NURS-4322 Final Exam Study Guide PDF
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This study guide covers various health topics, including types of prevention (primary, secondary, and tertiary), disease etiology, pathogenesis, and clinical manifestations. It also discusses prevalence, incidence, morbidity, mortality, and inflammation. Further topics addressed include respiratory and metabolic imbalances, conditions like epiglottitis, pneumothorax, pulmonary embolism, heart failure, kidney diseases, urinary incontinence, and anemia.
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NURS-4322 Final Exam Study Guide Types of Prevention ch1 primary secondary tertiary Primary ○ Removing risk factors so disease does not occur ○ Accomplished outside of health care system at community level ex: immunizations Secondary ○ Det...
NURS-4322 Final Exam Study Guide Types of Prevention ch1 primary secondary tertiary Primary ○ Removing risk factors so disease does not occur ○ Accomplished outside of health care system at community level ex: immunizations Secondary ○ Detecting disease when still curable ○ Clinical settings ex: pap smears Tertiary ○ Preventing further deterioration or reducing complications of a disease ○ Goes beyond treating the problem with which the person presents ex: antibiotic use Etiology, Pathogenesis, and Clinical Manifestations know and understand Etiology ○ “Etio” causation ○ Cause of a disease Pathogenesis ○ How the disease process evolves Clinical Manifestations ○ Signs and symptoms Prevalence and Incidence compare and contrast meanings Prevalence ○ A measure of existing disease in a population at a given point in time Incidence ○ The number of new cases arising in a population at risk during a specified time Morbidity and Mortality know what they mean Morbidity ○ Described the effect a disease has on a person life ○ Morbidity rate = examines how many people got a certain disease in a specific population Mortality ○ Pertains to the causes of death in a given population ○ Mortality rate = number of deaths in a year Cardinal Signs of Inflammation latin terms rubor, calor etc Rubor ○ Redness Calor ○ Heat Tumor ○ Swelling Dolor ○ Pain Functio Laesa ○ Loss of function Modes of transmission portals of entry sti’s know how to prevent Direct Contact Ingestion Inhalation Penetration Disease Course morbidity and mortality, know how to prevent Incubation ○ Pathogens WITHOUT producing recognizable symptoms Prodromal stage ○ Initial appearance of symptoms in host BEFORE a specific disease indication or severe symptoms develop (i.e., general malaise, mild fever, headache, fatigue) Acute stage ○ Host experiencing maximal impact of infection symptoms are pronounced allowing for pathogen identification Convalescent ○ Containment and progressive elimination of pathogen and resolution of symptoms Respiratory Alkalosis and Acidosis remember the numbers OPPOSITE ○ R.Alkalosis pH increases, CO2 decreases ○ R.Acidosis pH decreases, CO2 increases Metabolic Alkalosis and Acidosis remember the numbers. How lungs and kidneys help regulate ph EQUAL ○ M.Alkalosis pH increases, CO2 increases Decreases the contractility of the myocardium: vasodilation ○ M.Acidosis pH decreases, CO2 decreases Too many hydrogen protons and too little bicarbonate Hyperventilation and hypoventilation is the main way lungs help regulate pH. CO2 is made from cellular metabolism and mainly exhaled through the lungs Dyspnea subjective difficulty breathing in an individual Shortness of breath, is an uncomfortable feeling of difficulty breathing. Chest tightness, air hunger, or breathlessness 6-P’s of Dyspnea ○ Possible foreign body ○ Pulmonary bronchial constriction ○ Pulmonary embolism ○ Pneumothorax ○ Pneumonia ○ Pump failure Epiglottitis Airway inflammation → Obstruction Increased pulse and respirations Restlessness Retractions Anxiety increased Inspiratory stridor Drooling Pneumothorax (all types) Pneumothorax ○ Refers to the presence of air in the pleural space. ○ Causes partial or complete collapse of the affected lung Spontaneous Pneumothorax ○ Hypothesized to occur due to the rupture of an air-filled bleb, or blister, on the surface on the lung ○ Rupture of these blebs allows atmospheric air form the airways to enter the pleural cavity Open Pneumothorax/Communicating ○ Air enters the chest during inspiration and exits during