NR 507 Week 8 Final Exam / NR507 Week 8 Final Exam (V4)(NEW)(2022/2023): Advanced Pathophy, Exams of Nursing

Download NR 507 Week 8 Final Exam / NR507 Week 8 Final Exam (V4)(NEW)(2022/2023): Advanced Pathophy and more Exams Nursing in PDF only on Docsity! NR-507 Study Guide Chapters 1-5, 11-14, 16-20, 21-25, 27-3-33, 34-39, 40-47 1. Types of immunity-e.g. innate, active, etc (ch 7 ,191)  Innate immunity includes two lines of defense: natural barriers and inflammation Natural barriers are physical, mechanical, and biochemical barriers at the body’s surfaces and are in place at birth to prevent damage by substances in the environment and thwart infection by pathogenic microorganisms.  the natural epithelial barrier and inflammation confer innate resistance and protection, commonly referred to as innate, native, or natural immunity. Inflammation associated with infection usually initiates an adaptive process that results in a long-term and very effective immunity to the infecting microorganism, referred to as adaptive, acquired, or specific immunity.  Adaptive immunity is relatively slow to develop but has memory and more rapidly targets and eradicates a second infection with a particular disease-causing microorganism.  Innate immunity includes two lines of defense: natural barriers and inflammation. Natural barriers are physical, mechanical, and biochemical barriers at the body’s surfaces and are in place at birth to prevent damage by substances in the environment and thwart infection by pathogenic microorganisms BARRIERS INFLAMMATORY RESPONSE INNATE IMMUNITY ADAPTIVE (ACQUIRED) IMMUNI TY Level of defense First line of defense against infection and tissue injury Second line of defense; occurs as a response to tissue injury or infection Third line ofdefense; initiated when innate immune system signals the cells ofadaptive immunity Timing of defen se Constant Immediate response Delay between primary exposure to antigen and maximum response; immediate against secondary exposure to antigen Specificity Broadly specific Broadly specific Response is very specific toward “antigen” Cells Epithelial cells Mast cells, granulocytes (neutrophils, eosinophils, basophils), monocytes/macrophages , natural killer (NK) cells, platelets, endothelial cells T lymphocytes, B lymphocytes, macrophages, dendritic cells Memory No memory involved No memory involved Specific immunologic memory by T and B lymphocytes Peptides Defensins, cathelicidins, collectins, lactoferrin, bacterial toxins Complement, clotting factors, kinins Antibodies, complement Protection Protection includes anatomic barriers (i.e., skin and mucous membranes), cells and secretory molecules or cytokines (e.g., Protection includes vascular responses, cellular components (e.g., mast cells, neutrophils, macrophages), secretory Protection includes activated T and B lymphocytes, cytokines, and antibodies lysozymes, low pH of stomach and urine), and ciliary activity molecules or cytokines, and activation of plasma protein systems 2. Alveolar ventilation/perfusion- (ch, 34,pg 1238)  The relationship between arterial perfusion and alveolar gas pressure at the base of the lungs is best described as: arterial perfusion pressure exceeds alveolar gas pressure.  Effective gas exchange depends on an approximately even distribution of gas (ventilation) and blood (perfusion) in all portions of the lungs. The lungs are suspended from the hila in the thoracic cavity. When the individual is in an upright position (sitting or standing), gravity pulls the lungs down toward the diaphragm and compresses their lower portions or bases. 3. Dermatologic conditions e.g. pityriasis rosea (ch46, pg 1630/1631)  Psoriasis, pityriasis rosea, and lichen planus are inflammatory disorders characterized by papules, scales, plaques, and erythema  Psoriasis is a chronic, relapsing, proliferative, inflammatory disorder that involves the skin, scalp, and nails and can occur at any age.  