Introduction 

-Mitral regurgitation (MR) occurs due to the inability of the mitral valve to close adequately to prevent blood from returning back to the left atrium from the left ventricle during systole 

-Most common cause is mitral valve prolapse 

-Acute: papillary muscle rupture

-Chronic: Rheumatic fever, mitral valve prolapse 

Symptoms & Signs 

symptoms in proportion to  increase in left atrial pressure and pulmonary hypertension

– fatigue, exhaustion, atypical chest pain, progressive dyspnea, congestive heart failure, paroxysmal nocturnal dyspnea, orthopnea, pleural effusion, edema, increased jugular pressure

-A holosystolic murmur best heard at the apex, with radiation to the axilla 

-Handgrip exercise increases the intensity of the murmur 

Diagnosis 

ECG: left atrial abnormality, left ventricular hypertrophy 

Chest X-ray: can show LV enlargement, left atrial enlargement, and pulmonary edema 

Echocardiography: the diagnostic test of choice; can show mitral valve regurgitation, size of left atrium, left ventricle, pulmonary pressure 

Treatment 

Medications: Diuretics, ACE inhibitors Surgical: Mitral valve repair or replacement

Mitral Regurgitation 

Introduction 

-Mitral regurgitation (MR) occurs due to the inability of the mitral valve to close adequately to prevent blood from returning back to the left atrium from the left ventricle during systole 

-Most common cause is mitral valve prolapse 

-Acute: papillary muscle rupture

-Chronic: Rheumatic fever, mitral valve prolapse 

Symptoms & Signs 

symptoms in proportion to  increase in left atrial pressure and pulmonary hypertension

– fatigue, exhaustion, atypical chest pain, progressive dyspnea, congestive heart failure, paroxysmal nocturnal dyspnea, orthopnea, pleural effusion, edema, increased jugular pressure

-A holosystolic murmur best heard at the apex, with radiation to the axilla 

-Handgrip exercise increases the intensity of the murmur 

Diagnosis 

ECG: left atrial abnormality, left ventricular hypertrophy 

Chest X-ray: can show LV enlargement, left atrial enlargement, and pulmonary edema 

Echocardiography: the diagnostic test of choice; can show mitral valve regurgitation, size of left atrium, left ventricle, pulmonary pressure 

Treatment 

Medications: Diuretics, ACE inhibitors 

Surgical: Mitral valve repair or replacement

Introduction 

-The mitral valve has two leaflets, anterior and posterior

-Mitral stenosis is a condition where the mitral valve area is reduced, causing obstruction of blood flow from the left atrium into the left ventricle during left ventricular diastole

-MS can cause elevated left atrial pressure resulting in pulmonary hypertension, pulmonary edema, and right heart failure. 

-the most common cause of mitral valve stenosis: Rheumatic heart disease 

-Other causes include congenital, SLE, RA, myxoma 

Symptoms & signs 

-Rosy cheeks (mitral facies), Fatigue, exertional dyspnea, orthopnea, heart failure, atrial fibrillation, pulmonary hypertension, right-sided heart failure (ascites, pedal edema, weight gain), hemoptysis, hoarseness of voice (Ortner syndrome), systemic embolization 

-Accentuated first heart sound, an opening snap following the second heart sound, mid-diastolic low-pitched rumbling murmur best heard at the apex with the patient in the left lateral position 

Diagnosis 

ECG: tall peaked P waves, broad bifid P waves (P mitrale), right axis deviation,  LA abnormality, atrial fibrillation 

Echocardiography: thickened mitral valve leaflets, fish-mouth appearance of mitral valve, “hockey-stick” motion of the anterior leaflet, enlarged left atrium 

Chest x-ray: Left atrial enlargement, horizontal lines in the regions of the costophrenic angles representing interstitial edema (Kerley A and B lines) 

Treatment 

Asymptomatic: no treatment 

Symptomatic: Balloon valvuloplasty or valve replacement

Medications: diuretics, beta blockers,calcium channel blockers, anticoagulants

Patent Ductus Arteriosus

Introduction 

-Embryonic ductus arteriosus allows shunting of blood from the PA to the aorta, bypassing the lungs 