expiration Tension Pneumothorax ○ Air enters during inspiration but cannot leave the chest Pulse oximetry Painless, noninvasive procedure that measures the amount of oxygen in your blood Detects hypoxia Pulmonary embolism signs and symptoms, risk factors Right Sided Heart Failure Blockage in lung artery Occurs when a clump of material, most often a blood clot, gets stuck in an artery in the lungs blocking the flow of blood. Blood clots most commonly come from deep veins of your legs (DVT) Portions of lung served by each blocked artery can’t get blood and may die (pulmonary infarction). Makes it difficult for lungs to provide oxygen to the rest of your body. Risks of Immobilization understand development of dvt DVT ○ Occurs when a blood clot (thrombus) forms in one or more of the deep veins in the body, usually in legs. Swelling and pain Aortic aneurysm signs symp clinical manifestations Aneurysm in aorta Heart failure risk factors, pathophysiology Left Sided Heart Failure ○ Decreased cardiac output Activity intolerance and signs of decreased tissue perfusion ○ Pulmonary congestion Impaired gas exchange Cyanosis and signs of hypoxia Pulmonary edema Cough w/ frothy sputum Orthopnea Paroxysmal nocturnal dyspnea ○ Coronary Artery Disease ○ Myocardial Infarction ○ Hypertension Right Sided Heart Failure ○ Congestion of peripheral tissues Dependent edema and ascites GI tract congestion Anorexia, GI distress, weight loss Liver congestion Signs, related to impaired liver function ○ Pressure and volume overload ○ Pulmonary embolism ○ Pulmonary hypertension Cardiac Preload and Afterload how does it work with heart failure Preload ○ Pressure from volume of blood in ventricles at end of diastole (end diastolic pressure) ○ Increased in: Hypervolemia Regurgitation of cardiac valves Heart Failure Afterload ○ Resistance left ventricle must overcome to circulate blood ○ Increased in: Hypertension Vasoconstriction ○ Increased afterload = cardiac workload ○ Systole and Diastole understand meaning Systole ○ Period during which the ventricles are contracting Diastole ○ Period during which the ventricles are relaxed and filling with blood Cardiac output and stroke volume descriptive equations, what can reduce cardiac output and stroke volume (end sys and end diastolic) CO = SV x HR Stroke Volume (SV): ○ The amount of blood pumped w/ each beat ○ Changes in preload affect the SV; increase in EDV results in an increase in SV ○ Decrease in venous return and EDV leads to a decrease in SV Heart Rate (HR): ○ The number of times the heart beats each minute Glomerular filtration rate (GFR) understanding chronic kidney disease, measure From the bowman capsule, glomerular filtrate moves → tubular segments of nephron. While moving through the lumen of tubular segments, chemical composition of glomerular filtrate is changed by tubular transport of water and solutes Tubular transport can result in reabsorption of substances from the tubular filtrate → peritubular capillaries or secretion of substances from the peritubular capillaries → tubular filtrate Role of the Kidney in Blood Pressure Regulation flow chart, hormones Sympathetic Neural Stimulation effect of regulation of Renal blood flow (main image) Renin ○ Regulates BP ○ Converts angiotensin → angiotensin I, a precursor to vasoconstrictor angiotensin II, leading to increased blood pressure when BP drops too low Nephrotic Syndrome flow chart, what are clinical manifestations, what is happening that leads to this Not the specific glomerular disease but a constellation of clinical findings that result from an increase in glomerular permeability and loss of plasma proteins in the urine Characterized by: ○ Massive proteinuria (>3.5g/day) ○ Lipiduria (e.g., free fat, oval bodies, fatty casts) ○ Along w/ an associated hypoalbuminemia ( 300 mg/dL) Progression of Chronic Kidney Disease and common causes of CKD Hypertension and diabetic kidney disease are the two main causes of CKD in the United States Mild reduction of GFR ○ 60 → 89 Moderate reduction of GFR ○ 30 → 59 Severe reduction in GFR ○ 15 → 29 Kidney failure with a GFR ○ < 15 ○ w/ a need for a renal replacement therapy The manifestations of CKD include an accumulation of nitrogenous wastes; alterations in water, electrolyte, and acid-base balance; mineral and skeletal disorders; anemia and coagulation disorders; hypertension and alterations