Pityriasis rosea is a benign self-limiting inflammatory disorder that occurs more often in young adults, with seasonal peaks in the spring and fall. The cause is unknown but  thought to be associated with a virus (e.g., human herpesvirus 6 [HHV-6] and HHV-7) because of the timing and clustering of the outbreaks  Pityriasis rosea begins as a single lesion known as a herald patch that is circular, demarcated, and salmon-pink; is approximately 3 to 4 cm in diameter; and is usually located on the trunk  Lichen planus (LP) is a benign, autoimmune inflammatory disorder of the skin and mucous membranes with multiple clinical variations. The cause is unknown, but T cells, adhesion molecules, inflammatory cytokines, perforin, and antigen-presenting cells are involved.The infiltrate of T cells mediates immunoreactivity against basal layer keratinocytes, which have altered surface antigens and adhesion molecules  LP is also linked to hepatitis C virus. Some individuals develop lichenoid lesions after exposure to drugs or film-processing chemicals. The age of onset is usually between 30 and 70 years. The disorder begins with flat purple, polygonal, pruritic, nonscaling papules 2 to 4 mm in size, usually located on the wrists, ankles, lower legs, and genitalia  New lesions are pale pink and evolve into a dark violet. Persistent lesions may be thickened and red, forming hypertrophic LP. Oral lesions (oral lichen planus) appear as lacy white rings that must be differentiated from leukoplakia or oral candidiasis and they may be precancerous lesions 4. Croup (C 36,pg 1294)-  Croup illnesses can be divided into two categories: (1) acute laryngotracheobronchitis (croup) and (2) spasmodic croup. Diphtheria can be considered a croup illness but is now rare because of vaccinations. Croup illnesses are all characterized by infection and obstruction of the upper airways.  Croup is an acute laryngotracheobronchitis and most commonly occurs in children from 6 months to 3 years of age, with peak incidence at 2 years of age  The incidence of croup is highest in late autumn and winter, corresponding to the parainfluenza and RSV seasons, respectively. Croup is more common in boys than girls. In a significant portion of affected children, croup is a recurrent problem during childhood, and there is a family history of croup in about 15% of cases  Chickenpox (varicella) and herpes zoster (shingles) are produced by the varicella-zoster virus (VZV). VZV is a complex herpes group deoxyribonucleic acid (DNA) virus. The incubation period is 10 to 27 days, averaging 14 days. Productive infection occurs within keratinocytes such that the vesicular lesions occur in the epidermis, and an inflammatory infiltrate is often present 5. Types of anemia (ch 28,pg 987-1002)  Patch - A flat, nonpalpable, irregular-shaped macule more than 1 cm in diameter, Vitiligo, port-wine stains, mongolian spots, café-au-lait spots  Plaque- Elevated, firm, and rough lesion with flat top surface greater than 1 cm in diameter, Psoriasis, seborrheic and actinic keratosis  Wheal - Elevated, irregular-shaped area of cutaneous edema; solid, transient; variable diameter, Insect bites, urticaria, allergic reaction  Nodule- Elevated, firm, circumscribed lesion; deeper in dermis than a papule; 1-2 cm in diameter, Erythema nodosum, lipomas  Tumor- Elevated, solid lesion; may be clearly demarcated; deeper in dermis; greater than 2 cm in diameter, Neoplasms, benign tumor, lipoma, neurofibroma, hemangioma  Vesicle- Elevated, circumscribed, superficial, does not extend into dermis; filled with serous fluid; less than 1 cm in diameter, Varicella (chickenpox), herpes zoster (shingles), herpes simplex  Bulla - Vesicle greater than 1 cm in diameter, Blister, pemphigus vulgaris  Pustule- Elevated, superficial lesion; similar to a vesicle but filled with purulent fluid, Impetigo, acne  Cyst - Elevated, circumscribed, encapsulated lesion; in dermis or subcutaneous layer; filled with liquid or semisolid material, Sebaceous cyst, cystic acne  Telangiectasia - Fine (0.5-1.0 mm), irregular red lines produced by capillary dilation; can be associated with acne rosacea (face), venous hypertension (spider veins in legs), systemic sclerosis, or developmental abnormalities (port-wine birthmarks), Telangiectasia in rosacea 11. Chicken pox ( c 46,pg 1659)  an infectious viral disease that is spread by direct contact or through the air by coughing or sneezing; it causes a blister-like rash that first affects the face and trunk and then can spread over the rest of the body; symptoms include severe itching, fatigue, and fever. 