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endometrial cycle and the occurrence of ovulation uterine prolapse
polycystic ovarian syndrome (PCOS)
testicular cancer and conditions that increase risk symptoms that require evaluation for breast cancer signs of premenstrual dysphoric disorder dysfunctional uterine bleeding
pathophysiology of prostate cancer
HPV and the development of cervical cancer
body’s process for adapting to high hormone levels Cushing’s Syndrome
causes of hypoparathyroidism
lab results that point to primary hypothyroidism pathophysiology of thyroid storm
signs of thyrotoxicosis
dermatomes
substance release at the synapse Spondylolysis
location of the motor and sensory areas of the brain
pathophysiology of cerebral infarction and excitotoxins
agnosia
accumulation of blood in a subarachnoid hemorrhage
most common cause of meningitis
mechanisms responsible for the increase in antimicrobial resistance worldwide
functions of normal flora in the body
desensitization therapy
cells involved in “left shift” in the WBC count differential forms of immunity
major histocompatibility class I antigens
inflammatory chemicals blocked by anti-inflammatory drugs characteristics of acute phase reactant C-reactive protein
process by which a deep pressure ulcer heals
complications of the development of contractures during wound healing
causes of respiratory alkalosis
molecules that act as buffers in the blood
most common cardiac valve disease in women when myocardial ischemia may be reversible symptoms of stable angina
orthostatic hypotension isolated systolic hypertension
results of sustained controlled hypertension
the relationship of insulin resistance on the development of primary hypertension defects in the normal secretion of natriuretic hormones and the impact on renal system effects of increased sympathetic nervous system activity due to primary hypertension complications of unstable plaque in the coronary arteries
forms of dyslipidemia associated with the development of the fatty streak in atherosclerosis events that initiate the process of atherosclerosis
signs and symptoms of increased left atrial and pulmonary venous pressures in left sided heart differences between left and right sided heart failure
infective endocarditis
physiological response to hypoxia in anemia
populations at the highest risk for developing folate deficiency anemia causes of iron deficiency anemia
expected lab test results found in long standing iron deficiency anemia Sickle Cell Anemia
causes of aplastic anemia
underlying pathophysiologic mechanisms leading to autoimmune hemolytic anemia secondary polycythemia
anemia of chronic renal failure
conditions that result in pure water deficit (hypertonic volume depletion) osmoreceptors that stimulate thirst and the release of ADH
causes of hypernatremia
effects of increased aldosterone dependent edema
definition of isotonic
principle of capillary oncotic pressure types of fluid compartments in the body
most effective measure to prevent pulmonary embolus from developing in patients when the practitioner will note tactile fremitus
cause of acute airway obstruction in the patient with chronic bronchitis types of pneumothorax
results of the loss of alph-1-antitrypsin in emphysema the result of loss of surfactant in ARDS
Characteristics of Cheyne-Stokes respirations
An increase in stromal tissue in the late follicular phase is associated with a rise in androgen levels. Androgen production enhances the process of follicle atresia.
Luteal/secretory phase (premenstrual): Ovulation is the release of an ovum from a mature follicle and marks the beginning of the luteal/secretory phase of the menstrual cycle.
Ovarian follicle begins its transformation a corpus luteum (hence luteal phase) (see Fig. 24.8, A)
Pulsatile secretion of LH from the anterior pituitary stimulates the corpus luteum to secrete progesterone, which in turn initiates the secretory phase of endometrial development.
Glands from the endometrium start to secrete a thin glycogen-containing fluid (the secretory phase).
If conception occurs, the nutrient-laden endometrium is ready for implantation.
Human chorionic gonadotropin (HCG) is secreted 3 days after fertilization by the blastocytes and maintains the corpus luteum once implantation occurs at about day 6 or
If conception and implantation do not occur, the corpus luteum degenerates and STOPS production of progesterone and estrogen. Without progesterone or estrogen to maintain it, the endometrium becomes ischemic (“blood-starved”) and disintegrates, hence the name ischemic/menstrual phase. Menstruation then occurs, marking the beginning of another cycle.
Ovulation Occurs:
Ovulatory cycles- minimum length of 24 to 26.5 days:
Primary ovarian follicle requires 10 to 12.5 days to develop, and the luteal phase appears relatively fixed at 14 days (±3 days).
Menstrual blood flow usually lasts 3 to 7 days, but it may last as long as 8 days or stop after 1 to 2 days and still be considered within normal limits. Bleeding is consistently scant to heavy and varies from 30 to 80 mL, with most blood loss occurring during the first 3 days of menses.