-It normally closes immediately after birth 

-Failure to close results in left-to-right shunt 

-Risk factors: Down syndrome, rubella, 

Symptoms & signs 

-Usually asymptomatic at birth and during childhood 

-No symptoms in mild cases 

-Shortness of breath, sweating, almost always acyanotic but differential cyanosis can happen; lower extremities and sometimes the left hand show clubbing and cyanosis, but the right hand and head are always pink

-Continuous ‘machinery’  ‘to-and-fro’ murmur loudest over left pulmonary area below the left clavicle, widened pulse pressure, loud S2, accentuated in late systole at the time of S2, S2 is obliterated by the waxing and waning of the murmur 

Complications: Left heart dilation, pulmonary hypertension, Eisenmenger syndrome, heart failure, infective endocarditis 

Diagnosis 

Chest X-ray: normal 

ECG: normal or left atrial and ventricular hypertrophy 

Echocardiogram: left atrial and ventricular enlargement 

Treatment 

-Prior to birth, circulating prostaglandins keep the ductus patent, so a PDA can be closed by administering a prostaglandin inhibitor like indomethacin 

 Indomethacin is ineffective in term infants with PDA 

-Surgical ligation 

Tetralogy of Fallot 

Introduction

-Tetralogy of Fallot (TOF) is the most common form of cyanotic Congenital heart disease

-it is associated with trisomy 21 

–it has 4 anatomic components:

1.ventricular septal defect

2.right ventricular hypertrophy

3.pulmonary stenosis

4.overriding aorta 

-It results in not enough blood going to the lungs to get oxygen, and the oxygen-poor blood is pumped to the rest of the body

Symptoms & Signs 

-Clinical presentation depends on the degree of RV outflow obstruction 

-Most present by 6 months of age; -right to left shunt causes cyanosis, hypoxemia (blue illness); Baby ‘turning blue’ with feeding or crying, failure to thrive

‘Tet spells’: cyanotic episodes with deep breathing, irritability, prolonged crying, child squats to interrupt the spells 

-Harsh crescendo-decrescendo systolic ejection murmur best heard at the left upper sternal border (due to RVOT obstruction), single second heart sound 

-Most common residual defect after TOF surgery: pulmonary regurgitation 

Diagnosis 

ECG: The ECG reveals RVH and right axis deviation; in repaired tetralogy, there is often a right bundle branch block pattern.

Chest X-ray: Boot-shaped heart (coeur en sabot sign) 

Echocardiogram: Delineates TOF and quantifies degree of RV outflow obstruction 

Cardiac MRI and CT can quantitate both the pulmonary regurgitation and the RV volumes. 

Treatment 

-Surgical repair is the definitive treatment of choice 

-most adult patients have had surgical repair, 

-The goal of surgical repair is to alleviate the pulmonary stenosis and close the VSD

Introduction 

-VSD is a hole between the LV and RV 

-Most common congenital heart defect

-There are four types, classified by location: membranous, muscular, inlet and outlet  

-Muscular are the most common type 

-Membranous VSD are the most common type requiring surgical intervention (80% of cases) 

-There is no gender predilection 

-VSD allows oxygen-rich blood from the left ventricle flow into the right ventricle, which is pumped back to the lungs, even though this blood does not need oxygen. This puts more stress on heart and lungs 

Symptoms & Signs 

–Symptoms correlate with size 

-Poor weight gain, dizziness, feeling tired all the time, sweating, shortness of breath 

-Complications: cyanosis with pulmonary hypertension, Eisenmenger syndrome, endocarditis, heart failure 

–Small shunts are associated with loud, harsh holosystolic murmurs in the left third and fourth interspaces along the sternum with a narrowly split second heart sound 