12. Maternal immune system- (ch 8 & 9, pg 259-276)  The human neonate has a poorly developed immune response, particularly in the production of IgG. The fetus and neonate are protected in utero and during the first few postnatal months by maternalantibody that was actively transported across the placenta  The maternal antibodies are slowly catabolized after birth until they disappear altogether by about 10 months of age. The neonate begins producing IgG at birth, and the child’s antibodies reach protective levels after about 6 months of age.  The mother’s immune system produces the antibody, but because her cells do not express the target antigen, she has no symptoms of the disease.  Neonatal alloimmune disease may be secondary to maternal autoimmune diseases in which the mother produces an IgG autoantibody specific for maternal self-antigens that are found on fetal cells as well. Therefore, symptoms of the same autoimmune disease may affect mother and child, even though the autoantibody is being produced only by the mother’s immune system 13. Candidiasis exacerbation ( ch 10,313)  Candidiasis is a yeastlike fungal infection caused by C. albicans occurring on skin, on mucous membranes, and in the gastrointestinal tract.  Candida overgrowth may occur resulting in vaginitis or oropharyngeal infection (thrush). In those with an intact immune system the infection remains localized.  In immunocompromised individuals, particularly those with diminished levels of neutrophils (neutropenia), disseminated infection may occur. Candida is the most common fungal infection in people with cancer (particularly acute leukemia and other hematologic cancers), transplantation (bone marrow and solid organ), and HIV/AIDS. 14. Carbuncles (ch 46, pg 1635 15. Terms such as hypochromic, macrocytic, microcytic, etc ( ch 28 pg 983 ) MORPHOLOGY OF REMAINING ERYTHROCYTES NAME AND MECHANISM OF ANEMIA PRIMARY CAUSE Macrocytic- normochromic anemia: large, abnormally shaped erythrocytes but normal hemoglobin concentrations Pernicious anemia: lack of vitamin B12(cobalamin) for erythropoiesis; abnormal deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) synthesis in the erythroblast; premature cell death Congenital or acquired deficiency of intrinsic factor (IF); genetic disorder of DNA synthesis Folate deficiency anemia: lack of folate for erythropoiesis; premature cell death Dietary folate deficiency Microcytic-hypochromic a nemia: small, abnormally shaped erythrocytes and reduced hemoglobin concentration Iron deficiency anemia: lack of iron for hemoglobin production; insufficient hemoglobin Chronic blood loss; dietary iron deficiency; disruption of iron metabolism or iron cycle Sideroblastic anemia: dysfunctional iron uptake by erythroblasts and defective porphyrin and heme synthesis Congenital dysfunction of iron metabolism in erythroblasts; acquired dysfunction of iron metabolism as a result of drugs or toxins Thalassemia: impaired synthesis of α- or β- chain of hemoglobin A; phagocytosis of abnormal erythroblasts in the marrow Congenital genetic defect of globin synthesis Normocytic- normochromic anemia: normal size, normal hemoglobin concentration Aplastic anemia: insufficient erythropoiesis Depressed stem cell proliferation resulting in bone marrow aplasia Posthemorrhagic anemia: blood loss Acute or chronic hemorrhage that stimulates increased erythropoiesis, which eventually depletes body iron Hemolytic anemia: premature destruction (lysis) of mature erythrocytes in the circulation Increased fragility of erythrocytes Sickle cell anemia: abnormal hemoglobin synthesis, abnormal cell shape with susceptibility to damage, lysis, and phagocytosis Congenital dysfunction of hemoglobin synthesis Anemia of chronic disease: abnormally increased demand for new erythrocytes Chronic infection or inflammation; malignancy 16. Antibodies, IgG, IgA, etc- (ch 8, pg 229) ERYTHROCYTE VOLUME HEMOGLOBIN CONTENT Normal Normocytic Normochromic Increase d Macrocytic (higher mean corpuscular volume [MCV]) Hyperchromic (higher mean corpuscular hemoglobin concentration [MCHC]) Decrease d Microcytic (lower MCV) Hypochromic (lower MCHC)  There are five molecular classes of immunoglobulins (IgG, IgA, IgM, IgE, and IgD) that are characterized by antigenic, structural, and functional differences. Within two of the immunoglobulin classes are several distinct subclasses including four subclasses of IgG and two subclasses of IgA.  