SEARCH RESULTS FOR: Gynecomastia

Clinical Findings of Androgen Deficiency

Yu, Yan - Androgen Deficiency - FINAL.pptx Hypogonadism in Males:Clinical Findings of Androgen Deficiency? secretion volume from seminal vesicle and prostateAuthor: Yan YuReviewers:Peter VetereGillian GoobieHanan Bassyouni** MD at time of publicationLegend:Published June 18, 2013 on www.thecalgaryguide.comMechanismPathophysiologySign/Symptom/Lab FindingComplications? effect of testosterone on the brain? Libido(sensitive, but less specific)? [testosterone] : [estrogen] ratio at the male breast? ejaculate volume(a sensitive and specific sign)Gynecomastia (palpable breast tissue, not fat, directly under nipple)Fatigue,low mood, irrtabilityHot flashes, sweats(Can be nocturnal; occur only when hypogonadism is severe)Vasomotor neural response of unknown causeFewer spontaneous erections (i.e. in the morning)Lack of androgens (i.e. testosterone, DHT) in men past the age of pubertyIn advanced stages of the disease, after years of hypogonadism:(thus, less commonly seen)Low Bone Mass Density (BMD)Less testosterone to be converted into estrogen in bone? muscle bulk and strengthSmall, soft testicles(<4cm long on orchidometer)Lack of hormones to stimulate and maintain testicular hyperplasia/growthLoss of androgenic hair (on face, midline, and pubic area)Vertebral fracture (height loss), or other fragility fracturesIf sexual development is incomplete from puberty:Note: These clinical findings apply to many disorders, including:-Andropause-Hypopituitarism (suspect if other hormone abnormalities & Sx of mass lesion like visual field loss, diplopia, and headache exist)-Testicular Failure (if Hx of chemo, radiation, excess alcohol, and chronic liver disease)-Klinefelter's (if assoc. tall and eunuchoid stature, breast enlargement and cognitive deficiency - XXY)-Kallman's (if assoc. anosmia, and tall/eunuchoid stature)-Drugs (e.g. ketoconazole, anabolic steroids, spironolactone, digoxin, marijuana)Testosterone's inhibitory effect on estrogen is not enough to prevent breast growthDeficiency in testosterone during puberty delays fusion of epiphysesTall, eunuchoid statureNote: any disease involving an increase in aromatase activity (hyperthyroidism, cirrhosis, HCG-secreting tumors) will also cause relative estrogen excess & subsequent gynecomastia. 111 kB / 272 words

Viral-Hepatitis

Viral Hepatitis: Pathogenesis and clinical findings Infection with a virus that targets the Authors: Sean Spence Tyler Anker Yan Yu Reviewers: Dean Percy Crystal Liu Sam Lee* * MD at time of publication liver, e.g. HAV, HBV, HCV, HDV, HEV Hepatocytes are invaded & damaged Foreign particles and tissue damage activate immune systemàliver inflammation Lysis (bursting) of hepatocytes Infection with chronic viruses (HBV and HCV) persist over time and additional symptoms may develop RUQ pain/tenderness If infection is prolonged or severe, inflammation becomes systemic Release of hepatocyte’s cellular contents into the bloodstream Infection with acute viruses (HAV and HEV) resolve over time, and the symptoms above normalize Notes: • HDV can only infect people with concomitant HBV infection • HAV and HBV vaccines are the only ones that currently exist • Not all patients with viral hepatitis will develop each of these symptoms. The presentations vary. Fever, nausea, vomiting ↑ serum ALT, AST ↓ Hepatic metabolic activity (e.g. reduction of gluconeogenesis) ↓Serum Glucose ↓ Synthesis of plasma proteins (albumin, clotting factors, etc) ↓ Albumin, ↑ INR Abbreviations: • HAV - Hepatitis A Virus • HBV - Hepatitis B Virus • HCV - Hepatitis C Virus • HEV - Hepatitis E Virus • RUQ - Right Upper Quadrant • ALT - Alanine Aminotransferase • AST - Aspartate Aminotransferase • INR - International Normalized Ratio ↓ Bilirubin clearance from blood, bilirubin ends up under the skin Jaundice Portal Hypertension Encephalopathy, Splenomegaly, Esophageal Varices, Ascites, Caput Medusae, Edema Encephalopathy, Muscle Wasting, Metabolic Bone Disease, Terry’s Nails, Ascites, Bruising, Clubbing, Edema Spider Nevi, Altered Hair Patterns, Testicular Atrophy, Gynecomastia, Palmar Erythema Progressive deterioration in liver function, possibly ending up in cirrhosis. (See slide on “Cirrhosis: pathogenesis and complications” for more details on mechanisms and full explanations.) Hepatic Insufficiency Hyperestrogenism Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Re-Published January 12, 2020 on www.thecalgaryguide.com