Diagnosis

Chest X-ray: cardiomegaly, enlarged PA, increased vascular markings 

ECG: normal or right, left, or biventricular hypertrophy 

Echocardiogram: confirms diagnosis 

Treatment 

-Degree of shunting measured during cardiac catheterization dictates management 

-Asymptomatic small shunts do not require treatment 

-Medium and large VSDs may need to be fixed with surgery or heart catheterization 

Introduction

Coarctation of the aorta is the narrowing of the aorta where the ductus arteriosus (ligamentum arteriosum after regression) inserts 

Preductal: identified in infancy; early presentation of symptoms 

Postductal: identified in early adulthood; later presentation of symptoms 

-Most common site of coarctation is distal to the left subclavian artery

-Poses high risk for aortic aneurysm, dissection, rupture, CHF, stroke 

-Associations: Turner’s syndrome, Berry aneurysms, Bicuspid aortic valve 

Symptoms &  Signs 

Infants: pale skin, difficulty feeding, difficulty breathing, irritability 

Adults: Exertional dyspnea, headache, epistaxis and leg fatigue, 

-Hypertension in the arms, with low or normal pressure in the legs 

-Absent or weak and delayed femoral pulsations in comparison with the brachial or radial pulse 

-A continuous murmur loudest at left infrascapular region, posterior inter scapular area, 

-Lower blood pressure in the legs than in the arm

-Cyanosis in lower half of the body 

Diagnosis 

Radiography 

Rib notching: scalloping of the inferior portion of the ribs due to enlarged intercostal arteries 

3 sign: aortic arch and dilated left subclavian artery forming the upper curvature and poststenotic dilation of the descending aorta forming the lower

ECG: left ventricular hypertrophy, left atrial enlargement 

Echocardiography, CT, MRI

Treatment 

balloon angioplasty, Endovascular stenting, or surgery 

Introduction 

Pulmonic stenosis is a valvular abnormality that obstructs blood flow between the right ventricle and the pulmonary arteries 

Risk factors: German measles, rheumatic fever, Noonan sy1ndrome, carcinoid syndrome 

Untreated severe stenosis may result in RV failure 

Symptoms & Signs 

-mild cases are asymptomatic 

-moderate to severe cases may cause dyspnea on exertion, syncope, chest pain, RV failure

-cyanosis and clubbing if parent foramen ovale or ASD exists 

-a loud, harsh, high pitched systolic ejection murmur, a prominent thrill present in the left second and third interspaces parasternally

-the murmur radiates toward the left shoulder and increases with inspiration 

-this is the only right-sided auscultatory event that decreases with inspiration 

-a loud ejection click can be heard to precede the murmur

-the pulmonary component of S2 may be diminished, delayed, or absent

-Noonan syndrome: short stature, web neck, mental retardation, antimongoloid slanting of the eyes, hypogonadism 

Diagnosis 

ECG: right ventricular hypertrophy with right-axis deviation, prominent R waves in the right precordial leads

Chest radiography: dilated main and left pulmonary arteries, post-stenotic dilatation; greater vascular perfusion of the left lung than the right base (Chen sign)

Echocardiography: diagnostic tool of choice

Treatment 

-Percutaneous balloon valvuloplasty, Surgical commissurotomy or pulmonary valve replacement

-Endocarditis prophylaxis in certain cases 

Introduction

-Carcinoid tumor is a type of neuroendocrine tumor that grows from neuroendocrine cells

-They can arise in several organs throughout the body, most commonly in the digestive tract (appendix, ileum, rectum etc) or in the lungs 

Symptoms & Signs 

Some carcinoid tumors do not cause any symptoms and signs 

Classic triad: Cutaneous flushing, diarrhea and valvular heart disease

Carcinoid tumors in the GI: Nausea, vomiting, rectal pain, rectal bleeding, bowel obstruction, skin flushing, diarrhea, abdominal pain 

Carcinoid tumors in lungs: cough, hemoptysis, wheezing, shortness of breath, chest pain, diarrhea, skin flushing

Cardiac involvement: tricuspid regurgitation and pulmonary stenosis 

Diagnosis 

Imaging tests: CT, MRI, PET, nuclear scans, Octreotide scintigraphy

Labs: production of >15 mg/d of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the urine. 