IgG is the most abundant class of immunoglobulins; they constitute 80% to 85% of those circulating in the body and account for most of the protective activity against infections. As a result of selective transport across the placenta, maternal IgG is also the major class of antibody found in blood of the fetus and newborn. Four subclasses of IgG have been described: IgG1, IgG2, IgG3, and IgG4.  IgA can be divided into two subclasses, IgA1 and IgA2. IgA1 molecules are found predominantly in the blood, whereas IgA2 is the predominant class of antibody found in normal body secretions. The IgA molecules found in bodily secretions are dimers anchored together through a J chain and “secretory piece.” This secretory piece is attached to the IgAs inside mucosal epithelial cells and may function to protect these immunoglobulins against degradation by enzymes also found in the secretions.  IgM is the largest of the immunoglobulins and usually exists as a pentamer that is stabilized by a J(joining) chain. It is the first antibody produced during the initial, or primary, response to antigen. IgM is synthesized early in neonatal life, and its synthesis may be increased as a response to infection in utero. 17. Skin cancer ( ch 46 pg, 1641)  Basal cell carcinoma and squamous cell carcinoma are the most prevalent forms of cancer. Malignant melanoma is the most serious and the most common cause of death from skin cancer  Chronic ultraviolet (UV) radiation causes most skin cancers. Protection from UV radiation from the sun and artificial sources (e.g., tanning beds), particularly during the childhood years, significantly reduces the risk of skin cancer in later years. Areas commonly exposed to the sun’s rays—face, neck, and hands —are highly vulnerable for such lesions. Dark-skinned persons and those avoiding sunlight are significantly less likely to develop these malignant tumors. In dark-skinned persons, basal cells contain the pigment melanin, a protective factor against sun exposure  Basal cell carcinoma ( most common) is a surface epithelial tumor of the skin originating from undifferentiated basal or germinative cells. The tumors grow upward and laterally or downward to the dermal-epidermal junction. They usually have depressed centers and rolled borders. Early tumors are so small that they are not clinically apparent.  Squamous cell carcinoma (SCC) is a tumor of the epidermis and the second most common human cancer. characterized: in situ (Bowen disease [BD]) and invasive. Areas affected are the head and neck (75%) and the hands (15%), with 10% of squamous cell carcinomas occurring elsewhere on the body. 18. Parts of the heart in terms of function, such as pericardium ( ch 31, p 1085)  The heart wall has three layers—the epicardium, myocardium, and endocardium—and is enclosed in a double-walled membranous sac, the pericardium  The pericardial sac has several functions. It (1) prevents displacement of the heart during gravitational acceleration or deceleration, (2) acts as a physical barrier that protects the heart against infection and inflammation from the lungs and pleural space, and (3) contains pain receptors and mechanoreceptors that can elicit reflex changes in blood pressure and heart rate.  the outer layer of the pericardium, the parietal pericardium, is composed of a surface layer of mesothelium over a thin layer of connective tissue. The visceral pericardium, or epicardium, is the inner layer of the pericardium  At one point the visceral pericardium folds back and becomes continuous with the parietal pericardium, allowing the large vessels to enter and leave the heart without breaching the pericardial layer  The outer layer of the heart, the epicardium, provides a smooth surface that allows the heart to contract and relax within the pericardium with a minimal amount of friction.  the internal lining of the myocardium is composed of connective tissue and a layer of squamous cells called the endocardium  Gastroesophageal reflux disease is the regurgitation of chyme from the stomach into the esophagus, causing esophagitis from repeated exposure to acids and enzymes in the regurgitated gastric contents. 