in cardiovascular function; gastrointestinal disorders; neurologic complications; disorders of the skin integrity; and disorders of immunologic Process of bladder emptying autonomic nervous system involved Urine ○ Passes from the kidneys → the bladder through the ureters Ureters ○ Enter the bladder bilaterally at a location toward its base and close to the urethra Trigone ○ The triangular area bounded by the ureters and the urethra Micturition ○ The act of bladder emptying, involves both sensory and motor functions associated with bladder emptying. Types of Urinary Incontinence the four types Stress ○ Involuntary loss of urine associated with activities, such as coughing, that increase intra-abdominal pressure ○ Due to increased abdominal pressure under stress (weak pelvic floor muscle) Overactive bladder/Urge Incontinence ○ Urgency and frequency associated with hyperactivity of the detrusor muscle; may or may not involve involuntary loss of urine ○ Due to involuntary contraction of the bladder muscles Overflow ○ Involuntary loss of urine when intravascular pressure exceeds maximal urethral pressure in the absence of detrusor activity ○ Due to blockage of the urethra Functional ○ Lack of cognitive function to go to the bathroom resulting in spontaneous urination ○ Due to impaired functioning of the nervous system Serum what makes serum different from plasma DOESN’T have clotting factors like plasma Anemia Definition: ○ An abnormally low number of circulating red blood cells or level of hemoglobin, or both ○ Diminished oxygen-carrying capacity NOT a disease, but an indication of some disease process or alteration in body function Causes tissue hypoxia: fatigue, weakness, dyspnea, and angina. Brain hypoxia: headache, faintness, and dim vision Hypochromic (RBC have less color than normal, low hmg) Aplastic (bone marrow can’t produce enough RBC) Increase RBC destruction Secondary Decrease B12 (DNA synthesis) Erythroblastosis Fetalis (hemolytic disease in newborn) Hemoglobin Hmg is a vehicle for O2 and CO2 transport Lvls are normal when RBC are normal in size w/ normal amount of Hmg present Decreased Hmg lvl may indicate anemia Lvls of Hmg are affected by blood volume ○ Levels decreased w/ overhydration ○ Lvls increase w/ dehydration Normal Range ○ Men: 14-16 g/dL ○ Women: 12-16 g/dL Red blood cell production Red blood cells are produced → red bone marrow after birth Until 5 yrs of age, almost all bones produce red cells to meet growth needs; after 5 yrs, bone marrow activity gradually declines After 20, red cell production takes place mainly in membranous bones of the vertebrae, sternum, ribs, and pelvis W/ reduction in activity, red bone marrow is replaced w/ fatty yellow bone marrow Polycythemia Definition: ○ RBC mass increases Types: ○ Relative Loss of vascular fluid and is corrected by replacing the fluid ○ Primary Proliferative disease of bone marrow w/ an absolute increase in total RBC mass accompanied by elevated white cell and platelet counts ○ Secondary: Increased erythropoietin lvls caused by hypoxic conditions such as chronic failure and lung disease Disseminated intravascular coagulation (DIC) Paradox in hemostatic sequence, characterized by widespread coagulation and bleeding in vascular compartment Causes widespread of complications Begins w/ massive activation of the coagulation sequence as a result of unregulated generation of thrombin, resulting in systemic formation of fibrin Anticoagulants are reduced Characterization ○ Microemboli (small particle/blood clot, blocking a blood vessel) ○ Coagulation ○ Mainly bleeding problems Petechiae Purpura Oozing from puncture sites Severe hemorrhage (escapes of blood from a ruptured blood) Transfusion of fresh-frozen plasma, platelets, or fibrinogen, containing cryoprecipitate may correct the clotting factor deficiency Hemoglobin synthesis: iron cycle and destruction of red blood cells Hemoglobin synthesis ○ Rate of which Hmg is synthesized depends on the availability of iron for heme synthesis Iron levels Women: 2g Men: 6g ○ Deficiency in Hmg synthesis results in the diagnosis of iron deficiency anemia ○ Destruction of RBC ○ Life span of 4 months ○ Spleen is responsible for RBC destruction ○ RBC destruction and consequent bilirubin production are excessive, unconjugated bilirubin accumulates in the blood Results in yellow discoloration of skin (Jaundice) ○ Conjugated vs unconjugated bilirubin Conjugated bilirubin ○ From that has been processed by the liver. Soluble in water and can be excreted in bile ○ Unconjugated bilirubin is converted into conjugated bilirubin (conjugation) ○ Increased conjugated bilirubin → liver disease Unconjugated bilirubin ○ Form of bilirubin that is not yet processed by the liver ○ Insoluble in water and bound to albumin in the bloodstream ○ Produced from the breakdown of Hmg in old or damaged RBC Heme portion of Hmg is converted to bilirubin, which is transported to the liver ○ Hemolytic anemia 9low number of RBC due to too much hemolysis) ○ Increased unconjugated bilirubin → liver dysfunction Leukemias vs lymphomas Leukemias (BONE MARROW where BLOOD CELLS are PREVIEWED ○ Malignant neoplasms arising from transformation of single blood cell line derived from hematopoietic stem cells ○ Classification (cell lineage) Lymphocytic (lymphocytes) Myelocytic (granulocytes, monocytes) ○ ANT: Anemia - decrease Hmg Neutropenia - risk of infection Thrombocytopenia - bleeding ○ Leukemias = numerous immature WBC like ANTS in a colony Lymphomas (lymphatic system → LYMPH nodes or LYMPHOID tissues (spleen/thymus) Infectious mononucleosis (Mono) “Kissing Disease” Self-limited lymphoproliferative disorder Causes: ○ B-lymphocytotropic Epstein-barr virus (EBV), member of herpes virus family; transmitted in saliva ○ Fever, generalized lymphadenopathy, sore throat, and appearance in the blood of atypical lymphocytes and several antibodies ○ Highest incidence in adolescents and young adults ○ Treatment: Symptomatic and supportive Heat cramps, Heat Exhaustion, Heat Stroke Heat Cramps ○ Slow, painful, skeletal muscle cramps and spasm lasting 1-3 minutes. Muscles tender and skin moist cramping results from salt depletion when fluid losses from heavy sweating are replaced by water alone Heat Exhaustion ○ Skin moist, rectal temp 37.8 C (100F) to 40 C and heart rate is elevated. Signs of heat cramps may accompany Heat Stroke ○ Failure of thermoregulatory mechanisms resulting in excessive increases in body temp – core temp greater than 40 C (104F); hot, dry skin; absence of sweating; and possible CNS abnormalities such a delirium (mental state, confusion) convulsions and loss of consciousness Parkinson’s Disease Degeneration disorder of basal ganglia function that results in variable combinations of tremor, rigidity, and bradykinesia (slow movement) Slow progressive destruction of nigrostriatal pathway, w/ subsequent reduction in striatal concentrations of dopamine Mask-like, blank depression, stooped posture, pill rolling tremors; shuffling, propulsive gait; bradykinesia; possible mental deterioration, depression; muscle rigidity; has familial incidence, more common in men Amyotrophic lateral sclerosis (ALS) Lou Gehrig Disease Devastating neurologic disorder that selectively affects motor function Typically follows a progressive course, w/ a mean survival period of 2-5 years from onset symptoms Affects the LMNs of spinal cord; motor nuclei of brainstem (hypoglossal nuclei); and the UMNs of cerebral cortex. More extensive in the distal parts of the affected tracts rather than the proximal parts Multiple Sclerosis Demyelinating disease of the CNS Inflammation and destruction of mostly the CNS myelin. Characterized by exacerbations and remissions over many years in several different sites in the CNS ○ Initially, there is normal or near-normal neurologic function between exacerbations ○ As disease progresses, there is less improvement between exacerbations and increasing neurologic dysfunction Nystagmus Diplopia Blurred vision Dysarthia Dysphagia Intention tremor Alzheimer Disease Specific brain disease that accounts for 60-80% of dementia cases Initial change is subtle ○ short -term memory loss ○ Mild changes in personality ○ Randomly forget important and unimportant details Moderate state ○ Global impairment of cognitive functioning ○ Changes in higher cortical functioning needed for language, spatial relationships, and problem solving; disorientation, lack of insight, and inability to carry out the activities of daily living, extreme confusion ○ ○ Severe alzheimer disease is the last state of the disease A loss of ability to respond to the environment Require total care Bedridden ○ Death can occur as a result of complications related to chronic debilitation ○ No curative treatment for AD. medications such as cholinesterase inhibitors and NMDA antagonist may slow progression and improve depression, agitation, or sleep disorders ○ Two major goals of care are maintaining socialization and providing support caregivers ○ 5 A’s of Alzheimer’s Disease Anomia – inability to remember names of things Apraxia – misuse of objects because of failure to identify them Agnosia – inability to recognize familiar objects, tastes, sounds, and other sensations Amnesia – memory loss Aphasia – inability to express oneself through speech Vascular Dementia General term describing problems w/reasoning, planning, judgement, memory and other thought processes caused by brain damage from impaired blood flow to your brian Negative Feedback Loop Most common mechanism of hormone control, some feature of hormone action directly or indirectly inhibits further hormone secretion so that the hormone level returns to an ideal level or set point W/ negative feedback, the most common mechanism of hormone control, some feature of hormone active directly or indirectly inhibits further hormone secretion so that the hormone level returns to an ideal level or set point. In the simple neg feedback loop, the amount of hormones or its effect on a physiologic mechanism regulates the response of the endocrine gland Diabetes Mellitus Chronic complications of Dm include disorders of the microvascular (i.e., neuropathies, nephropathies and retinopathies), disorders of gastrointestinal motility, macrovascular complications (i.e., coronary artery, cerebral vascular, and peripheral vascular disease), and food ulcers People w/ DM are more susceptible to infections. Level of chronic hyperglycemia is the best predictive factor for diabetic complications; therefore, glycemic control is a primary goal of diabetic treatment Type II ○ Majority of DM cases (90-95%) ○ Presence of hyperglycemia in association w/ relative insulin deficiency ○ Formerly called adult-onset or non-insulin dependent DM ○ Strong genetic component ○ High, normal, or low insulin levels (insulin resistance) ○ Deranged secretion of insulin by the pancreatic beta cells ○ Increased glucose production by the liver ○ Hyperglycemia DM refers to a group of common metabolic disorders characterized by hyperglycemia resulting from imbalances b/w secretion and cellular responsiveness to insulin. A person w/ uncontrolled diabetes is unable to transport glucose → cells. In result, body cells are starved, and breakdown of fat and protein is increased to generate cellular energy Hypoglycemia Low sugar Onset rapid 1-3 years Anxious, sweaty, hungry, confused, blurred or double vision, shaky, irritable, cool, clammy skin Needs blood sugar, increased > 70 mg/dL Healthy blood sugar levels varies by person, but its generally below 70 mg/dL for people w/ diabetes and below 55 mg/dL for people w/o diabetes ○ TIRED Tachycardia (inc HR) Irritable Restless Excessive hunger Diaphoresis (excessive sweating), Depression Sensory Neuropathy Microvascular complications of DM are related to production of advanced glycation end products (AGEs), as reflected in the hmg A1C measure. AGEs induce vascular damage by stimulating an inc production of reactive oxygen species (ROS). these ROS are thought to damage endothelial cells by dec the production of vascular endothelial relaxing factor NO, this leading to endothelial dysfunction In type II DM: ○ Damage from AGEs may be compounded by the inc oxidative stress, chronis systemic inflammation, and dyslipidemia associated w/ the metabolic syndrome (as described previously). The types of microvascular complications that occur in DM can include neuropathy, retinopathy, nephropathy, and disorders of gastrointestinal motility. In the US, diabetes is a leading cause of vision loss and blindness as well as chronic kidney disease Role of Gastric Mucosa what cells produce gastric mucosa, what does it protect One of the important characteristics of the gastric mucosa is resistance to the highly acidic secretions that is produces It also protects the stomach from pepsin Epithelial, parietal, chief & G cells w/in the stomach mucosa produce and secrete approx 20 mEq of HCl → several hundred milliliters of gastric secretions (or gastric juices) each hour Pyloric Sphincter what is role At the end of the pyloric channel, the circular layer smooth