The European Menopause and Andropause Society has released guidelines for assessment of the endometrium, which is usually the main source of spotting or bleeding.In post-menopausal women, however, any unscheduled vaginal bleeding is of concern and requires an appropriate investigation to rule out the possibility of malignant diseases. Urogenital symptoms that may appear during menopause and continue through postmenopause include:

painful intercourse
vaginal dryness
atrophic vaginitis – thinning of the membranes of the vulva, the vagina, the cervix, and the outer urinary tract, along with considerable shrinking and loss in elasticity of all of the outer and inner genital areas. Urinary urgency and burning

Other physical
Other physical symptoms of menopause include lack of energy, joint soreness, stiffness, back pain, breast enlargement, breast pain,
heart palpitations, headache, dizziness, dry, itchy skin, thinning, tingling skin, rosacea,  weight gain, urinary incontinence,urinary urgency,
interrupted sleeping patterns, heavy night sweats, and hot flashes. Mood and memory effects
Psychological symptoms include anxiety, poor memory, inability to concentrate, depressive mood, irritability, mood swings, and less interest in sexual activity.Menopause-related cognitive impairment can be confused with the mild cognitive impairment that precedes dementia. Tentative evidence has found that forgetfulness affects about half of menopausal women and is probably caused by the effects of declining estrogen levels on the brain, or perhaps by reduced blood flow to the brain during hot flashes. Long-term effects
Cardiovascular health
Exposure to endogenous estrogen during reproductive years provides women with protection against cardiovascular disease, which is lost around 10 years after the onset of menopause.
This is a disorder where the tricuspid valve fails to close properly, allowing backward flow of blood. Other structural defects which lead to RVH include tetralogy of Fallot, ventricular septal defects, pulmonary valve stenosis, and atrial septal defects. RVH is also associated with abdominal obesity, elevated fasting blood glucose, high systolic blood pressure, and fractional shortening of the left ventricular mid-wall.Other risk factors for RVH include smoking, sleep apnea, and strenuous activity. These increase the risk of heart and lung disease and hence RVH. Pathophysiology
Right ventricular hypertrophy can be both a physiological and pathophysiological process. It becomes pathophysiological (damaging) when there is excessive hypertrophy. The pathophysiological process mainly occurs through aberrant signalling of the neuroendocrine hormones; angiotensin II, endothelin-1 and the catecholamines (e.g. noradrenaline). Angiotensin-II and endothelin-1
Angiotensin-II and endothelin-1 are hormones that bind to the angiotensin (AT) and endothelin (ET) receptors. These are G-protein coupled receptors that act via internal signalling pathways. Through several intermediates, these pathways directly or indirectly increase reactive oxygen species (ROS) production causing accumulation in myocardial cells. This can subsequently induce necrotic cell death, fibrosis, and mitochondrial dysfunction.This has been demonstrated in animal studies. Protein Kinase C (PKC) is an intermediate molecule in the signalling pathway and mice lacking PKC shown resistance to heart failure compared to mice overexpressing PKC which shown heart dysfunction.Targeting the renin–angiotensin (RAAS) system (using angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers) are a well-recognized clinical approach for reversing maladaptive cardiac hypertrophy independently of blood pressure. Catecholamines
Catecholamines levels increase due to increased sympathetic nervous system activity.