24. Hypersensitivity reaction ( ch 9 ,p262)-  Hypersensitivity is an altered immunologic response to an antigen that results in disease or damage to the host. Hypersensitivity reactions can be classified in two ways: by the source of the antigen that the immune system is attacking MECHANISM Autoimmunity Self-antigens TYPE I (IMMUNOGLOB ULIN E–[IgE] MEDIATED IMMEDIATE TYPE II (TISSUE SPECIFIC) IgG and IgM IMMEDIATE TYPE III (IMMUNE COMPLEX) IgG and IgM IMMEDIATE TYPE IV (CELL MEDIATED) NO ANTIBODY INVOLVED DELAYED Alloimmunity Another person’s antigens ++++ + + ++ Hay fever; Environmental antigens Hemolysis in drug allergies; Graves Disease Gluten (wheat) allergy Poison ivy allergy ± ++ +++ + May contribute to some type III reactions Autoimmune thrombocytop enia Systemic lupus erythematosu s; Arthus Reactions; Raynaud Phenomena Hashimoto thyroiditis ± ++ + ++ May contribute to some type III reactions Hemolytic disease of the newborn Anaphylaxis to IgA in IV gamma globulin Graft rejection 25. Congenital intrinsic factor deficiency( ch 28, 988)  Deficiency in IF secretion may be congenital or, more often, an autoimmune process directed against gastric parietal cells. Congenital IF deficiency is a genetic disorder that demonstrates an autosomal recessive inheritance pattern. The autoimmune form of the disease also has a genetic component, as do most autoimmune diseases  The principal disorder in PA is an absence of intrinsic factor (IF), a transporter required for absorption of dietary vitamin B12, which is essential for nuclear maturation and DNA synthesis in erythrocytes. IF is secreted by gastric parietal cells and complexes with dietary vitamin B12 in the small intestine. The B12-IF complex binds to cell surface receptors in the ileum and is transported across the intestinal mucosa. 26. Acid base imbalance – (ch 3 p 1236)  Pathophysiologic changes in the concentration of hydrogen ion or base in the blood lead to acid-base imbalances.  An abnormal increase or decrease in bicarbonate concentration causes metabolic acidosis or metabolic alkalosis; changes in the rate of alveolar ventilation produce respiratory acidosis or respiratory alkalosis.  Metabolic acidosis is caused by an increase in the concentrations of non-carbonic acids or by loss of bicarbonate from the extracellular fluid.  Metabolic alkalosis occurs with an increase in bicarbonate concentration usually caused by loss of metabolic acids from conditions such as vomiting, gastrointestinal suctioning, excessive bicarbonate intake, hyperaldosteronism, and diuretic therapy.  Respiratory acidosis occurs with a decrease of alveolar ventilation and an increase in levels of carbon dioxide, or hypercapnia.  Respiratory alkalosis occurs with alveolar hyperventilation and excessive reduction of carbon dioxide concentration, or hypocapnia. 27. Acute epiglottitis(ch 36,pg 1296)  Historically, acute epiglottitis was caused by Haemophilus influenzae type B (Hib). Since the advent of Hib immunization, the overall incidence of acute epiglottitis in children has decreased significantly, although Hib still accounts for approximately 25% of the cases seen in children. Infants less than 1 year of age are at greater risk.Current pediatric cases usually represent Hib vaccine failures or are caused by alternative pathogens, such as groups A, B, C, F, and G streptococci, Streptococcus pneumoniae, Candidaspecies, Staphylococcus aureus, and viral pathogens. Thermal injuries, trauma, and posttransplant lymphoproliferative disorder also have been reported as causes of epiglottitis.  Acute epiglottitis is a life-threatening emergency. The essentials are early recognition, avoidance of disturbing the child (which could worsen the obstruction), and securing the airway. 28. Types of gastric ulcers-signs and symptoms, characteristics ( ch 41, pg 1437-1438)  The clinical manifestations of gastric ulcers are similar to those of duodenal ulcers . The pattern of pain, food, and relief is common, but the pain of gastric ulcers also occurs immediately after eating.  Gastric ulcers also tend to be chronic rather than alternate between periods of remission and exacerbation and cause more anorexia, vomiting, and weight loss than duodenal ulcers.  