muscle thickens to form the pyloric sphincter. Role: ○ Serves as a valve that controls the rate of stomach emptying and prevents the regurgitation of intestinal contents back into the stomach Steatorrhea what can cause fatty stool, what diseases come with fatty stool Fatty stool caused by low fat absorption in the small intestine and due to the removal of the gallbladder gastroesophageal reflux disease clinical manifestations Symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus or into the oral cavity (including larynx) or the lunch. Clinical manifestations: ○ Regurgitation ○ Pain radiates to back and neck ○ Heartburn ○ Dyspepsia ○ Increased burping, bloating and pain after meals role of bile salts Form micelles that transport these substances to the surface of the intestinal villi. ○ Here, they are taken into the epithelial cells and used to form new triglycerides ○ Hepatitis A B C transmission, clinical manifestations, role of vaccines Hepatitis A (HAV) ○ Usually benign, self limited disease ○ Fecal–oral route ○ Hepatitis w/ a vowel comes from the bowel Hepatitis B (HBV) ○ (US) declining in incidence since 1990, mainly bc of effective vaccination strategies. ○ Transmitted through inoculation w/infected blood or serum. ○ Highly preventable among injecting drug users, heterosexuals w/ multiple sex partners and men who have sex w/ men. ○ Health care workers are at risk owing to blood exposure and accidental needle injuries. Hep B vaccine provides long-term protection 9up to 20 years in some) against HBV infection ○ Body fluids Hepatitis C (HCV) ○ Estimated that 2.4 million people in the united states are living w/ chronic hep C. Before 1990, the main route of transmission of HCV was through contaminated blood transfusions or blood products. ○ Currently, recreational injecting drug use is the most common mode of HCV transmission in the united states and canada ○ Circulation Cholelithiasis contributes to the buildup of gallstones Gallstones ○ Precipitation of substances contained in bile, mainly cholesterol and bilirubin Peptic Ulcers etiology Ulcerative disorders that occur in areas of the upper gastrointestinal tract that are exposed to acid–pepsin secretions Spontaneous remissions and exacerbations are common Causes ○ H. pylori ○ Aspirin ○ Age ○ Warfarin ○ smoking Aspirin and NSAID use H. Pylori etiology Most common cause of chronic gastritis Chronic inflammatory disease of the antrum and body of the stomach Appendicitis study quadrants for gastrointestinal tract to know where pain would be inflamed , swollen and gangrenous, and it eventually perforates if not treated Abrupt onset, w/ pain referred to the epigastric or periumbilical area Palpation of the abdomen usually reveals a deep tenderness, which is pain that occurs when pressure is applied to the area and then released, and spasm of the overlying abdominal muscles are common Epigastric and periumbilical area Peritonitis Risk factors: ○ Abdominal surgery ○ Ectopic pregnancy ○ Perforation: Trauma Ulcer Appendix rupture Diverticulum Signs & Symptoms ○ Increased pulse ○ Shock ○ Dehydration ○ Pain ○ Decreased bowel sounds ○ Universal sign Tenderness over involved area ○ Fever ○ N&V ○ anorexia Esophageal Cancer Squamous cell carcinoma ○ Alc and tobacco use Adenocarcinoma ○ Barrett esophagus Dysphagia Weight loss Anorexia Fatigue Painful swallowing Not easily caught Diverticulitis Pain in lower left quadrant Nausea and vomiting Tenderness in the lower left quadrant A slight fever An elevated white blood cell county Crohn disease Recurrect, granulomatous type of inflammatory response that can affect any area of the gastrointestinal tract from the mouth of to the anus Abdominal pain and distention Portal Hypertension flowchart, what can cause, when present where is it most likely to back flow and what was backflow cause Characteristics: ○ Increased resistance to flow in the portal venous system and sustained portal vein pressure. Ascites Esophageal varices Splenomegaly Obstruction of blood flow in the portal circulation, w/ portal hypertension and diversion of blood flow to other venous channels, including the gastric and esophageal veins Liver Blood Flow know primary arteries and veins, which are oxygen rich and poor Hepatic portal vein ○ Digestive tract and major abdominal organs Hepatic veins ○ Valveless veins that empty into the inferior vena cava