Treatment 

Surgery, medications (octreotide), chemotherapy (5FU plus streptozocin or doxorubicin), radiation 

Introduction

Pheochromocytomas are neoplasms of the chromaffin cells of the adrenal medulla or paraganglial cells of extramedullary sites (paragangliomas) 

-These tumors secrete excessive amounts of epinephrine, norepinephrine, or both or even dopamine

-Most pheochromocytomas secrete norepinephrine 

-Pheochromocytoma was classically referred to as the “tumor of tens” because it was considered that 10% are hereditary, 10% are malignant, 10% are asymptomatic, 10% are extra-adrenal, 10% are extra-abdominal,10% are multiple, 10% are bilateral

– They can occur at any age, have no gender predilection

-Peak incidence: in the fourth and fifth decades of life

-Familial causes: Multiple Endocrine Neoplasia type 2 (MEN 2), von Hippel-Lindau disease, von Recklinghausen neurofibromatosis type 1 (NF-1) 

Symptoms & Signs 

-The classic pentad of symptoms: Episodic headache, palpitations, unusual sweating, pallor and orthostasis

-Other symptoms: Anxiety, irritability, flushing, chest pain, shortness of breath, nausea, vomiting, abdominal pain

-The most common clinical sign: Hypertension 

-Typical paroxysm: Sudden headache, palpitations, and sweating produced by anxiety or activities that compress the tumor (bending, defecation, deep palpation of the abdomen etc) 

Diagnosis 

24-hour urinary tests: Catecholamines, Fractionated metanephrines, total metanephrines

Plasma tests: Catecholamines, Free metanephrines

Imaging: CT, MRI, MIBG scintigraphy, Somatostatin receptor scintigraphy

Most sensitive test: Plasma fractionated free metanephrines

Most specific test: Urinary total metanephrines 

Treatment 

Definitive treatment: Surgery 

First administer alpha blockers, then beta blockers

α-blockers: Phenoxybenzamine, prazosin, terazosin, doxazosin

beta blockers: Propranolol, atenolol, metoprolol, carvedilol, bisoprolol, esmolol 

Calcium channel blockers: Nicardipine 

Introduction 

Primary aldosteronism occurs when the adrenal glands produce too much of the steroid hormone aldosterone, which helps control sodium and potassium excretion 

-Excessive aldosterone production increases sodium retention and suppresses plasma renin 

-It increases renal potassium excretion, which can lead to hypokalemia 

-The most common cause of refractory hypertension in young and middle-aged adults: Primary aldosteronism 

-Most frequent cause of primary aldosteronism: Bilateral adrenal cortical hyperplasia 

Symptoms & signs

Fatigue, edema, tingling, muscle weakness, excessive thirst, frequent urination, visual disturbances, normotension, hypertension, paresthesias with tetany, headache, polyuria and polydipsia 

Diagnosis

Labs: low plasma renin; low potassium;  Elevated plasma and urine aldosterone levels, sodium bicarbonate levels 

Imaging: Adrenal CT 

Treatment 

Unilateral Adrenal adenoma: usually treated by adrenalectomy 

Bilateral adrenal hyperplasia: usually treated with medical therapy 

Medications: Spironolactone, Eplerenone, Amiloride

Primary aldosteronism (Conn’s syndrome)

Introduction 

Primary aldosteronism occurs when the adrenal glands produce too much of the steroid hormone aldosterone, which helps control sodium and potassium excretion 

-Excessive aldosterone production increases sodium retention and suppresses plasma renin 

-It increases renal potassium excretion, which can lead to hypokalemia 

-The most common cause of refractory hypertension in young and middle-aged adults: Primary aldosteronism 

-Most frequent cause of primary aldosteronism: Bilateral adrenal cortical hyperplasia 