On set age 50 to 70 years of age, family history- usually negative, gender – equal in men and women, stress factors- increased , ulcerogenic drugs- normal use, cancer risk – increased, Pahtophysiology- Helicobacter pylori incfection – often present (6o% to 80%) abnormal mucus- may be present, parietal call mass – normal or decreased, acid production- normal or decreased, serum gastrin – increased, serum pepsiogen – normal , associated gastritis – more common , clinical manifestations - pain – located in upper abdomen, inttermittent, pain antacid-relief pattern, food pain pattern, clinical course- chronic ulcer without pattern of remissionn and exacerbation 29. Lupus (ch 9,p277)  Systemic lupus erythematosus (SLE) is a chronic, multisystem, inflammatory disease and is one of the most common, complex, and serious of the autoimmune disorders. SLE is characterized by the production of a large variety of autoantibodies against nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, and many other self-components. The most characteristic autoantibodies produced in SLE are against nucleic acids (e.g., single-stranded deoxyribonucleic acid [DNA], double-stranded DNA), histones, ribonucleoproteins, and other nuclear materials. 30. General adaptation syndrome (ch 11,p 339)  Selye concluded that this triad or syndrome of manifestations represented a nonspecific response to noxious stimuli, naming it the general adaptation syndrome (GAS). He identified three successive stages of the GAS: (1) the alarm stage or reaction, in which the central nervous system (CNS) is aroused and the body’s defenses are mobilized (e.g., “fight or flight”); (2) the stage of resistance or adaptation, during which mobilization contributes to “fight or flight”; and (3) the stage of exhaustion, where continuous stress causes the progressive breakdown of compensatory mechanisms (acquired adaptations) and homeostasis. Exhaustion marks the onset of certain diseases (diseases of adaptation). 31. Ventilation/perfusion ratio ( ch 34, pg 1238-1239)  The relationship between ventilation and perfusion is expressed as a ratio called the ventilation- perfusion ratio, or ˙V/˙Q.The normal ˙V/˙Q ratio is 0.8. This is the amount by which perfusion exceeds ventilation under normal conditions. 32. Bile salt deficiencies ( ch 41,pg 1440)  Conjugated bile acids (bile salts) are necessary for the digestion and absorption of fats. Bile salts are conjugated in the bile that is synthesized from cholesterol and secreted from the liver. When bile enters the duodenum, the bile salts aggregate with fatty acids and monoglycerides to form micelles. Micelle formation makes fat molecules more soluble and allows them to pass through the unstirred layer at the brush border of the small intestinal villi  Clinical manifestations of bile salt deficiency are related to poor intestinal absorption of fat and fat- soluble vitamins (A, D, E, and K). Increased fat in the stools (steatorrhea) leads to diarrhea and decreased plasma proteins. The losses of fat-soluble vitamins and their effects include the following:  1.Vitamin A deficiency results in night blindness.  2.Vitamin D deficiency results in decreased calcium absorption with bone demineralization (osteoporosis), bone pain, and fractures.  3.Vitamin K deficiency prolongs prothrombin time, leading to spontaneous development of purpura (bruising) and petechiae.  4.Vitamin E deficiency has uncertain effects but may cause testicular atrophy and neurologic defects in children.  The most effective treatment for fat-soluble vitamin deficiency is to increase the amount of medium- chain triglycerides in the diet, for example, by using coconut oil for cooking. Vitamins A, D, and K are given parenterally. 33. Clonal selection (ch 12, pg373)  This is referred to as clonal proliferation or clonal expansion . As a clone with a mutation proliferates, it may become an early stage tumor, for example, a carcinoma in situ or a benign colonic polyp. Additional heritable changes can occur in these early lesions that permit progression to more advanced tumors. The process of tumor development is a form of darwinian evolution; cells with a genetic change that confers a survival advantage out-compete their neighbors. The progressive accumulation of distinct advantageous (from the point of view of the cancer cell, not the individual!) mutations leads from normal cells to fully malignant cancers. 