SEARCH RESULTS FOR: Endometriosis

Primary Spontaneous Pneumothorax: Pathogenesis and clinical findings

Primary Spontaneous Pneumothorax: Pathogenesis and clinical findings Thoracic Tall, thin endometriosis males Genetic Factors (i.e. FLCN mutations, HCY, MFS, CTD) Malnutrition Smoking Structurally compromised lung parenchyma Notes: • PSPs usually occur at rest • Respiratory symptoms vary in severity • Suspect thoracic endometriosis in young women with recurrent PSPs that coincide with menstruation • *Pathophysiology of tension pneumothorax is described in a separate slide Air leaks into the subcutaneous tissue Subcutaneous emphysema Authors: Lauren Hampton Reviewers: Kening (Midas) Kang Natalie Morgunov Sadie Kutz Usama Malik Leila Barss* * MD at time of publication Thoracic Ischemia endometriosis Mechanical forces of respiration create blebs Inflammation disrupts mesotheial and/or bullae ~ cell layer of the visceral pleura 47 Spontaneous rupture of blebs or bullae 47 Sudden onset pleuritic chest pain 71r Primary spontaneous pneumothorax: Presence or introduction of air in the pleural space in a patient WITHOUT diagnosed or clinically apparent lung disease Tachycardia Abbreviations: Communication occurs between the alveoli and pleural space • FLCN- Folliculin gene • HCY- Homocystinuria • MFS- Marfan syndrome Alveolar pressure > pleural pressure • CTD- Connective tissue disease • PSP- Primary spontaneous Air from the lungs enters the pleural space pneumothorax • V/Q- ventilation/perfusion Air separates the chest from /1` intrapleural pressure • Sp02- oxygen saturation the lung parenchyma Small areas of lung collapse Blood flow to areas of On affected side: under un-opposed intrinsic atelectasis is maintained -• Si, chest wall expansion elastic recoil while ventilation 4, t resonance to percussion Si, or absent tactile fremitus Si, or absent breath sounds 4, lung compliance Shunting and V/Q mismatch Pleural line on chest x-ray 1` work of breathing Tension pneumothorax* Accessory muscle use, 4• Sp02, Sudden onset dyspnea, Tachycardia Hypotension, Juglar venous Tachypnea distension, Pulsus paradoxus

Pathogenesis-of-Female-Infertility

Pathogenesis of Female Infertility Author: Simonne Horwitz Reviewers: Claire Lothian, Hannah Yaphe, Yan Yu*, Nicole Paterson* * MD at time of publication Extreme stress, eating disorder, excessive exercise, intracranial tumor, or hyperprolactinemia* ↓ Gonadotropin releasing hormone (GnRN) from hypothalamus ↓ release of Luteinizing hormone (LH) & Follicle stimulating hormone (FSH) by pituitary ↓ release of estrogen by ovaries Anovulation (oocyte is not released) Fewer follicles available to ovulate * Causes of Hyperprolactinemia include: prolactinoma (prolactin-producing tumor), hypothalamic infiltrate or mass, chest wall irritation, hypothyroidism, renal or liver disease (↓ prolactin clearance), dopamine antagonists that ↑ prolactin secretion (antipsychotics, anti- depressants, anti-emetics) Polycystic ovary syndrome (see PCOS: Pathogenesis and Clinical findings) ↑ androgen production & ↑ estrogen earlier in the menstrual cycle ↓ FSHà↓ follicle growth ↑ rate of follicle depletion Oocyte not available every month for fertilization Premature ovarian insufficiency due to unexplained causes, chemotherapy, radiation, autoimmune ovarian destruction, Turner’s & Fragile X Syndromes Damage in germ cells that accumulates over a woman’s lifetime Age-related changes in quality of granulosa cells surrounding oocyte Genetic damage accumulates, such as ↑ rates of meiotic nondisjunction (failure of chromosomes to separate during gamete cell division) Tubal occlusion or ↓ transport of oocyte tubal cilia dysfunction through fallopian tube ↓ quality of oocytes Normal transport of oocyte & sperm through fallopian tube is impaired ↓ facilitation of sperm transportation Inhibits normal zygote implantation Chlamydial or gonorrhoeal pathogens Previous tubal surgery or ectopic pregnancy surgery tissue removal ↓ transport of oocyte through fallopian tube Female Infertility Previous abdominal infection or surgery Endometriosis Congenital malformations or trauma / surgery to cervix Uterine leiomyomata (benign smooth muscle monoclonal tumor) or polyp Intrauterine procedures Pelvic adhesions (scar-like tissue that tether together abdominal organs) may distort the shape and normal anatomy of the fallopian tube Ectopic endometrial cells implant & Local inflammatory response grow along pathway of egg/sperm further ↓ egg/sperm mobility Inability of cervix to produce normal mucus, and/or sperm physically unable to enter the cervix Submucosal or intracavitary component disrupts uterine lining Trauma to basalis layer of endometrium Intrauterine scarring or synechiae (adhesions) ↓ vascularization & endometrial regrowth Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published October 25, 2020 on www.thecalgaryguide.com