Symptoms & signs

Fatigue, edema, tingling, muscle weakness, excessive thirst, frequent urination, visual disturbances, normotension, hypertension, paresthesias with tetany, headache, polyuria and polydipsia 

Diagnosis

Labs: low plasma renin; low potassium;  Elevated plasma and urine aldosterone levels, sodium bicarbonate levels 

Imaging: Adrenal CT 

Treatment 

Unilateral Adrenal adenoma: usually treated by adrenalectomy 

Bilateral adrenal hyperplasia: usually treated with medical therapy 

Medications: Spironolactone, Eplerenone, Amiloride

Introduction

Cushing syndrome is a hormonal disorder which occurs when body has too much of the hormone cortisol over time 

-it more frequently affects women

-the most common cause of Cushing’s syndrome: use of glucocorticoids 

Symptoms & Signs 

General: fatigue, backache, headache, central obesity with a rounded, rosy face (moon face), a fat pad in the upper back between the clavicles (buffalo hump), protuberant abdomen  

CNS: irritability, emotional lability, depression, psychosis, insomnia   

Musculoskeletal: Proximal muscle weakness (Difficulty standing up from a seated position, or climbing stairs), osteopenia, osteoporosis 

Reproductive: Oligomenorrhea, amenorrhea, erectile dysfunction, infertility 

Cardiovascular: Hypertension, hypercoagulation 

Endocrine: Glucose intolerance, diabetes

Skin: purple striae, easy bruisability, hyperpigmentation, hirsutism

Diagnosis 

Labs: 24-hour urinary free cortisol and creatinine, Late-night (10–11 PM) salivary cortisol determinations, Petrosal sinus sampling, overnight dexamethasone suppression test, plasma ACTH level, plasma DHEAS (dehydroepiandrosterone sulfate (DHEAS) level

Imaging: CT of the adrenals, MRI of the pituitary

Treatment 

Medications: Spironolactone, eplerenone, flutamide, cabergoline, Pasireotide, Ketoconazole, Metyrapone, Mitotane 

Surgery: transsphenoidal selective resection of the pituitary adenoma (Pituitary Cushing disease), Adrenalectomy (Adrenal Cushing disease) 

Introduction

-Primary adrenocortical insufficiency (Addison disease) is a syndrome resulting from the chronic deficiency of cortisol caused by adrenocortical insufficiency 

-Secondary adrenocortical insufficiency is due to ACTH deficiency, caused by exogenous glucocorticoid therapy, pituitary or hypothalamic tumors 

-in primary adrenal insufficiency, low or absent cortisol level results in hypersecretion of ACTH by the pituitary

-ACTH stimulates melanocyte activity, resulting in generalized hyperpigmentation, which is the most specific sign of primary adrenal insufficiency

-Addison’s disease occurs when >90% of adrenal tissue is destroyed

-The most common cause is autoimmune destruction 

Symptoms & Signs 

General: Weakness, malaise, anorexia, weight loss, craving for salt 

Vascular: postural hypotension

GI: Nausea, vomiting, diarrhea, constipation, abdominal pain

Musculoskeletal: Myalgia, arthralgia 

Metabolic: Hypoglycemia, hyponatremia,hyperkalemia 

Psychiatric: Personality changes 

Dermatological: Hyperpigmentation of the buccal mucosa and gums preceded by generalized hyperpigmentation of the skin, loss of axillary and pubic hair, vitiligo,calcification of auricular cartilage (petrified ears), longitudinal pigmented bands in the nails  

Gynecological: Amenorrhea, ovarian failure, infertility

Obstetrical: preterm delivery, low-birth weight newborn, increase in cesarean delivery

Emergency: Shock, coma, and death, if untreated

Diagnosis 

Labs: hyponatremia, hyperkalemia, acidosis, elevated serum creatinine and blood urea nitrogen, hypoglycemia, hypercalcemia

Hematology: Normochromic, normochromic anemia, neutropenia, eosinophilia, and lymphocytosis

Best screening test/Definitive diagnosis: Failure to respond adequately to corticotropin stimulation test

