NR 507 Week 8 Final Study Guide - Highlight Areas

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Contributor

Matthew Perry

Category

Nursing

Course

NR 507 Advanced Pathophysiology

Institute

Chamberlain

Pages

49

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PATHO FINAL EXAM STUDY GUIDE Reproductive Endometrial cycle and the occurrence of ovulation -menstrual cyclestarts with menarche (first menstruation) ends with menopause (cessation of menstrual flow for 1 year) -Cycles -anovulatory at first may vary in length from 10 to 60 days or more. -As adolescence proceeds into adulthood, regular patterns of menstruation and ovulation are established at intervals ranging from 21 to 45 days. -Menstruation continues to recur in a recognizable and characteristic pattern during adulthood, with the length of the menstrual cycle varying considerably among women. commonly accepted cycle average is 28 (27 to 30) days, with rhythmic intervals of 21 to 35 days considered normal. -Approximately 2 to 8 years before menopause, cycles begin to lengthen again with variation related to changing hormone levels -2 phases: follicular/proliferative phase (postmenstrual) -lasts until about day 14. endometrium grows to form a lush lining inside of the uterus. GnRH, activin, and inhibin from granulosa cells cause rise in FSH levels (stimulates number of follicles) FSH rescues dominant ovarian follicle from apoptosis day 5-7 Estrogen and FSH make primary follicle more sensitive to FSH Estrogen levels increase, FSH levels drop because of inhibin-B increase from dominant follicle Estrogen causes cells of endometrium to proliferate and stimulate LH production Surge in FSH and LH require for final follicular growth and ovulation Androgen enhances process of follicle atresia luteal/secretory phase (premenstrual) this is where the body secretes the hormones estrogen and progesterone. -These hormones work together to prepare the lining of the uterus for implantation. -lasts for 12 days -During menstruation (menses), the functional layer of the endometrium disintegrates and is discharged through the vagina. The estrogen and progesterone start to decline and the endometrial lining begins to shed. This lasts for 3-5 days and the process restarts. Menstruation is followed by the follicular/proliferative phase. -Ovulation is the release of an ovum from a mature follicle and marks the beginning of the luteal/secretory phase of the menstrual cycle. The ovarian follicle begins its transformation into a corpus luteum hence the name luteal phase. Pulsatile secretion of the LH from the anterior pituitary stimulates the corpus luteum to secrete progesterone. -This will initiate the secretory phase of endometrial development. Glands and blood vessels in the endometrium branch and curl through a functional layer, and the glands begin to secrete a thin glycogen-containing fluid= the secretory phase. *If conception occurs the nutrient-laden endometrium is ready for implantation. Release of ovum from mature follicle Beginning of luteal/secretory phase Follicle begins transformation into corpus luteum (luteal phase) Secretion of LH from anterior pituitary stimulate corpus luteum to secrete progesterone Progesterone initiates secretory phase Glands and blood vessels in endometrium branch secrete thin glycogen-containing fluid (secretory phase) If conception occurs endometrium is ready for implantation HCG secreted 3 days after fertilization by blastocytes and maintains corpus luteum after fertilization at day 6-7 HCG detected in blood/urine 8-10 days after ovulation Production of estrogen and progesterone continues until placenta can maintain hormonal production If no conception/implantation corpus luteum degenerates and ends progesterone/estrogen production Endometrium becomes ischemic and disintegrates (ischemic menstrual phase) Menstruation occurs (3-7 days)=beginning of new cycle Ovulatory cycle – 24-26.5 days Primary ovarian follicle 10-12.5 days Luteal phase - around day 14 Uterine prolapse -descent of the cervix or entire uterus into the vaginal canal -In severe cases the uterus falls completely through the vagina and protrudes from the introitus. Can be caused by cystocele (lowering of bladder wall into vaginal canal) or retrocele (bulging of rectum through vaginal canal) -Symptoms of other pelvic floor disorders also may be present. -Causes due to weakness of the pelvic musculature, ligaments, and fascia or obstetric trauma and lacerations sustained during labor and delivery. Pregnancy, obesity, prolonged standing, and chronic constipation are associated with stretching of the fascia and prolapse over time. Women with connective tissue disorders are also at risk, so there is a strong genetic/familial component. In addition, risk of prolapse increases with age because of cumulative effects of stress on the pelvic floor. -Because estrogen improves vascularity of the pelvic area, postmenopausal women are at risk since their fascia and pelvis musculature lose resilience with diminished estrogen levels Treatment is often progressive with less aggressive treatments tried first. -The pelvic fascia may be strengthened through Kegel exercises (repetitive isometric tightening and relaxing of the pubococcygeal muscles) or by estrogen therapy in menopausal women. -Maintaining a healthy body mass index (BMI), preventing constipation, and treating chronic cough or constipation may help as well. -A common treatment is a pessary, which is a removable device that, when placed in the vagina, holds the uterus in position. Surgical repair with or without hysterectomy is the treatment of last resort. Symptoms: Urinary Sensation of incomplete emptying of bladder Urinary incontinence Urinary frequency/urgency Bladder “splinting” to accomplish voiding Bowel Constipation or feeling of rectal fullness or blockage Difficult defecation Stool or flatus incontinence Urgency Manual “splinting” of posterior vaginal wall to accomplish defecation Pain and Bulging Vaginal, bladder, rectum Pelvic pressure, bulging, pain Lower back pain Sexual Dyspareunia Decreased sensation, lubrication, arousal Polycystic ovarian syndrome -most common cause of anovulation and ovulatory dysfunction in women. 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--presence alone does not establish the diagnosis. -The diagnosis is one of exclusion, and all other disorders potentially responsible for the clinical findings also must be ruled out, including thyroid dysfunction, hyperprolactinemia, and congenital adrenal hyperplasia. associated with metabolic dysfunction, including dyslipidemia, insulin resistance, and obesity Insulin stimulates androgen secretion by the ovarian stroma and reduces serum sex hormone–binding globulin (SHBG) directly and independently. The net effect is an increase in free testosterone levels. Excessive androgens affect follicular growth, and insulin affects follicular decline by suppressing apoptosis and enabling follicles to persist there appears to be a genetic ovarian defect in PCOS, which makes the ovary either more susceptible to or sensitive to insulin's stimulation of androgen production -A HYPERANDROGENIC STATE IS A CARDINAL GEATURE IN THE PATHOGENSIS OF PCOS -3 X LIKELY TO HAVE INSULIN RESISTENCE. - *FSH is low and LH are high. -**Women with PCOS 3 x greater of developing uterine cancer. Clinical Manifestations: *Appear within 2 years of puberty. *May not present until normal menstrual function or pregnancy. o anovulation, hyperandrogenism, and insulin resistance  dysfunctional bleeding or amenorrhea, hirsutism, acne, acanthosis nigricans, and infertility. Management: *Goals are to suppress androgen, instituting menstruation, restore fertility, and reduce endocrine disturbance. **FIRST LINE TREATMENT= COMBINED ORAL CONTRACEPTIVES** -Insulin resistance= metformin **FOR OBESE WOMEN LIFESTYLE MODIFICATIONS ARE FIRST LINE** -CLOMIPHENE CITRATE CAN BE USED TO FACILITATE OVULATION* Testicular cancer and conditions that increase risk -Highly treatable, usually curable cancer most often develops in young and middle aged men. -Rare, but most common form of cancer between young men 15-35. -More common on R side than left. -testicular cancer has been linked to exposure to abnormal levels of estrogen -testicular cancer is a risk factor for men with undescended testicles -Germ cell tumors arising from male gametes: seminomans and nonseminomas. -Seminomas are most common, least aggressive. -Nonseminomas include embryonal carcinomas, teratomas, and choriocarcinomas, most aggressive but rare. -Neoplasm cause is unknown. -Genetic predisposition is suggested d/t incidence in brothers, identical twins and close male relatives. -Risk factors: cryptochordism- neoplasms develop more commonly in contralateral testis. Abnormal testicular development, HIV and AIDS, Klinefelter syndrome, and hx of testicular cancer. Symptoms that require evaluation for breast cancer CLINICAL MANIFESTATIONPATHOPHYSIOLOGY Chest pain Metastasis to the lung Dilated blood vessels Obstruction of venous return by a fast-growing tumor; obstruction dilates superficial veins Dimpling of the skin Can occur with invasion of the dermal lymphatics because of retraction of Cooper ligament or involvement of the pectoralis fascia Edema Local inflammation or lymphatic obstruction Edema of the arm Obstruction of lymphatic drainage in the axilla Hemorrhage Erosion of blood vessels Local pain Local obstruction caused by the tumor Nipple/areolar eczema Paget disease Nipple discharge in a nonlactating woman Spontaneous and intermittent discharge caused by tumor obstruction Nipple retraction Shortening of the mammary ducts Pitting of the skin (similar to the surface of an orange [peau d'orange]) Obstruction of the subcutaneous lymphatics, resulting in the accumulation of fluid Reddened skin, local tenderness, and warmth Inflammation Skin retraction Involvement of the suspensory ligaments Ulceration Tumor necrosis Signs of premenstrual dysphoric disorder cyclic recurrence (in the luteal phase of the menstrual cycle) of distressing physical, psychologic, or behavioral changes that impair interpersonal relationships or interfere with usual activities and resolve after menstruation. -linked with the complex hormonal changes of the menstrual cycle. many theories on the cause(s) of the disorder, including that the drop in estrogen level following ovulation and the immediate rise in progesterone level interact with hormones and neurotransmitters to cause symptoms -the neurotransmitters serotonin, gamma-aminobutyric acid (GABA), and noradrenaline may have mediating or moderating roles on symptom manifestation. -These NT 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). Emotional symptoms,  depression, anger, irritability, and fatigue, have been reported as the most prominent and the most distressing, physical symptoms seem to be the least prevalent and problematic. breast tenderness, abdominal bloating, headache, and swelling of extremities. -diagnosis based on prospective health history and symptoms, with completion of a 2-month prospective symptom questionnaire, which is considered the gold standard -Diagnostic Criteria for PDD: ≥5 symptoms below: occur in most cycles during the week before menses onset, improve within a few days after menses onset, and diminish in the week postmenses One (or more) of the following symptoms must be present: Marked affective lability Marked irritability or anger or increased interpersonal conflicts Marked anxiety, tension One (or more) of the following symptoms must also be present: Decreased interest Difficulty concentrating Easy fatigability, low energy Increase or decrease in sleep Feelings of being overwhelmed Physical symptoms such as breast tenderness, muscle or joint aches, “bloating” or weight gain NOTE: Criteria A–C must be present for most menstrual cycles in the preceding year Symptoms are associated with significant distress or interferences with work, school, relationships The disturbance is not merely an exacerbation of another disorder such as major depression, panic disorder, persistent depressive disorder, or a personality disorder Criterion A should be confirmed by prospective daily ratings in at least two symptomatic cycles The symptoms are not due to physiological effects of a substance or another medical condition -treatment is symptomatic Dysfunctional uterine bleeding -heavy or irregular bleeding in the absence of organic disease, such as submucous fibroids, endometrial polyps, blood dyscrasias, pregnancy, infection, or systemic disease. -common symptom of POS 50% of perimenopausal women will experience dysfunctional uterine bleeding that is heavy and unpredictable. -Increased endometrial bleeding is correlated with a change from ovulatory to anovulatory cycles and is associated with unopposed high estrogen levels the week before menses -accounts for 70% of all hysterectomies and almost all endometrial ablation procedures. Occurs more in women ages 40-50 because they are at the end of their reproductive years and are more likely to ovulate irregularly abnormal uterine bleeding in duration, volume, frequency, regularity present for 6 mos can be acute or chronic classified by cause of bleeding: o PALM (structural)-COEIN(non structural) (Polyp, Adenomyosis, Leiomyoma, Malignancy, Coagulopathy, Ovulatory Dysfunction, endometrial, Iatrogenic, Not yet classified) Treatment: first find cause, NSAIDs- first line of treatment (reduce prostaglandin synthesis=vasoconstriction), birth control Pathophysiology of prostate cancer More than 95% of prostatic neoplasms are histologically similar to adenocarcinomas and rely on androgen- dependent signaling for their development and progression Most of these neoplasms occur in the periphery of the prostate. -the biologic aggressiveness of the neoplasm appears to be related to the degree of differentiation rather than the size of the tumor relationship between hormones and the pathophysiology of prostate carcinogenesis is incomplete and controversial. The main issues and controversies include the sources of androgen production outside of the testes, or extratesticular sources (e.g., from adrenal DHEA and from prostate cholesterol [de novo], itself); the role of prostatic androgen receptor (AR) the role of estrogens (e.g., genotoxicity), aromatase enzyme, and the estrogen receptors (ERs) ER-α and ER-β; the role of the surrounding microenvironment or stroma. One mechanistic effect of estrogen is determined by the two receptors ER-α and ER-β. ER-α leads to abnormal proliferation, inflammation, and the development of premalignant lesions. Increased expression of ER-α has been found to be associated with prostate cancer progression, metastasis A specific oncogene is regulated by ERs, and those hormones that stimulate the ER-α receptor–like (i.e., agonists) endogenous estrogens can stimulate oncogene expression. In contrast, ER-β leads to antiproliferative and antiinflammatory effects, differentiation and maturation of prostatic epithelial cells, and potentially anticarcinogenic effects that act in concert or balance the actions of ER-α and androgens No symptoms until it’s advanced Slow urinary stream, hematuria, urinary hesitancy, incomplete emptying, dysuria Testing: DRE (location/size/nodules on prostate gland), biopsy, PSA (blood test for elevated prostate specific antigen levels) Prevention: Less meat (especially red meat = iron), fat (cook meat at high temp) Less milk More fruits and veggies (tomatoes and broccoli) No Western diet (proinflammatory) Keep BMI within range Vitamin E (prevention = antioxidant, from egg yolk, nuts, oil), Vitamin D, green tea (antioxidant) HPV and the development of cervical cancer -cervical cancer is almost exclusively caused by cervical human papillomavirus (HPV) infection. Infection with “high-risk” (oncogenic) types of HPV is a necessary precursor to development of cervical dysplasia, otherwise known as the precancerous cell changes that lead to invasive cancer -precancerous dysplasia, also called cervical intraepithelial carcinoma (CIN) and cervical carcinoma in situ (CIS), is a more advanced form of these cell changes. -cervical dysplasia can be detected noninvasively through examination of the cervical cells. If dysplasia is detected early, treatment is available to prevent invasive cancer. HPV strains 16 and 18 are most often implicated as causing 70% of all cervical cancers Most HPV infections are cleared by the immune system; the vast majority of infections do not cause cervical cancer. Risk factors: Smoking has been shown to increase the risks of persistent infection and later development of cervical cancer; in addition, women who have had many children, have a long history of oral contraceptive use, multiple sex partners, herpes, venereal infections, and are immunocompromised also are at higher risk of cervical cancer. S/SX: abnormal bleeding, vaginal discharge, bleeding between periods, heavy periods, flank pain, stool/urine leakage screening: pap smear, colonoscopy, cone biopsy -There are two main cell types of the cervix: squamous epithelium cells and columnar epithelial cells. The line where the two cells types meet, known as the transformation zone, is very vulnerable to the oncogenic effects of HPV, and this is where carcinoma in situ is most likely to develop In this zone, columnar epithelium is constantly being replaced by squamous epithelium in a process known as metaplasia. Metaplasia is thought to be affected by hormonal levels. Because