34. Obstructive sleep apnea (ch 16,pg 504)  Obstructive sleep apnea syndrome (OSAS) is a disorder of breathing during sleep related to upper airway obstruction that is associated with reduced blood oxygen saturation and hypercapnia. The typical classification of the severity of this disease uses the Apnea Hypopnea Index (AHI). This index represents how many apnea (total airway closure) or hypopnea (partial airway closure) episodes occur per night—the number of which is then divided by the night’s total sleep time to give an average number of apnea or hypopnea episodes per hour. 35. Large bowel obstruction (ch 41,pg 1431)  Chronic or partial obstructions are more often associated with tumors or inflammatory disorders, particularly of the large intestine. Intussusception is rare in adults compared with the more frequent 43. Cervical immunoglobulin- (ch 23, pg 775)  The external cervical os is a very small opening that contains thick, sticky mucus (the mucous plug) during the luteal phase of the menstrual cycle and all of pregnancy. During ovulation the mucus changes under the influence of estrogen and forms watery strands, or spinnbarkeit mucus, to facilitate the transport of sperm into the uterus  the downward flow of cervical secretions moves microorganisms away from the cervix and uterus. In women of reproductive age, the pH of these secretions is inhospitable to most bacteria. Furthermore, mucosal secretions contain enzymes and antibodies (mostly immunoglobulin A) of the secretory (humoral) immune system  These defenses do not always prevent infection, even if they are intact. Besides infection, uterine pathophysiology includes displacement of the uterus within the pelvis, benign growths (fibroids) of the uterine wall, hyperplasia of the endometrium, endometriosis, and cancer. 44. Concept of pain ( ch 16 p 485)  Pain is one of the body’s most important adaptive and protective mechanisms and all definitions suggest it is a complex phenomenon and cannot be characterized as only a response to injury  Waddell defines pain as “…a symptom, not a clinical sign, diagnosis or disease.…”2 A clear understanding of the complexities of the pain experience—specifically one that encompasses an individual’s emotions, cognition, motivation, prior history, and even issues of secondary gain—is needed to manage pain and to further understand the pain processes. “The inability to communicate verbally does not negate the possibility that an individual is experiencing pain and is in need of appropriate pain- relieving treatment. Pain is always subjective. 45. Autosomal dominant diseases ( ch 4 pg 153)  Parents at risk for producing children with a genetic disease nearly always ask the question, “What is the chance that our child will have this disease?” The probability that a family member will have a genetic disease is termed the recurrence risk. When one parent is affected by an autosomal dominant disease (and is a heterozygote) and the other is normal, the recurrence risks for each child are one half.  Huntington disease is another well-known autosomal dominant condition and its main features are progressive dementia and increasingly uncontrollable movements of the limbs  One of the key features of this disease is that symptoms are not usually seen until age 40 years or later, a pattern known as age-dependent penetrance. TYPE MECHANISM OF INCREASED PRESSURE Open-angle Obstruction of outflow of aqueous humor at trabecular meshwork or Schlemm canal; myopia may be a risk factor Normal or low-tension Form of open-angle glaucoma with symptomless damage to the optic nerve and gradual vision loss when intraocular pressure is within normal range (12-20 mmHg) Narrow-angle (angle- closure) Forward displacement of iris toward cornea with narrowing of iridocorneal angle and obstruction to outflow of aqueous humor from anterior chamber Acute angle-closure Acute closure of iridocorneal angle with a sudden rise in intraocular pressure, producing pain, redness, and visual disturbances Chronic angle-closure Progressive, permanent closure of anterior chamber angle Secondary Open- or closed-angle obstruction caused by, for example, uveitis, hemorrhage, rupture of lens or tumors Congenital glaucoma Malformation of trabecular meshwork and excess extracellular matrix in outer meshwork 46. Congenital murmurs ( ch 32 pg 1168-1170)  Aortic stenosis – congenital bicuspid valve, degenerative (calcification) changes with aging, rheumatic fever, left ventricular hypertrophy followed by left heart failure; decreased blood flow with myocardial ischemia, pulmonary edema: dyspnea on exertion, syncope especially on exertion, pain- angina pectoris, systolic murmur heard best at the right parasternal second intercostal space and radiating to the neck.  