-MRI to rule out pituitary or hypothalamic tumor 

-CT scan of the adrenal glands

-Secondary Adrenal insufficiency: Diminished pigmentation, Normal serum potassium 

Treatment 

-Register with a medical alert system 

-Patient should be instructed in the self-administration of steroids

-Lifelong replacement therapy of glucocorticoids and mineralocorticoids 

-Medications: Hydrocortisone, prednisone, dexamethasone, fludrocortisone 

-Acute adrenocortical insufficiency: Medical emergency, parenteral hydrocortisone, correction of fluid and electrolytes 

Introduction

Paget disease (Osteitis deformans) is a chronic, localized bone-remodeling disorder of abnormal osteoclasts that drive increased bone resorption accompanied by accelerated, disordered bone formation that results in disorganized, fragile bone

-It was originally described by Sir James Paget in 1877 

-It most commonly involves the pelvis, vertebrae, skull, humerus, femur and tibia 

-it predominantly affects Caucasian individuals over the age of 40 

Symptoms & Signs 

-Most patients are asymptomatic 

-Most common presenting symptom is pain, often worse at night  

-Bowing of weight-bearing bones, stress fractures (Chalk stick fractures), 

-Enlargement of the parietal or frontal bones (frontal bossing), increased head size, softening of the base of the skull (platybasia)

Complications of Paget disease: 

Rheumatologic: Osteoarthritis, gout, vertebral collapse 

Neurologic: Basilar impression, peripheral nerve entrapment, spinal cord and root compression 

Otologic: Cranial nerve dysfunction (especially deafness) 

Ophthalmic: Loss of vision 

Neoplastic: Osteosarcoma, giant cell tumor 

Cardiac: High-output heart failure 

Metabolic: Hypercalcemia 

Diagnosis 

X rays: Focal lytic, radiolucent areas with a coarse trabecular pattern and bone thickening, described as osteoporosis circumscripta “cotton-wool” skull, enlarged “picture-frame” vertebrae, “ivory vertebrae”

Labs: Normal calcium, phosphate levels, Elevated serum alkaline phosphatase

Bone resorption markers: Elevated serum or urine N-telopeptide or C-telopeptide measured in the blood or urine

Treatment 

-Adequate calcium and vitamin D intake 

-Mainstay of pharmacologic therapy: Bisphosphonates 

-The treatment of choice: Zoledronic acid 

-Other medications: Pamidronate, Risedronate, Alendronate, Tiludronate

-Serial serum alkaline phosphatase determinations are done to evaluate the response to treatment 

Introduction 

Rickets: Defective bone mineralization in children before epiphyseal fusion

Osteomalacia: Defective bone mineralization in adults with fused epiphyses

-The most common cause of osteomalacia: Vitamin D deficiency 

-Drug-induced osteomalacia caused by phenytoin, carbamazepine, valproate, phenobarbital 

Calcipenic rickets occurs in 4 forms:

Nutritional rickets 

Vitamin D-dependent rickets type I

Hereditary vitamin D resistant rickets

Defects in vitamin D metabolism 

Hypophosphatemic rickets occurs in 2 forms: 

-nutritional hypophosphatemic rickets 

-X-linked hypophosphatemic rickets 

Symptoms & Signs 

-can be asymptomatic 

-Weakness, apathy, listlessness, bone pain, proximal muscle weakness

-spasms, convulsions, thickened and widened wrists and ankles 

-Craniotabes: thinning of the bones of the skull, soft, misshapen head, widened sutures, frontal bossing, muscle hypotonia, pronounced potbelly, bowing of the legs, waddling gait  

-Delayed eruption of teeth, pitted teeth 

-Rachitic rosary: Enlargement and cupping of the costochondral junctions resulting in widening of the chest 

-Genu Valgum: ‘Knock knees’ 

-Genu Varum: ‘Bowed legs’ 

-Harrison Groove: Tug of the diaphragm against the softened lower ribs may produce an indentation at the point of insertion of the diaphragm

