol KCL at 125 mls per hour). - Check blood glucose and electrolytes at the end of the operation or at 1- to 2-hourly intervals. - Monitor blood glucose during surgery at least every 30 minutes. Continue this as long as blood glucose is between 5-10 mmol/L. Reduce insulin to 5 units if less than 5 mmol/L and increase to 15 units if blood glucose is 10-20 mmol/L (new infusion needed of course). - After surgery, check glucose every 2 hours and electrolytes every 6-12 hours, adjusting infusions as necessary. Continue infusions but, when eating normally, restart subcutaneous insulin (as before surgery). - Pre and post operative antibiotic to guard against infection and slow wound healing - Local anesthesia with low concentration of adrenaline. ## Type 2 diabetes mellitus - Preoperatively, control should be assessed. - Patients controlled by diet alone do not usually need any special measures, providing control on diet is adequate. - It is better to use short-acting drugs (for example glipizide). - Remember that the hypoglycemic effect of sulphonylureas is enhanced by some drugs (for Example: aspirin, sulphonamides, anticoagulants). - Metformin should be discontinued 48 hours prior to and subsequent to surgery in order to reduce the risk of lactic acidosis. - If control is inadequate, insulin may be needed. - Insulin can be required in the postoperative phase temporarily. - On the day of surgery keep 'nil by mouth' as usual and omit short-acting sulphonylurea. - Monitor blood glucose as for type 1 diabetes above. If blood glucose is >13 mmol/L, use insulin to control (small doses of soluble insulin). - For major surgery or where there is prolonged postoperative starvation, use glucose and insulin infusions as set out above # Complications: - Hypoglycemia & hypoglycemic coma. - Nocturnal hypoglycemia. - Blurring of vision: osmotic changes of lens. - Acute neuropathy: may occur paradoxically with controlling hyperglycemia by insulin. - Insulin edema: mild LL edema (salt & water retention). - Weight gain. - Insulin lipodystrophy: - Insulin lipoatrophy: Autoimmune reaction to non-human insulin. - Insulin lipohypertrophy: lipogenic effect of insulin. - Allergy: use human insulin - Insulin resistance: defined as daily requirements > 200 IU due to: - Obesity: commonest cause for mild resistance - Antibodies against insulin preparations (non-human). - Antibodies against insulin receptors. # THANK YOU www.must.edu.eg The image is of a modern building in front of a sunset sky. 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