Menstrual discharge consists of blood, mucus, and desquamated endometrial tissue and does not clot under normal circumstances. It is usually dark and produces a characteristic musty odor on oxidation. Environmental factors such as severe emotional stress, illness, malnutrition, obesity, and seasonal variation may affect the length of the menstrual cycle.
Uterine prolapse : is descent of the cervix or entire uterus into the vaginal canal (Fig. 25.11). In severe cases the uterus falls completely through the vagina and protrudes from the introitus.
Symptoms of other pelvic floor disorders also may be present.
Polycystic ovary syndrome (PCOS): is the most common cause of anovulation and ovulatory dysfunction in women. PCOS is defined as having at least two of the following three features:
-irregular ovulation,
-elevated levels of androgens (e.g., testosterone), and
-the appearance of polycystic ovaries on ultrasound.
Polycystic ovaries do not have to be present to diagnose PCOS, and conversely their presence alone does not establish the diagnosis. (2 out of 3 need to be present).
PCOS is associated with metabolic dysfunction , including dyslipidemia, insulin resistance, and obesity.
Cause of PCOS is unknown, a genetic basis is suspected.
Symptoms are related to anovulation, hyperandrogenism, and insulin resistance and include dysfunctional bleeding or amenorrhea, hirsutism, acne, acanthosis nigricans, and infertility.
Goals of treatment include reversing signs and symptoms of androgen excess, instituting cyclic menstruation, restoring fertility, and ameliorating any associated metabolic or endocrine, or both, disturbances.
adulthood; (5) have been diagnosed with breast cancer or other breast health problems, such as lobular carcinoma in situ (LCIS), DCIS, atypical ductal hyperplasia, or typical lobular hyperplasia; and (6) high breast density. A high-risk breast cancer condition is postpartum breast cancer with immune suppression and delayed involution. Pg 792-
Pathophysiology Chest pain Metastasis to lung Dilated blood vessels Obstruction of venous return by fast growing tumor Dimpling of skin Can occur with invasion of dermal lymphatic because of retraction of cooper ligament Edema of arm Local inflammation of lymphatic obstruction Hemorrhage Erosion of blood vessels Local pain Local obstruction by tumor Nipple/areolar eczema Paget disease Nipple discharge in a no lactating woman Spontaneous and intermittent d/c caused by tumor obstruction Nipple retraction Shortening of mammary ducts Pitting of the skin Obstruction of sub lymphatic, resulting in fluid accumulation Reddened skin, local tenderness, warmth Inflammation Skin retraction Involvement of suspensory ligaments Ulceration Tumor necrosis
hormones and neurotransmitters to cause symptoms. Furthermore, the neurotransmitters serotonin, gamma-aminobutyric acid (GABA), and noradrenaline may have mediating or moderating roles on symptom manifestation. These neurotransmitters have demonstrated interactions with estrogen and progesterone and all of these are neuroactive with known mood and behavior effects, including negative mood, irritability, aggression, and impulse control. Sex steroids also interact with the renin-angiotensin-aldosterone system (RAAS), which explains some PMS/PMDD signs and symptoms (e.g., water retention, bloating, weight gain). There is a predisposition of PMS to occur in families, perhaps because of genetics or shared environment; however, no genes have been identified. Pg 766
Dysfunctional Uterine Bleeding or Abnormal Uterine Bleeding (AUB) - Abnormal uterine bleeding is defined as bleeding between monthly periods, prolonged bleeding, or an extremely heavy flow. Causes include overgrowth of fibrosis and polyps, blood disorders, polycystic ovary syndrome, hormone changes during menopause, and cancer of the uterus or cervix. Treatments include hormones, non-steroidal anti-inflammatory drugs and surgery.
· 50% of perimenopausal women will experience dysfunctional uterine bleeding characterized as heavy and unpredictable bleeding · Increased endometrial bleeding is correlated with a change from ovulatory to anovulatory cycles (when a woman skips ovulation) and is associated with unopposed high estrogen levels the week before menses. · caused by submucosal myomas and endometrial polyps, or metrorrhagia (midcycle bleeding) · First line of therapy is medical and hormonal management for normal uterus only
Prostatic adenocarcinoma is a heterogeneous group of tumors with a diverse spectrum of molecular and pathologic characteristics, and therefore clinical behaviors and challenges. The biologic aggressiveness of the neoplasm appears to be related to the degree of differentiation rather than the size of the tumor.
tract ureters as well. If rectal obstruction occurs, a man may experience a large-bowel obstruction or difficulty in defecation. Symptoms of late disease include bone pain at sites of bone metastasis, edema of the lower extremities, enlargement of lymph nodes, enlargement of the liver, development of pathologic bone fractures, and mental confusion associated with brain metastases.