Kyphoscoliosis or lumbar lordosis is common

-Hypocalcemia: fatigue,lethargy, irritability, depression, paresthesias in the circumoral area, muscle cramps, carpopedal spasm, convulsions, tetany, laryngospasm, and stridor 

-Hypophosphatemia: muscle weakness, reduced endurance, dysphagia, diplopia, cardiomyopathy, respiratory muscle weakness and impaired cognition

Diagnosis 

Histology: Transcortical bone biopsy 

Radiographs: bilateral bowing deformity of the femora, metaphyseal flaring, physeal widening 

Treatment 

-vitamin D 

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Introduction

Osteoporosis is a systemic skeletal disease characterized by low bone mass, microarchitectural deterioration of the bone tissue, compromised bone strength resulting in bone fragility and increased risk of fractures

-It is more common in women than in men

-The World Health Organization has established criteria for defining osteopenia and osteoporosis based on the T score: 

T score greater than or equal to –1.0, normal; 

T score –1.0 to –2.5, osteopenia 

T score less than –2.5, osteoporosis; 

T score less than –2.5 with a fracture, severe osteoporosis.

-Medication-induced osteoporosis: Glucocorticoids are the most common cause of medication-induced osteoporosis; diabetes medications, thiazolidinediones,SSRIs, proton pump inhibitors, warfarin 

Symptoms & Signs 

-Osteoporosis is often a ‘silent disease’

-Complications: loss of height from vertebral fractures, kyphosis from vertebral fractures, chronic back pain, restrictive lung capacity from thoracic vertebral fractures, hip fractures, low self-esteem, decreased quality of life and independence, isolation and depression

-Most important consequence of osteoporosis: Fractures 

-Most frequent sites of fractures: thoracic and lumbar vertebral bodies, proximal hip, pelvis, proximal humerus, and distal radius 

-The most common osteoporotic fracture: Vertebra

-the most disastrous osteoporotic fracture:Proximal femur

Diagnosis 

-CBC, CMP, 24-hour urine collection of calcium, serum 25-hydroxy vitamin D, PTH

-Most commonly used tool to determine bone density: Dual-Energy X-ray Absorptiometry (DEXA) 

-Other techniques: single-energy x-ray absorptiometry (SXA), quantitative CT, and ultrasound (US)

-Fracture risk increases with age at any T-score.

Treatment 

Lifestyle modifications: Discontinue smoking, alcohol consumption, Exercise, hip protectors 

Nutritional supplements: Calcium, Vitamin D, protein intake, good sun exposure 

Medications: 

Bisphosphonates: Alendronate, Risedronate, Ibandronate, Zoledronic acid 

PTH analogs: Teriparatide, Abaloparatide, limited to 2-year treatment

SERMS: Raloxifene,tamoxifen; up to 5-year treatment 

RANKL inhibitor: Denosumab; up to 10-year treatment 

Sclerostin inhibitor: Romosozumab; limited to 12 monthly doses 

Hyperparathyroidism is a common disorder of calcium, phosphorus, and bone metabolism caused by increased circulating levels of parathyroid hormone (PTH) 

– PTH decreases urinary excretion of calcium and increases urinary excretion of phosphate.

-it is the most common disorder of parathyroid function

-it is categorized as primary, secondary, or tertiary depending on the etiology

-Causes: solitary parathyroid adenoma (85%), hyperplasia, multiple adenomas, carcinoma 

Primary hyperparathyroidism: 

-The most common cause of hypercalcemia 

-in the outpatient setting: Primary hyperparathyroidism 

-in the inpatient setting: Malignancy 

-It occurs at all ages, affects women more than men, most commonly in the seventh decade 

Secondary hyperparathyroidism: 

-PTH levels are elevated in response to chronic hypocalcemia

-Most common causes are chronic renal failure, vitamin D deficiency

Tertiary hyperparathyroidism: 

-Autonomous hypersecretion of PTH and hypercalcemia 

Symptoms & Signs 

-Classic description: “bones, stones, abdominal groans, psychic moans, with fatigue overtones.”