Hepatic artery Portal circulation: ○ Blood from the gastrointestinal tract, spleen and pancreas travels to the liver through the portal vein before moving into the vena cave for return to the heart. ○ 70% blood in portal vein 30% is from the hepatic artery Erectile Dysfunction risk factors Atherosclerosis include obesity, physical inactivity, high cholesterol levels, high blood pressure, and cigarette smoking Functions of the Prostate Gland Fibromuscular, glandular organ inferior to the bladder. Secretes thin, alkaline fluid w/ citric acid, calcium, acid phosphate, a clotting enzyme and profibrinolysin. Eliminates urine through the prostatic urethra Hypogonadism signs and symptoms SIGNS: ○ Reduced body hair ○ Gynecomastia ○ Reduced testicular volume ○ Obesity Reduced muscle mass ○ Anemia ○ Reduced bone density SYMPTOMS: ○ Sexual dysfunction ○ Low motivation / vitality ○ Poor concentration / memory ○ Hot flushes / sweating ○ Infertility Primary ○ Testicular failure Secondary ○ Failure to stimulate testes via gonadotropins Tertiary ○ Lack of stimulus to secrete gonadotropins testicular torsion physical negative affects Viability rapidly after 6 hours from the onset of symptoms. It is the most common acute scrotal disorder in the pediatric and young adult population, occurring in 1 in 4000 males under 25 years Twisting of the spermatic cord and loss of blood supply to the ipsilateral testical. Considered a urologic emergency, early diagnosis and treatment are critical to preserving the testical and fertility Effects of Progesterone Growth of the alveolar structures Protection against cancer During pregnancy ○ Increased levels of EPT significantly alter the breasts. ○ Estrogen stimulates inc vascularity of the breasts and the growth and extension of the ductile structures causing “heaviness” of the breasts. ○ Progesterone causes marked budding and growth of the alveolar structures Menopause physiology and risk factors after menopause Vaginal dryness Urinary stress incontinence Urgency Nocturia Vaginitis Urinary tract infection Diminished levels of estrogen ○ Subcutaneous fat decrease ○ Skin elasticity ○ Body hair Vasomotor instability ○ Hot flashes Osteoporosis Cardiovascular disease Menopause ○ Represents the gradual cessation of ovarian function and resultant diminished levels of estrogen Human papillomavirus (HPV) Prevalence ○ HPV is the most common STI in the US and about 80% women will get at least one type of HPV in their lifetime Transmission ○ HPV is spread through vaginal, oral, or anal sex, or through intimate skin-to-skin contact w/ an infected person Symptoms ○ HPV usually has no symptoms and goes away on its own, so many people don’t know they have it Pelvic Inflammatory Disease An inflammation of the upper reproductive tract that involves ○ The uterus (endometritis) ○ The fallopian tubes (salpingitis) ○ The ovaries (oophoritis) Clinical manifestations ○ A polymicrobial infection; most likely caused by Neisseria gonorrhoeae and chlamydia trachomatis Symptoms: ○ Lower abdominal pain ○ Purulent cervical discharge ○ Fever >101 Risk Factors: ○ 16-24 years of age ○ Nulliparity ○ History of multiple sexual partners ○ Previous history of PID ○ IUD use Gonorrhea Agent ○ Pyogenic, gram-negative diplococcus that evokes inflammatory reactions characterized by purulent exudates Host ○ Humans are the only host Growth ○ Warm, mucus-secreting epithelium Portal of entry ○ Genitourinary tract, eyes, oropharynx, anorectum, or skin Transmission ○ Heterosexual or homosexual intercourse Genital Herpes STIs ○ Sexually transmitted infections (STIs) encompass a broad range of infectious diseases that are spread by sexual contact Portals of Entry for STIs ○ Mouth ○ Genitalia ○ Urinary meatus ○ Rectum ○ skin Syphilis Primary ○ Appearance of a chance at the site of exposure Secondary ○ Lasts from 1 week to 6 months Tertiary ○ Delayed response of the untreated disease Chlamydia Most prevalent STI in the US, w/ an incidence estimated to be more than twice that of gonorrhea Untreated it can lead PID which causes greater fallopian tube damage Bacterial vaginosis Characteristics: ○ Homogeneous discharge ○ Production of a fishy, amine odor when a 10% potassium hydroxide solution is dropped onto the secretions ○ Vaginal pH above 4.5 (usually 5.0 to 6.0) ○ Appearance of characteristics “clue cells” on wet-mount microscopic studies