Human Papillomavirus Infection (HPV)- a nonenveloped, circular, double stranded DNA virus, one of the papovaviruses, that belongs to the Papovaviridae family.
· Transmission is through physical contact with infected skin, mucosa, or fluids · Initial infection follows trauma to the epithelium that allows the virus to reach and infect the basal cells of the epithelium- such minor trauma may occur during sexual intercourse · HPV infection may occur months to years before symptoms appear, such as warts or precancerous lesion · HPV may enter the nuclear DNA and change the expression of cell proteins, leading either to increased but noncancerous cell growth ( warts) or to unchecked cell growth (cancer)
· Caused by cervical human papillomavirus (HPV) infection · Infection with “high risk” oncogenic type of HPV is necessary precursor to development of cervical dysplasia (precancerous cell changes that lead to invasive cancer). More advance form of this changes is called precancerous dysplasia also known as cervical intraepithelial carcinoma (CIN) and cervical carcinoma in situ (CIS). · Most sexually active women will contract HPV at some point in their lifetime. Most of this infection are asymptomatic and resolve spontaneously. · High risk HPV persist and cause abnormal cellular changes that can become cancerous · Risk factors- women with multiple sexual partners, smoking, women who have had many children, long history of oral contraceptive use, and immunocompromised.
Transformation zone (TZ)- the line where 2 cells type meet (squamous epithelial cells and columnar epithelial cells. TZ is very vulnerable to the oncogenic effects of HPV, this is where carcinoma in situ most likely developed.
Metaplasia- the constant replacement of columnar epithelium by squamous epithelium. It is affected by hormonal level.
Body’s process for adapting to high hormone levels: Negative-feedback systems are important in maintaining hormone concentrations within physiologic ranges. The lack of negative-feedback inhibition on hormonal release often results in pathologic conditions. hormonal imbalances and related conditions are caused by excessive hormone production, which is the result of failure to “turn off” the system.
High concentrations of hormone decrease the number of receptors, called down-regulation. Thus the cell can adjust its sensitivity to the concentration of the signaling hormone. The receptors on the plasma membrane are continuously synthesized and degraded, so that changes in receptor concentration may occur within hours. Various physiochemical conditions also can affect both the receptor number and the affinity of the hormone for its receptor. Some of these physiochemical conditions are the fluidity and structure of the plasma membrane, pH, temperature, ion concentration, diet, and the presence of other
Cushing’s Syndrome : overproduction of anterior pituitary ACTH by a pituitary adenoma; chronic excess cortisol (at any age)
With ACTH-dependent hypercortisolism, the excess ACTH stimulates excess production of cortisol and there is loss of feedback control of ACTH secretion. Whatever the cause, two observations consistently apply to individuals with Cushing syndrome : (1) they do not have diurnal or circadian secretion patterns of ACTH and cortisol, and (2) they do not increase ACTH and cortisol secretion in response to a stressor.
Exogenous result from administration of glucocorticoids. Endogenous either corticotropin dependent (most common & caused by ACTH-secreting pituitary tumor) or corticotropin independent (usually caused by an adrenal cortical tumor).
Clinical features: weight gain in trunk, face, and cervical areas. “truncal obesity, moon face, buffalo hump”. Transient weight gain from sodium and water retention may be present because of the mineralocorticoid effects of cortisol, exhibited when cortisol is present in high levels. Glucose intolerance occurs because of cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by the liver. Protein wasting is caused by the catabolic effects of cortisol on peripheral tissues. Muscle wasting leads to muscle weakness and is especially obvious in the muscles of the extremities with thinning of the limbs. In bone, loss of the protein matrix and increases in bone resorption lead to osteoporosis and can result in pathologic fractures, vertebral
compression fractures, bone and back pain, kyphosis, and reduced height. Hypercalciuria may result in renal stones, which are
experienced by approximately 20% of individuals with this disease. Loss of collagen also leads to thin, weakened integumentary tissues through which capillaries are more visible; the tissues are easily stretched by adipose deposits.