epithelial-ovarian-cancer-pathogenesis-and-clinical-findings

Epithelial Ovarian Cancer: Pathogenesis and clinical findings Authors: Brian Yu Chieh Cheng, Yan Yu* Reviewers: Mehul Gupta, Hannah Yaphe, Sarah Glaze* * MD at time of publication See Epithelial Ovarian Cancer Risk Factors slide BRCA1 or BRCA2 mutationà faulty double strand DNA repairà↑ mutations & loss of controlled cell division Asymptomatic serous tubal intraepithelial carcinoma (STIC) lesions of the fallopian tube fimbria develop overtime STIC cells may break off from the fallopian tube & become trapped during inclusion cyst formation As part of the ovarian cycle, the coelomic epithelium (CE) of the ovary is ruptured & repaired after ovulation Incomplete repair of the CE results in invagination of the rupture site, forming a benign cortical inclusion cyst CE cells trapped during cyst formation undergoes metaplasia to tubal or other types of epithelium Endometriosis Endometriosis causes endometrial tissue to start growing on ovarian CE Endometrial cells trapped during cyst formation progresses to endometrioma or “chocolate cysts” Immune cell infiltration & cytokine release inside the ovary results in dysregulated inflammation Cancer cells proliferate in distant organs, invading & destroying native cells Organ failure Metastatic spread to liver, lung, brain & lymph nodes Lymphadenopathy Systemic immune activation ↑ metabolic consumption ↑ capillary surface area & permeability Fatigue & weight loss ↑ fluid entry into Ascites peritoneal cavity Further somatic mutation accumulation leads to malignant transformation of epithelium Tumor growth stimulates new blood vessel formation to supply itself with nutrients & O2 Omental / peritoneal seeding of cancer cells Early-stage disease Asymptomatic Epithelial Ovarian Cancer In late-stage disease, tumor may secrete a glycoprotein called mucin 16, also known as CA-125 (sensitive but non-specific biomarker for ovarian cancer) ↑ serum CA-125 levels Cancer cells proliferate inward & eventually ruptures the ovary Cancer cells are released into the peritoneal cavity Tumor growth in local organs (bladder/uterus) progresses to symptomatic cancer ↑ tumor volume & local tumor spread directly disrupts neighboring structures Pelvic/abdominal pain Palpable pelvic/abdominal mass Altered urinary frequency Compression of colon/bladder Change in bowel habits Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published August 15, 2021 on www.thecalgaryguide.com

Ectopic Pregnancy

Ectopic Pregnancy: Pathogenesis and Clinical Findings In vitro fertilization Tubal disorders leading to infertility and unknown procedural causes Previous ectopic pregnancy Underlying tubal disorder leading to previous ectopic Pelvic inflammatory disease (PID) Endometriosis Tubal surgery or disorders Age >35 Risk factor accumulation over time Smoking Impairment in tubal motility; impaired immunity (risk factor for PID) Tubal scarring leading to adhesions, obstruction, and alteration of tubal function Ectopic Pregnancy: Implantation of developing blastocyst outside the uterine cavity, most commonly in fallopian tube (other locations: interstitial > cornual > cervical > ovarian > abdominal) Embryo releases human chorionic gonadotropin (β-hCG), which supports corpus luteum to continue producing progesterone On transvaginal ultrasound: Extrauterine gestational sac with a yolk sac or embryo Embryo & trophoblast deathàloss of hormone support for the decidua (modified endometrial lining) Progesterone maintains the endometrial lining, preventing it from shedding Missed period Penetration of ovum into muscular wall of fallopian tube Tubal distention àTubal rupture Intra-abdominal hemorrhage Pregnancy cannot survive without the uterine endometrium Maternal blood extrudes through fimbriae of fallopian tubes and into peritoneal cavity Lower abdominal pain (including peritonitis in cases of hemoperitoneum) Hemoperitoneum (blood in the peritoneal cavity) Sloughing of decidua out of the uterus through the vagina Vaginal bleeding (usually in first trimester) Cessation of human chorionic gonadotropin (β-hCG) release from embryo β-hCG plateaus or decreases Authors: Jemimah Raffé-Devine Tahsin Khan Yan Yu* Reviewers: Brianna Ghali Bishwas Paudel Mackenzie Grisdale Christina Schweitzer Ron Cusano* Jadine Paw* * MD at time of publication Syncope ↓ Level of consciousness Positive β-hCG, but rising <35% over 2 days Discriminatory zone: β-hCG >2000 + absence of intrauterine pregnancy Hypotension Shock Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Oct 1, 2017, updated Oct 19, 2021 on www.thecalgaryguide.com

