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The document discusses the effects of Tamoxifen on hormonal imbalances and the resulting physiological changes, including the stimulation of growth factors and cellular proliferation in the endometrium. It highlights the development of endometrial polyps, their structural integrity issues, and the associated risks of abnormal uterine bleeding and infertility. Additionally, it outlines the inflammatory response and tissue remodeling processes that contribute to pelvic pain and menstrual irregularities.

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Katrina Jhane Mercado
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12 views1 page

Safari

The document discusses the effects of Tamoxifen on hormonal imbalances and the resulting physiological changes, including the stimulation of growth factors and cellular proliferation in the endometrium. It highlights the development of endometrial polyps, their structural integrity issues, and the associated risks of abnormal uterine bleeding and infertility. Additionally, it outlines the inflammatory response and tissue remodeling processes that contribute to pelvic pain and menstrual irregularities.

Uploaded by

Katrina Jhane Mercado
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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Age Tamoxifen Use – orally Hormonal Imbalances

Obesity taken (Hormone replacement


Family History therapy or Tamoxifen
Metabolic Disorders Use)
Absorbed in the bloodstream through GI tract Chronic inflammation
Mechanical factors

Transported into the liver

Metabolized into active forms

Enters the bloodstream → circulates to different


body tissues

Binds to estrogen receptors in the


endometrium

Disrupts the progesterone action


Binds to er-a receptors

Er-a activation Unopposed estrogen like


stimulation

Partial agonist effects in the endometrium →


persistent receptor activation

Stimulates upregulation of growth


factors

Insulin-like Growth Factor (IGF) Vascular Endothelial Growth Factor (VEGF)

Stimulates cellular proliferation Inhibits apoptosis Promotes excessive angiogenesis


(lacks proper regulation)

Continuous cell growth →


accumulation of cells Fragile and dysfunctional blood vessels

Stromal and glandular


cell growth

Endometrial Polyps

Polyps lack structural integrity of blood


vessels

Poor blood flow Easily ruptured

Abnormal uterine bleeding


Localized hypoxia in the endometrial
polyps
If persistent, gradual iron
loss over time
Tissue damage

Impaired hemoglobin
production
Segmented Neutrophils (70.4 Inflammatory response stimulation (vasodilation, immune cell
%)- High and Monocytes activation (neutrophils & macrophages) ,macrophages releases
(5.2%)) Slightly High secretes cytokines)
Hemoglobin (11.6 g/L)
Low and MCV (79.6 fL)
Macrophages releases growth Slightly Low
factors
Release of prostaglandins

VEGF production → reinforcing PDGF (Platelet-Derived Growth Factor) →


Stimulates nociceptors in abnormal angiogenesis recruits fibroblasts to the injury site
pelvic tissue

Transforming Growth Factor-β (TGF-β) and FGF


Pelvic Pain/Discomfort released → promotes fibroblast proliferation

Fibroblasts releases ECM (collagen,


fibronectin, hyaluronic acid) for tissue repair

Persistent TGF- β activation keeps fibroblasts active

Stimulates TIMPs production Fibroblasts turns into myofibroblasts

Inhibits ECM breakdown → enhances Secrete excessive extracellular matrix (ECM)


collagen deposition – collagen and fibronectin

Tissue becomes thick and stiff Strengthened polyp tissue

Less receptive to embryo


implantation Thick-walled, rigid and vascularized polyps Prevent proper endometrial shedding

Localized hypoxia Menstrual irregularities


Infertility

VEGF production → reinforcing angiogenesis Large polyps losing support


Structural distortion of the uterus

Polypoid mass (4.7 × 4.3 cm)


Uterus: Retroverted, mildly globular Continuous fibrosis prolapsing from the endocervical
with heterogeneous texture canal

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