Atrophic vaginitis: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
====Pathogenesis==== | ====Pathogenesis==== | ||
The pathogenesis of atrophic vaginitis is related to decreased estrogen levels. The following are the manifestations of decreased estrogen levels:<ref name="pmid20042564">{{cite journal |vauthors=Mac Bride MB, Rhodes DJ, Shuster LT |title=Vulvovaginal atrophy |journal=Mayo Clin. Proc. |volume=85 |issue=1 |pages=87–94 |year=2010 |pmid=20042564 |pmc=2800285 |doi=10.4065/mcp.2009.0413 |url=}}</ref><ref name="pmid9332260">{{cite journal |vauthors=Pandit L, Ouslander JG |title=Postmenopausal vaginal atrophy and atrophic vaginitis |journal=Am. J. Med. Sci. |volume=314 |issue=4 |pages=228–31 |year=1997 |pmid=9332260 |doi= |url=}}</ref> | The pathogenesis of atrophic vaginitis is related to decreased estrogen levels. The following are the manifestations of decreased estrogen levels:<ref name="pmid20042564">{{cite journal |vauthors=Mac Bride MB, Rhodes DJ, Shuster LT |title=Vulvovaginal atrophy |journal=Mayo Clin. Proc. |volume=85 |issue=1 |pages=87–94 |year=2010 |pmid=20042564 |pmc=2800285 |doi=10.4065/mcp.2009.0413 |url=}}</ref><ref name="pmid9332260">{{cite journal |vauthors=Pandit L, Ouslander JG |title=Postmenopausal vaginal atrophy and atrophic vaginitis |journal=Am. J. Med. Sci. |volume=314 |issue=4 |pages=228–31 |year=1997 |pmid=9332260 |doi= |url=}}</ref><ref name="pmid27472999">{{cite journal |vauthors=Gandhi J, Chen A, Dagur G, Suh Y, Smith N, Cali B, Khan SA |title=Genitourinary syndrome of menopause: an overview of clinical manifestations, pathophysiology, etiology, evaluation, and management |journal=Am. J. Obstet. Gynecol. |volume= |issue= |pages= |year=2016 |pmid=27472999 |doi=10.1016/j.ajog.2016.07.045 |url=}}</ref> | ||
*A hypoestrogenic state, such as that seen in menopause, causes the vaginal epithelium to lose its rugae, as well as become thin and pale or erythematous with fine petechial hemorrhages. | *A hypoestrogenic state, such as that seen in menopause, causes the vaginal epithelium to lose its rugae, as well as become thin and pale or erythematous with fine petechial hemorrhages. | ||
*Decreased glycogen content within the epithelium due to decreased thickness leads to less glycogen content available for the [[lactobacilli]] to utilize and turn it into [[lactic acid]]. As a result, the vaginal pH rises with a resultant overgrowth of other bacteria, such as [[group B streptococci]], [[Staphylococci]] and diptheroids. | *Decreased glycogen content within the epithelium due to decreased thickness leads to less glycogen content available for the [[lactobacilli]] to utilize and turn it into [[lactic acid]]. As a result, the vaginal pH rises with a resultant overgrowth of other bacteria, such as [[group B streptococci]], [[Staphylococci]] and diptheroids. As a result, vaginal infections, [[UTI]] and inflammation become more common in the setting of atrophic vaginitis. | ||
====Genetics==== | ====Genetics==== | ||
Revision as of 01:20, 24 October 2016
For patient information, click here
| Atrophic vaginitis | |
| ICD-10 | N95.2 |
|---|---|
| ICD-9 | 627.3 |
| DiseasesDB | 32516 |
| MedlinePlus | 000892 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]
Synonyms and keywords: Atrophic vulvovaginitis; vaginal atrophy; urogenital atrophy; genitourinary syndrome of menopause
Overview
Historical Perspective
Classification
Pathophysiology
Pathogenesis
The pathogenesis of atrophic vaginitis is related to decreased estrogen levels. The following are the manifestations of decreased estrogen levels:[1][2][3]
- A hypoestrogenic state, such as that seen in menopause, causes the vaginal epithelium to lose its rugae, as well as become thin and pale or erythematous with fine petechial hemorrhages.
- Decreased glycogen content within the epithelium due to decreased thickness leads to less glycogen content available for the lactobacilli to utilize and turn it into lactic acid. As a result, the vaginal pH rises with a resultant overgrowth of other bacteria, such as group B streptococci, Staphylococci and diptheroids. As a result, vaginal infections, UTI and inflammation become more common in the setting of atrophic vaginitis.
Genetics
Gross Pathology
Microscopic Pathology
Associated Conditions
Causes
Epidemiology and Demographics
Risk Factors
Screening
Differentiating atrophic vaginitis from other diseases
Atrophic vaginitis must be differentiated from other disease processes that may present with similar symptoms. These can be divided into 3 categories:[1]
- Vaginal infections: Candida vulvovaginitis, bacterial vaginosis and trichomoniasis
- Vulvovaginal dermatoses: lichen sclerosus, lichen planus and lichen simplex chronicus
- Cancer and precancerous lesions: vulvar intraepithelial neoplasia, vulvar cancer and extramammary Paget disease
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Symptoms of atrophic vaginitis can be divided into two categories:[1][2][3]
- External Genital Symptoms
- Vaginal dryness
- Vaginal irritation
- Vaginal itching
- Vaginal discharge
- Painful sexual intercourse (dyspareunia)
- Postcoital bleeding
- Urological Symptoms
- Burning on urination (dysuria)
- Urinary frequency
- Urinary urgency
- Nocturia
- Urge incontinence
- Stress incontinence
- Recurrent urinary tract infections (UTI)
Physical Examination
Laboratory Findings
CT
MRI
Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
The mainstay of treatment of atrophic vaginitis is medical therapy. It can be categorized into two groups:[1]
- Nonhormonal therapy: this includes vaginal moisturizers and lubricants
- Hormonal therapy: this includes vaginally administered local estrogens
Primary Prevention
Secondary Prevention
References
- ↑ 1.0 1.1 1.2 1.3 Mac Bride MB, Rhodes DJ, Shuster LT (2010). "Vulvovaginal atrophy". Mayo Clin. Proc. 85 (1): 87–94. doi:10.4065/mcp.2009.0413. PMC 2800285. PMID 20042564.
- ↑ 2.0 2.1 Pandit L, Ouslander JG (1997). "Postmenopausal vaginal atrophy and atrophic vaginitis". Am. J. Med. Sci. 314 (4): 228–31. PMID 9332260.
- ↑ 3.0 3.1 Gandhi J, Chen A, Dagur G, Suh Y, Smith N, Cali B, Khan SA (2016). "Genitourinary syndrome of menopause: an overview of clinical manifestations, pathophysiology, etiology, evaluation, and management". Am. J. Obstet. Gynecol. doi:10.1016/j.ajog.2016.07.045. PMID 27472999.