-Primary hyperparathyroidism is often asymptomatic 

General: Fatigue, weakness, irritability 

Psychiatric: Depression, dementia, and confusion

Cardiovascular: Hypertension, palpitations,prolonged P-R interval, shortened Q-T interval, bradyarrhythmias, heart block, asystole  

Gastrointestinal: Anorexia, nausea, vomiting, heartburn, peptic ulcer, weight loss, constipation, abdominal pain, pancreatitis 

Bone: osteoporosis, bone pain, osteitis fibrosa cystica 

Rheumatologic: arthralgia, myalgia, and gout

Neurological: Paresthesias, headaches, diminished deep tendon reflexes, insomnia, irritability 

Dermatologic: Pruritus 

Renal: Nephrolithiasis, polyuria, polydipsia, and renal failure 

Diagnosis 

1. Laboratory findings: Elevated serum calcium, ionized calcium; Elevated PTH; Low or low-normal phosphate levels; Elevated alkaline phosphatase

2.Other tests: Radiographs: Extensive areas of demineralization with areas of increased bone density (“Salt and pepper” skull); Electrocardiography & echocardiography

Treatment 

Medications: Calcium mimetics such as Cinacalcet, Bisphosphonates, Denosumab, Vitamin D and vitamin D analogs

Surgical treatment: Parathyroidectomy 

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Pseudohypoparathyroidism (PHP) is a genetic disorder of end-organ insensitivity to the effect of PTH, which results in hypocalcemia, hyperphosphatemia, and increased PTH levels

Symptoms & Signs 

-As the name implies, patients with pseudohypoparathyroidism have signs and symptoms characteristic of hypoparathyroidism

-PHP may be associated by a characteristic phenotype known as Albright Hereditary Osteodystrophy (AHO) which includes short stature, round facies, shortening of the fourth metacarpals (brachydactyly), and osteoma cutis 

-Examination of the clenched fist reveals a characteristic depression where the knuckle of the fourth metacarpal should be located.

Diagnosis 

-A high concentration of serum PTH, low serum calcium, high phosphate, and 

signs and symptoms of hypoparathyroidism

-patients with pseudohypoparathyroidism do not respond to infused PTH

Treatment 

Treatment is the same as for hypoparathyroidism

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Introduction 

-The four parathyroid glands produce and secrete PTH

-Hypoparathyroidism develops when the parathyroid glands fail to secrete sufficient quantities of PTH, resulting in a low calcium level and a high phosphorus level 

-The most common cause of hypoparathyroidism is neck surgery with removal or destruction of the parathyroid glands

-Other causes include congenital abnormalities of the third and fourth pharyngeal pouches (DiGeorge syndrome), autoimmune or drug induced or radiation induced hypothyroidism 

Symptoms & Signs 

Skin: Dry, scaly skin, coarse hair

Ocular: Cataracts, Papilledema 

Dental: enamel hypoplasia, defective root formation, delayed teeth eruption

Respiratory: Bronchospasm, laryngospasm, stridor 

Cardiac: Heart failure, Prolonged QT interval on ECG

Psychological: Confusion, behavioral changes, psychosis 

Neuromuscular: numbness, tingling, carpopedal spasms, seizures, Parkinsonism

Tetany: Spontaneous tonic muscular contractions; Classically diagnosed by Chvostek sign and Trousseau sign

Chvostek sign: twitching or contraction of the facial muscles in response to tapping the facial nerve at a point anterior to the ear and above the zygomatic bone

Trousseau sign: it is elicited by inflating the sphygmomanometer with the cuff around the arm above the systolic blood pressure for 3 min; The wrist and metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers adduct

Diagnosis 

Labs: Inappropriately low or undetectable PTH level, low calcium level, high phosphorus level

EKG: a prolonged QT interval on the ECG

Treatment 

Recombinant PTH; IV or oral calcium, Vitamin D supplementation; correction of hypomagnesemia