Potassium-Sparing-Diuretics-Mechanism-of-Action-and-Side-Effects

Potassium-Sparing Diuretics: Mechanism of Action and Side Effects Potassium-Sparing Diuretics Authors: Samin Dolatabadi, Yan Yu* Reviewers: Jessica Krahn, Timothy Fu, Juliya Hemmett* * MD at time of publication Epithelium Sodium Channel Blockers (Amiloride and Triamterene) Inhibit Na+ channels (involved in Na+ reabsorption) in the luminal membrane of the principal cells in the cortical collecting duct Aldosterone Antagonists (Spironolactone and Eplerenone) Competitively blocks mineralocorticoid receptors and ↓ aldosterone effect in the renal tubules and throughout the body ↓ aldosterone effectà↓ expression of basolateral Na+/K+ pumps & luminal epithelium Na+ channels on the principal cells of cortical collecting duct Spironolactone’s molecular structure is similar to that of steroid hormonesàspironolactone can also block androgen receptors Anti-androgenic effects (due to ↓ androgen function in reproductive organs, skin, and on brain centers) Triamterene can form triamterene crystals and granular casts (unclear mechanism) ↓ Na+ reabsorption by principal cells ↓ in serum Na+ concentration: Hyponatremia ↓ K+ pumped out into the tubule by principal cells Crystals & casts obstruct tubular lumen → inflammation (unclear mechanism) Triamterene crystals are directly cytotoxic to tubular cells Only ~2-5% of Na+ filtered by the glomerulus is normally reabsorbed in the cortical collecting ductàthe ↑ in Na+ retained in cortical collecting duct is mild Water follows Na+ to maintain a balanced osmotic pressureà↑ in water in cortical collecting duct available for excretion ↑ positive charges in lumen relative to surroundings generates an electropositive tubular lumen Unfavorable electrical gradient ↓ secretion of positive charged ions into electropositive lumen ↓ libido Menstrual abnormalities (in women) ↓ acne Gynecomastia (in men) ↓ secretion of K+ ↑ in serum K+ concentration: Hyperkalemia Cardiac Arrythmias (See relevant slide on Hyperkalemia: Clinical Findings) Interstitial inflammation and tubular injury Drug-induced Nephrotoxicity Mild Diuresis ↓ blood volume ↓ Blood pressure/ Hypotension ↓ secretion of H+ ↑ in serum H+ concentration: Metabolic Acidosis Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published February 15, 2021 on www.thecalgaryguide.com

Gynecomastia

Gynecomastia: Pathogenesis Authors: Sara Cho Reviewers: Michelle J. Chen Samuel Fineblit* *MD at time of publication Physiologic causes Puberty Placenta transfers maternal estrogens to newborn male babies Older age (>60 years) Hyperthyroidism Klinefelter Syndrome (males with > 1 X chromosome) Liver cirrhosis Certain tumors (e.g., germ cell, adrenal, Leydig cell, Sertoli cell) Anabolic steroid usage (containing testosterone) Finasteride (treatment for benign prostate hyperplasia and male pattern baldness) Cimetidine - inhibits stomach acid production Spironolactone (diuretic used to treat high blood pressure and heart failure) Ketoconazole (antifungal) Cytotoxic agents (e.g. alkylating agents, vincristine, methotrexate) Imbalance between estrogens and androgens Estrogen stimulates breast tissue growth in newborn Changes in metabolic rate ↑ fat production Unclear mechanism ↑ Proinflammatory mediators and cytokines (e.g. prostaglandin E2, TNF⍺, IL-1, IL-6, cyclooxygenase-2) Prostaglandin E2 and IL- 6 upregulate aromatase enzyme expression Available estrogen is higher than available testosterone ↑ Aromatase enzyme activity, converting androgens to estrogen ↓ Testosterone release from the testes ↓ Testosterone ↑ Serum sex hormone binding globulin (SHBG) SHBG binds estrogen with less affinity to testosterone Thyroid hormone stimulates liver to express more sex hormone binding globulin Thyroid hormone stimulates aromatase activity Overexpression of aromatase enzyme Seminiferous tubules in the testes hyalinize and fibrose Suppression of the hypothalamic pituitary thyroid axis through an unclear mechanism Tumor may produce estradiol Tumor produces β- human chorionic gonadotropin (β-HCG) ↑ serum testosterone Inhibits 5-α reductase Blocks binding of 5-DHT to androgen receptors ↓ 2-hydroxylation of estradiol Mimics structures of testosterone Inhibits 17,20 desmolase and 17α-hydroxylase Damage to Leydig cells in testes ↑ Estrogen to androgen ratio Pathological causes Impaired spermatogenesis and testosterone production ↓ GnRH secretion from hypothalamus ↓ Testosterone ↓ Luteinizing hormone (LH) release from anterior pituitary ↓ 5-DHT and/or testosterone binding to androgen receptors in chest tissue ↓ inhibition of breast development Normal or increased estrogen acts on estrogen receptor on chest tissue Estrogen receptors stimulate breast development Estradiol negatively feedbacks on luteinizing hormone β-HCG stimulates LH receptors on Leydig cells in the testes Aromatase enzyme converts excess testosterone into estrogen and estradiol ↓ conversion of testosterone to 5- dihydrotestosterone (5-DHT), a more potent form of testosterone Glandular proliferation in male breasts Gynecomastia (development of breast tissue in males) Drug side- effects ↓ Metabolism of estradiol Competitively binds to androgen receptors ↑ Serum estradiol levels Exhibits physical attributes that do not align with gender identity Psychological distress In some cases, hormones stabilize Involution and atrophy of ducts Gynecomastia resolves ↓ Steroid synthesis ↓ Androstenedione produced (testosterone precursors) ↓ Serum testosterone levels ↓ Testosterone production Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Jun 9, 2024 on www.thecalgaryguide.com