epithelial-ovarian-cancer-subtypes-molecular-alterations-risk-factors

Epithelial Ovarian Cancer: Subtypes, Molecular Alterations & Risk Factors Risk factors associated with developing specific subtypes of epithelial ovarian cancer Authors: Brian Yu Chieh Cheng Reviewers: Ayaa Alkhaleefa, Parker Lieb, Tara Shannon, Sarah Glaze* * MD at time of publication No known subtype specific risk factors Smoking Introduction of carcinogenic material ↑Rate of cancer causing genetic mutations 2) Mucinous carcinoma Ovarian endometriosis (implantation of endometrial tissue on the ovaries) ↑ Chance of endometrioma (cyst comprised of endometrial tissue) formation in ovaries See Endometriosis Slide Familial BRCA1 or BRCA2 mutation Impaired double strand DNA repair mechanism results in accumulation of DNA damage 5) High grade serous carcinoma Lynch syndrome (autosomal dominant mutations in DNA repair genes) Impaired DNA mismatch repair mechanismà accumulation of DNA damage 1) Low grade serous carcinoma 3) Clear cell carcinoma 4) Endometrioid carcinoma Either clear cell, endometrioid carcinomas, or a mix of both subtypes General risk factors for developing all epithelial ovarian cancer (unknown pathogenesis) 1. Old age 2. Family history of breast or ovarian cancer 3. Post-menopausal hormone replacement therapy 4. Irregular age of menarche & menopause 5. High number of lifetime ovulation events / nulliparity Alteration in genes like KRAS, NRAS, BRAF, ERBB2 & CDKN2A Alteration in genes like ARID1A, PIK3CA & ERBB2 Alteration in genes like POLE & TP53 Molecular alterations in genes like TP53 and/or CCNE1 Molecular alterations commonly associated with specific epithelial ovarian cancer subtypes Legend: Pathophysiology Mechanism Sign/Symptom/Lab Findings Complications Published August 30, 2022 on www.thecalgaryguide.com

Endometriose Pathogenese und Komplikationen

Endometriose: Pathogenese und Komplikationen

Endometriosis

Endometriosis: Pathogenesis, clinical findings, & complications Risk factors Theories of endometrial tissue migration Genetic causes (family history & specific gene loci) Transfer of endometrial tissue away from the uterus during pelvic surgery, vaginal delivery, or cesarean section Sampson’s theory: Retrograde flow of endometrial tissue through fallopian tubes Long menstrual flows (↑ retrograde menstruation) Coelomic metaplasia theory: Undifferentiated mesothelial cells from the peritoneal cavity differentiate into endometrial cells during fetal development. May also occur in patients with testes Implantation theory: Menstrual endometrium implants onto pelvic structures ↓ Cellular antioxidant capacity (↑ cell damage) Alcohol use (mechanism unclear) Early menarche (↑ estrogen exposure) Stem cell theory: Endometrial stem/ Embryonic rest theory: Residual progenitor cells from menstrual embryonic cells from Müllerian Dissemination theory: Endometrial blood or neonatal uterine bleeding or Wolffian ducts are misplaced tissue transported through bloodstream implant in the pelvic cavity during organogenesis or lymphatics to extrauterine structures (e.g., brain, pericardium) Cells differentiate into endometrial-like tissue Ovary releases estrogen & progesterone Endometriosis Endometrial glands & stroma (structural support tissue) found outside the uterus Ectopic endometrial-like tissue on bladder Ectopic endometrial-like tissue in posterior cul-de-sac Monthly proliferation (by estrogen) and stabilization (by progesterone) of endometrial tissue Chronic inflammation of surrounding tissues & fibrosis/adhesion formation Tissue inflammation & fibrosis/adhesions push on & displace pelvic organs Ectopic tissue abnormally activates nerve signaling pathways responsible for bladder contraction Bladder wall contractions activate nociceptors (pain sensors) Penetrative intercourse involving the posterior vagina applies ↑ pressure to tethered & immobile pelvic structures Feces moves down colon into rectum & applies pressure to the tethered rectum Monthly progesterone withdrawal Dyspareunia (pain with deep intercourse) Dyschezia (pain with bowel movements) ↑ Urinary frequency & urgency Pain with micturition (urination) Endometrial tissue sloughs off from a basal tissue layer (menstruation**) Extra-uterine endometrial- like tissue cannot evacuate the implantation site Retrograde menstruation in ovary ↑ the presence of ectopic endometrial-like tissue & blood (mechanism poorly understood) Old blood fills endometrial-like tissue on ovary Endometrioma (chocolate cyst) Chronic cyclical local inflammation (release of pro-inflammatory chemicals) Nociceptors near ectopic endometrial-like tissue activate Pain signals & release of inflammatory mediators subsides over time Cyclic dysmenorrhea (menstrual pain) Repair of inflammation Ectopic endometrial-like tissue becomes fibrotic (scarred) Significant ↑ scar tissue Nodule formation ↓ Hormone levels post-menopause Accumulation of inflammatory fluid within scar tissue ↑ Risk of scar tissue obstructing or kinking fallopian tubes Endometrial tissue stops proliferating Hormone-dependent symptoms (e.g., dysmenorrhea) cease Cyst formation Embryos unable to pass through fallopian tube to uterus Author: Joshua Seto Kayla Nelson Reviewers: Yan Yu Sean Spence Jessica Revington Infertility Colin Birch*, Rachel Wang* * MD at time of publication **See corresponding Calgary Guide slide Legend: Published December 20, 2013, revised September 24, 2025 on www.thecalgaryguide.com Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications