NR 507 Week 8 Final Exam Study Guide (Variant 1)/Patho Final Study guide Completed, Exams of Nursing

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Final Study guide

REPRODUCTIVE:

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 ENDOCRINE 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 NEUROLOGICAL 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

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GENITOURINARY

diet and the prevention of prostate cancer Impact of Benign Prostatic Hypertrophy (BPH) on the urinary system GENETICS the role of DNA in genetics transcription effects of genetic mutations Trisomy Down Syndrome Klinefelter syndrome Duchenne muscular dystrophy Neurofibromatosis diseases that have multifactorial traits multifactorial inheritance MUSCULOSKELETAL ions that initiate muscle contraction growth of long bones in children bones belonging to the appendicular skeleton IMMUNITY & INFLAMMATION how vaccines are formed populations at risk for getting systemic fungal infections and parasitic infections systemic manifestations of infection 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

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major histocompatibility class I antigens

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inflammatory chemicals blocked by anti-inflammatory drugs characteristics of acute phase reactant C-reactive protein DERMATOLOGY process by which a deep pressure ulcer heals complications of the development of contractures during wound healing ACID/BASE causes of respiratory alkalosis molecules that act as buffers in the blood CARDIOVASCULAR 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 PERIPHERAL VASCULAR DISEASE pathophysiology of deep vein thrombosis Vichow’s triad

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HEMATOLOGY

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 FLUIDS & ELECTROLYTES 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 PULMONARY 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

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Characteristics of Cheyne-Stokes respirations

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SHOCK

causes of hypovolemic shock; how the body maintains glucose levels during shock

Reproductive:

The Menstrual (Ovarian) Cycle: Purpose: Pregnancy and menstrual bleeding (the menses). Starts with Menarche (first menstruation) ends with menopause (cessation of menstrual flow for 1 year). Cycles are anovulatory at first and may vary in length from 10 to 60 days then regular patterns of menstruation and ovulation occur lasting from 21 to 45 days. CYCLE: Commonly accepted cycle average is 28 (27 to 30) days, with rhythmic intervals of 21 to 35 days (Normal). Phases of the Menstrual Cycle: (two phases) 1- the follicular/proliferative phase (postmenstrual) followed by 2- the luteal/secretory phase (premenstrual). Menstruation (menses),the functional layer of the endometrium disintegrates and is discharged through the vagina. Follicular/proliferative phase: GnRH and a balance between activin and inhibin from the granulosa cells contribute to the rise of FSH levels, which stimulates several follicles. The pulsatile secretion of FSH from the anterior pituitary gland rescues a dominant ovarian follicle from apoptosis by days 5 to 7 of the cycle. Together estrogen and FSH increase FSH receptors in the granulosa cells of the primary follicleà making them more sensitive to FSH. FSH and estrogen combine to induce production of LH receptors on the granulosa cells, promoting LH stimulation to combine with FSH stimulation causing a more rapid secretion of follicular estrogen. As estrogen levels increase, FSH levels drop because of an increase in inhibin-B secreted by the granulosa cells in the dominant follicle. This drop in FSH level decreases the growth of less-developed follicles. Estrogen causes cells of the endometrium to proliferate and stimulates production of LH. A surge in both FSH and LH levels is required for final

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follicular growth and ovulation.

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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

7. HCG can be detected in maternal blood and urine 8 to 10 days after ovulation. 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.

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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.

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First-line treatment of PCOS includes combined oral contraceptives (COCs) for management of symptoms (e.g., hirsutism, acne) and to establish regular menses. For those women with PCOS who are overweight or obese, lifestyle modifications, including regular exercise and weight loss, also are considered first-line treatments. Women with insulin resistance, or those women who do not respond to contraceptive therapy, may benefit from the insulin sensitizer metformin. If COCs are not used and pregnancy is not desired, progesterone therapy is recommended to oppose estrogen's effects on the endometrium and as a means to initiate monthly withdrawal bleeding (at the expense of continued hirsutism). Clomiphene citrate, an antiestrogen, can be used to facilitate ovulation and can be combined with metformin for improved outcomes. Management of PCOS is a nearly lifelong process because the effects of the syndrome persist past childbearing years.

testicular cancer and conditions that increase risk; symptoms that

require evaluation for breast cancer; signs of premenstrual dysphoric

disorder;

Testicular cancer - testicular cancer is highly treatable and mostly often develops in young and middle aged men. 90% of testicular cancers are germ cell tumors arising from the male gametes. Germ cell tumors constitute 90% of testicular cancers and are classified in to seminomas and nonseminomas. Seminomas are the most common and the least aggressive, and make up 30% to 35% of testicular cancers. Nonseminomas make up 60% and include embryonal carcinomas (20%-25%), teratomas (5%-10%), and choriocarcinomas (<1%) which are the most aggressive but rare form of testicular cancer. pg 844. Conditions that increase risk of testicular cancer- the cause of testicular cancer is unknown, but a genetic predisposition is suggested since there is higher incidence among brothers’ identical twins and other close male relatives. Risk factors include history of cryptorchidism, abnormal testicular development, human immunodeficiency virus (HIV) and AIDS, klinefelter syndrome and history of testicular cancer. Pg 845 Symptoms that require evaluation for breast cancer- More than two-thirds of breast cancer cases occur in women older than 55 years. The median age for breast cancer diagnosis was 61 years of age. Some women younger than age 45 may have a higher risk for getting breast cancer compared with other women their age if they have the following risks factors: (1) close relatives (parents, siblings, or children) who were diagnosed with breast or ovarian cancer when they were younger than 45, especially if more than one relative was diagnosed or a male relative had breast cancer; (2) alterations in certain breast genes (BRCA1 and BRCA2), or having close relatives with these alterations; (3) Ashkenazi Jewish heritage; (4) treatment with radiation therapy to the breast or chest during childhood or early adulthood; (5) have been diagnosed with breast cancer or other breast health problems, such as

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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-

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Signs and symptoms of breast cancer may include:

• Change in the size, shape or appearance of a breast
• Changes to the skin over the breast, such as dimpling
• A newly inverted nipple
• Peeling, scaling, crusting or flaking of the pigmented area of skin surrounding the nipple (areola) or breast skin
• Redness or pitting of the skin over your breast, like the skin of an orange Clinical manifestation 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 Signs of premenstrual dysphoric disorder- Premenstrual syndrome (PMS) and premenstrual dysphoric disorder (PMDD) are the 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. The psychologic and physiologic changes of PMS/PMDD occur in the luteal phase of ovulatory cycles and are linked with the complex hormonal changes of the menstrual cycle. There are 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

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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 Clinical manifestations includes

• Emotional symptoms, particularly depression, anger, irritability, and fatigue, have been reported as the most prominent and the most distressing.
• Physical symptoms include breast tenderness, abdominal bloating, headache, and swelling of extremities. Pg 766

dysfunctional uterine bleeding; pathophysiology of prostate cancer;

HPV and the development of cervical cancer

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 Pathophysiology of Prostate Cancer 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.

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(1) Androgens act as strong tumor promoters through androgen receptor–mediated mechanisms to enhance the carcinogenic activity of strong endogenous DNA toxic carcinogens, including reactive estrogen metabolites and estrogen, and prostate-generated reactive oxygen species; (2) Alterations in autocrine/paracrine growth-stimulating and growth-inhibiting factors between the prostate tumor cells and microenvironment influence cancer pathogenesis; and (3) possibly unknown environmental-lifestyle carcinogens may contribute to prostate cancer. All of these factors are modulated by diet and genetic determinants, such as hereditary susceptibility genes and polymorphic genes, which encode receptors and enzymes involved in the metabolism and action of steroid hormones. · Prostate cancer develops in an androgen-dependent epithelium and is usually androgen sensitive. Androgens are synthesized not only in the testis, accounting for 50% to 60% of the total testosterone in the prostate, but also in the prostate gland itself. · Prostate cancer cells have been reported to make androgens from cholesterol · Prostate cancer is the most commonly diagnosed non–skin cancer in men in the United States, with a lifetime risk for diagnosis currently estimated at 15.9% · Second most frequently diagnosed cancer and the sixth leading cause of death worldwide. · Intraprostatic conversion - the hormone dehydroepiandrosterone (DHEA) produced by the adrenal glands is converted to testosterone and then into DHT in the prostate. · Prostate cancer is rare before age 50 years and very few men die from it before 60 years of age. 75% of all prostate cancer is diagnosed in men older than 65. · With aging, most of the androgen-metabolizing enzymes undergo significant alteration and older age, race (black), and family history remain the well-established risk factors. · Dietary factors modulate the risk of advanced prostate cancer · Epidemiologic studies have found total fat intake, animal and saturated fat, red meat, and dairy products are associated with an increase in prostate cancer risk. · Obesity is linked to advanced and aggressive prostate cancer. · Prostate cancer diagnosis- PSA (Prostate- specific antigen) testing · Chronic exposure to arsenic, as well as estrogen, is a known risk factor for prostate cancer. Clinical Manifestations Prostatic cancer- Causes no symptoms until it is far advanced. The first manifestations of disease are those of bladder outlet obstruction: slow urinary stream, hesitancy, incomplete emptying, frequency, nocturia, and dysuria. Unlike the symptoms of obstruction caused by BPH, the symptoms of obstruction caused by prostatic cancer are

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progressive and do not remit. Local extension of prostatic cancer can obstruct the upper urinary

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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) Cervical 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.

Endocrine: body’s process for adapting to high hormone levels;

Cushing’s Syndrome; causes of hypoparathyroidism;

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.

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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. Hypoparathyroidism CX: low PTH levels. Usually caused by damage to the PT glands during thyroid surgery & anatomic proximity of PT glands to thyroid. Assoc c genetic syndromes, including familial HX & DiGeorge syndrome (velocardiofacial

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syndrome) & idiopathic or autoimmune form of the disease. Low mag can cause a decrease of PTH secretion & function

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Lab Results That Point to Primary Hypothyroidism

~ decreased T3 + T4 plus increased TSH + TRH *primary hypothyroidism is due to dysfunction of the thyroid itself (Lack of the thyroid hormone negative feedback loop) -thyroid is unable to secrete adequate T3 + T -hypothalamus detects low levels and sends thyroid releasing hormone (TRH) to anterior pituitary -anterior pituitary releases thyroid stimulating hormone (TSH)

Pathophysiology of Thyroid Storm

-acute life threatening, hypermetabolic state -induced by excessive release of thyroid hormones *TH required for metabolism and function of blood cells, normal muscle functioning, and skin/hair/nail integrity *TH effect cell metabolism by altering protein, fat, and glucose metabolism which leads to increased heat production and 02 consumption -may occur spontaneously -most often occurs in patients with undiagnosed or partially treated severe hypothyroidism who are then subjected to excessive stress (infection, trauma, emotional, etc.) *Signs and Symptoms -hyperthermia -tachycardia -high output heart failure -agitation/delirium -nausea/vomiting/diarrhea **Can be fatal if not treated within 48 hours!

Signs of Thyrotoxicosis

-Thin hair

-Exophthalmos (Bulging eyes due to elevated eyelid and

decreased blinking)

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-Enlarged thyroid (goiter)

Diffuse-warm on

palpation Nodular

Solitary “toxic” nodule

-Heart Failure- tachycardia (need to dissipate heat)

-Weightloss- due to increased metabolism

-Diarrhea- increased gastric motility

-Hyperreflexia- due to increased sensitivity of muscles

-Pretibial myxedema

(Table 22.2)

(Figure 22.7)

Neurological:

dermatomes; substance release at the synapse; Spondylolysis;

location of the motor and sensory areas of the brain;

Dermatones: Specific areas of cutaneous (skin) innervation at these spinal cord segments. The dermatomes of various spinal nerves are distributed in a fairly regular pattern, although adjacent regions between dermatomes can be innervated by more than one spinal nerve.

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Substance release at synapse The region between adjacent neurons is called a synapse. Impulses are transmitted across the synapse by chemical and electrical conduction. The conducting substance is called a neurotransmitter and it is often formed in the neuron, transported to the synaptic knobs (boutons) of the presynaptic neuron’s axon, and stored in synaptic vesicles within the knobs. Action potentials in the presynaptic neuron cause the synaptic vesicles to release their neurotransmitter(s) through the plasma membrane into the synaptic cleft (the space between the neurons), where they bind to specific neurotransmitter (protein) receptor sites on the plasma membrane of the postsynaptic neuron Spondylolysis Degenerative process of the vertebral column and associated with soft tissue. Characterized by a structural defect of spine involving lamina or neural arch of vertebra. Most common site affected is the lumbar spine. This defect occurs in the portion of the lamina between the superior and inferior articular facets called the pars interarticularis. Mechanical pressure may cause a forward displacement of the deficient vertebra called spondylolisthesis. Heredity plays a significant role, and spondylolysis is associated with an increased incidence of other congenital spinal defects. As a result of torsional and rotational stress, “microfractures” occur at the affected site and eventually cause dissolution of the pars interarticularis. Location of motor and sensory areas of the brain The special senses of vision, hearing, touch, smell, and taste are the means by which individuals perceive stimuli that are essential for interacting with the environment. Special sensory receptors are connected to specific areas of the brain through the afferent pathways of the peripheral and central nervous system (CNS). Each of the special senses thus involves a connected system of organs and tissues that receives stimuli and sends sensory messages to areas of the CNS, where they are

pathophysiology of cerebral infarction and excitotoxins; agnosia;

accumulation of blood in a subarachnoid hemorrhage; most common

cause of meningitis;

Pathophysiology of cerebral infarct and excitotoxins ; agnosia, accumulation of blood in a subarachnoid hemorrhage; most common cause of meningitis. Cerebral infarction (CI) occurs when an area of the brain loses blood supply because of vascular occlusion. Causes: abrupt vascular occlusion is most common (embolus & thrombi), gradual vessel occlusion (atheroma), & vessel stenosis (not completely occluded) *underlying causes- atherosclerosis/ hypotension There is a central core of necrosis or irreversible ischemia during infarction. This is surrounded by the penumbra (borderline ischemia area). Borderline area can be improved when reperfusion occurs. CI’s can be ischemic or hemorrhagic.

• ischemic: affected softens/ pale in 6-12 hours, necrosis & welling occurs 48-72 hrs. *infiltration of macrophages and phagocytosis of necrotic tissue occurs

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• resolves within two weeks but leaves a cavity and glacial scarring

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• hemorrhagic : bleeding occurs into the area through leaking vessels when the embolic fragments resolve and reperfusion begins *hemorrhagic transformation of ischemic infarcts may be exacerbated by thrombolytic *patients are at risk for reperfusion injury (oxidative stress) Excitotoxins- (excito= overstimulated by allowing ca+ to enter cell) Definition: a neurotransmitter that can cause brain cell injury/ death. -Brain cell damage is mediated by excitotoxins during stroke and prolonged seizures *common excitotoxins are glutamate and aspartame Agnosia- commonly caused by cerebral accident or from any brain injury pathology Definition: A pattern recognition deficit caused by dysfuction in primary sensory area or interpreter area of cerebral cortex (Temporo-occipital area). -can be tactile, visual, or auditory (usually affects only one sense) examples: visual- can’t recognize faces, tactile- can’t recognize object by touch Subarachnoid hemorrhage (SAH): the escape of blood from a defective/ injured vasculature to the subarachnoid space. 50% mortality rate and 1/3 are dependent care after SAH. Can reoccur (especially from aneurysms) People at risk: ppl. with intracranial aneurysm or intracranial A-V malformation, htn, family hx of SAH, head injury Contributing factors: heavy alcohol use, anticoagulation, smoking Pathophysiology of SAH: Blood increases intracranial volume which is irritating to meningeal and other neural tissue = inflammatory response. -blood coats nerve roots, clogs arachnoid granulations, clogs foramina within ventricular system. Impairs CSF reabsorption and circulation. -ICP is increased initially then returns to baseline in ten minutes -autoregulation of blood flow is impaired -SBP increases -expanding hematoma=space occupying results in compression/ displacement of brain tissue, decreased cerebral perfusion pressure, decreased cerebral blood flow, edema and inflammation result in cell death Meningitis : inflammation of the or spinal cord, can be bacterial, viral,fungal,parasitic, or caused by toxins.

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-most common- bacterial: pneumococcus (streptococcus pneumonia) and Meningococcus (Neisseria meningitidis). Affects 5-10 per 100,000 ppl. -most cases are sporadic but outbreaks occur in places such as dorms, military bases, and Africa -spread by droplet/ respiratory secretions -often predisposed by otitis/ sinusitis

Genitourinary:

- Diet and the prevention of prostate cancer

o Our book states that epidemiologic evidence is inconsistent

for the prevention of prostate cancer in relation to diet, studies are giving attention to having a diet higher in fruits and vegetables and cutting down on animal products. This was done in the trial called MEAL or Men’s Eating and Living Study. ▪ The thought behind MEAL is that it will slow the progression of the indolent form to the aggressive form of prostate cancer ▪ Increased total fat, animal fat, red meat and dairy products are associated with a higher risk of prostate cancer ▪ Dietary fat increases androgens, oxidative stress and reactive oxygen species

- Impact of Benign Prostatic Hypertrophy (BPH) on the urinary system: page 847-848 in text book o BPH is caused by hyperplasia not hypertrophy even though, the terms are used interchangeably- so it is an enlargement related to the number of cells increasing not the size of the cells o Preclinical manifestations are inflammation which plays a role in the progress and symptoms that present o As time passes the tissue around the urethra compress causing symptoms o LUTS=lower urinary tract symptoms ▪ Urge to urinate often ▪ Delay in starting to urinate ▪ Decreased force behind urination ▪ Urine retention ▪ Can cause overflow incontinence o More serious complications ▪ Hematuria (blood in urine) ▪ Bladder and/or kidney infections ▪ Bladder calculi ▪ Hydronephrosis