metaplastic cells are at increased risk of incorporating foreign or abnormal genetic material, neoplastic changes are most common in the transformation zone. Endocrine Body’s process for adapting to high hormone levels -hormone release regulated by: chemical factors (ex: blood glucose, calcium levels) endocrine factors (ex: hormone from one endocrine gland controlling another endocrine gland neural control -Feedback systemsprovide precise monitoring and control of cellular environment. Negative feedback (most common) occurs when a changing chemical, neural, or endocrine response DECREASES the subsequent synthesis and secretion of a hormone. Positive feedback occurs when a neural, chemical, or endocrine response INCREASES the synthesis and secretion of a hormone. o also occurs when an increased hormone level further increases the synthesis and secretion of that same hormone. o ex: female reproductive system. The cyclic rise of estradiol levels provides positive feedback on the anterior pituitary and hypothalamus, causing a subsequent increase in gonadotropin- releasing hormone and follicle-stimulating hormone -The sensitivity or affinity of the target cell to a particular hormone is related to the concentration of receptors per cell: the more receptors, the higher the affinity (or the more sensitive) the cell is to the stimulating effects of the hormone. Low concentrations of hormone increase the number of receptors per cellupregulation High concentrations of hormone decrease the number or affinity of receptorsdownregulation Causes of hypoparathyroidism **Low PTH levels -most commonly caused by damage to or removal of the parathyroid glands during thyroid surgery due to anatomic proximity of the parathyroid glands to the thyroid Hypomagnesemia also can cause a decrease in PTH secretion and function associated with genetic syndromes including familial hypoparathyroidism and DiGeorge syndrome (velocardiofacial syndrome), and an idiopathic or autoimmune form of the disease. Lab results that point to primary hypothyroidism -diagnosis is made by documentation of the clinical symptoms of hypothyroidism AND by measurement of: increased levels of TSH decreased levels of TH (total T3 and both total and free T4). Cushing’s Syndrome -refers to clinical manifestations resulting from chronic exposure to excess endogenous cortisol - cortisol is lipid soluble hormone (glucocorticoids) -more common in women. Cortisol levels are controlled by negative feedback- high levels of cortisol tell hypothalamus and pituitary to decrease CRH+ACTH (less stimulation to make cortisol) In Cushing’s cortisol is constantly higher than normal (effects are exaggerated) Excess cortisol: severe muscle, skin, bone breakdown, elevated blood glucose (causes high insulin levels) High insulin levels target adipocytes in body = activation of lipoprotein lipase = belly fat, back of the neck, moon shape face High cortisol causes hyperextension More effect on catecholamines on blood vessels Water retention Inhibits gonadotropin releasing hormone: messed up ovarian and testicular function Decreases inflammatory response = more susceptible to infection Can be caused by exogenous cortisol: medications (steroids to treat autoimmune inflammatory disorders) Can cause negative feedback on hypothalamus or pituitary Decrease in CRH and ACTH = no cortisol production in zona fasciculata (adrenal gland) over time there will be lack of stimulation (atrophic zona fasciculata) No more endogenous cortisol made but still high levels of exogenous cortisol = Cushing’s symptom develops or endogenous: excess cortisol made by the body caused by pituitary adenoma (benign tumor on pituitary gland) = Cushing’s disease grows in size and secretases too much ACTH causes overstimulation of zona fasciculata = grows larger and makes more cortisol caused by ectopic sources of ACTH (Small cell lung cancer) o ACTH is coming from somewhere else and not pituitary Caused by tumors of adrenal gland Adrenal adenoma (benign) or adrenal carcinoma Cells in zona fasciculata divide abnormally and make excess cortisol Causes negative feedback and suppresses production of CRH and ACTH but the adrenal gland with tumor doesn’t get effected because of the cancer cells but the non-cancerous adrenal gland shrinks Cushing disease  excess endogenous secretion of ACTH (corticotropin) Hyperfunction of adrenal cortex that causes increased secretion of cortisol (hypercortisolism) leads to Cushing disease or Cushing syndrome ACTH-dependent hypercortisolism (about 80%) -from overproduction of pituitary ACTH by a pituitary adenoma (most common and can occur at any age) OR by an ectopic secreting nonpituitary tumor, such as a small cell carcinoma of the lung (more common in older adults). excess ACTH stimulates excess production of cortisol and there is loss of feedback control of ACTH secretion secretion of cortisol and adrenal androgens is increased cortocotropin-releasing horming (CRH) is inhibited -ACTH-independent hypercortisolism (about 20%) is caused by cortisol secretion from a rare benign or malignant tumor of one or both adrenal glands ACTH-independent secreting tumors of the adrenal cortex generally secrete only cortisol. Elevated cortisol levels suppress CRH and ACTH secretion from the hypothalamus and anterior pituitaryleads to low levels of ACTH cause atrophy of the remaining normal portions of the adrenal cortex over time alters the cortisol-secreting activity of normal cells. When the secretion of cortisol by the tumor exceeds normal cortisol levels, symptoms of 428375263248hypercortisolism develop -No matter the cause 2 consistent observations with individuals with Cushings syndrome: they do not have diurnal or circadian secretion patterns of ACTH and cortisol they do not increase ACTH and cortisol secretion in response to a stressor. Exogenous result from administration of glucocorticoids. Clinical manifestations: Weight gain most common feature & results from the accumulation of adipose tissue in the trunk, facial, and cervical areas. “truncal [central] obesity,” “moon face,” & “buffalo hump” Glucose intolerance- results from cortisol-induced resistance & increased gluconeogenesis & glycogen storage by the liver protein wasting-caused by catabolic effects of cortisol on peripheral tissues. results in muscle weakness and increased bone resorption which leads to osteoporosis (pathologic fractures, kyphosis, reduced height) vascular sensitivity to catecholamines is increasedvasoconstriction & HTN Chonically elevated cortisol supresses immune system increased infection susceptibility & poor wound healing -diagnostic: urinary and serum cortisol and serum ACTH concentration. Other tests include the dexamethasone suppression test and bilateral inferior petrosal sinus sampling. Treatment is specific for the cause of hypercorticoadrenalism and includes medication, radiation, and surgery. Thyroid Gland Thyroxine- comes in two forms T3 and T4, both bind to thyroxine receptors, cause cells to use more energy (metabolic hormone) TRH (thyroid releasing hormone) made in hypothalamus travels to anterior pituitary (thyrotropes) and makes TSH (thyroid stimulating hormone) goes to thyroid gland and makes T3 and T4 aka TH Thyroid hormones high= TH goes back to hypothalamus and activates negative feedback mechanism Stops TRH production in hypothalamus, therefore low TSH and then T3 and T4 Thyroid hormones low = TH goes back to hypothalamus and activates negative feedback but now hypothalamus makes extra TRH, TSH and T3/T4 To make enough thyroxine you need enough iodine (diet) Negative feedback look can be the cause of thyroid imbalance Causes of hypoparathyroidism  high TSH **Low PTH levels = NOT MAKING ENOUGH THYROXINE -most commonly caused by damage to or removal of the parathyroid glands during thyroid surgery due to anatomic proximity of the parathyroid glands to the thyroid Hypomagnesemia also can cause a decrease in PTH secretion and function -hypocalcemia  Chvostek and Trousseau signs, phosphate retention associated with genetic syndromes including familial hypoparathyroidism and DiGeorge syndrome (velocardiofacial syndrome), and an idiopathic or autoimmune form of the disease. Lab results that point to primary hypothyroidism -diagnosis is made by documentation of the clinical symptoms of hypothyroidism AND by measurement of: increased levels of TSH decreased levels of TH (total T3 and both total and free T4). Causes: autoimmune disease (hashimoto’s = own antibodies damage thyroid gland) -Symptoms: foggy thinking, depression, fatigue, low HR/BP, anemia (cold, pale, tired), cells don’t make enough ATP (low energy) Pathophysiology of thyroid storm  too much thyroxine, low on TSH o - Th

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