Tricuspid regurgitation – congenital, right heart failure, dyspnea, palpitations, murmur throughout systole heard best at the left lower sternal border. 47. Lactose intolerance (CH 42,PG 1500)-  Lactose intolerance is the inability to digest lactose (milk sugar). It is caused by inadequate production of lactase and is a common cause of diarrhea in children, particularly nonwhite children younger than 7 years of age. The malabsorption of lactose results in osmotic diarrhea, in which fluids move by osmosis from the vascular compartment into the intestinal lumen. The undigested sugar is processed by the colonic bacteria, and intestinal gas is produced.  The diarrhea is accompanied by abdominal pain, bloating, and flatulence. Diagnosis includes elimination of dietary lactose or hydrogen breath testing. Treatment consists of using lactase-treated dairy products or lactase supplements or reducing dairy product consumption. Other sources of dietary calcium or supplements need to be provided if dairy products are eliminated. Some children can tolerate lactose in fermented forms, such as cheese and yogurt  a condition caused by lactase deficiency in which lactose is not metabolized, making it impossible for the small intestine to absorb it and causing excessive gas production and diarrhea when exposed to lactose-containing foods. 48. Angiotensin-renin system ( ch 5, ch 37 pg 1327)  Aldosterone synthesis and secretion are regulated primarily by the renin-angiotensin-aldosterone system  A major hormonal regulator of renal blood flow is the renin-angiotensin-aldosterone system (RAAS), which can increase systemic arterial pressure and increase sodium reabsorption. Renin is an enzyme formed and stored in granular cells of the afferent arterioles of the JGA  The release of renin is principally triggered by decreased blood pressure in the afferent arterioles, which reduces stretch of the juxtaglomerular cells; decreased sodium chloride concentrations in the distal convoluted tubule; sympathetic nerve stimulation of β-adrenergic receptors on the juxtaglomerular cells; and release of prostaglandins 49. AIDS (ch 10pg 322)  AIDS is a viral disease caused by the human immunodeficiency virus (HIV). HIV infects and depletes a portion of the immune system (Th cells), making individuals extremely susceptible to life-threatening infections and malignancies  HIV is a blood-borne pathogen present in body fluids (e.g., blood, vaginal fluid, semen, breast milk) with the typical routes of transmission: blood or blood products, intravenous drug abuse, heterosexual and homosexual activity, and maternal-child transmission before or during birth. 50. Carcinoma ( ch 12 pg 363 ) BENIGN TUMORS MALIGNANT TUMORS Grow slowly Grow rapidly Have a well-defined capsule Are not encapsulated Are not invasive Invade local structures and tissues Are well differentiated; look like the tissue from which they arose Are poorly differentiated; may not be able to determine tissue of origin Have a low mitotic index; dividing cells are rare High mitotic index; many dividing cells Do not metastasize Can spread distantly, often through blood vessels and lymphatics 51. Hormonal regulation of calcium ( ch 3 pg 119)  Calcium (Ca++) is a necessary ion for many fundamental metabolic processes. It is the major cation associated with the structure of bones and teeth. It serves as an enzymatic cofactor for blood clotting and is required for hormone secretion and the function of cell receptors. Plasma membrane stability and permeability are directly related to calcium ions, as is the transmission of nerve impulses and the contraction of muscles. Intracellular calcium is located primarily in the mitochondria.  Calcium and phosphate balance is regulated by three hormones: parathyroid hormone (PTH), vitamin D, and calcitonin  The parathyroid glands secrete PTH in response to low levels of serum calcium  As calcium levels increase, an opposite adaptation occurs, leading to suppression of PTH secretion, decreased renal vitamin D activation, decreased intestinal calcium absorption, and increased renal phosphate reabsorption. 52. Neural tube defect- (ch 20,pg 663)and )ch 5,pg 167)  lack of closure of the neural groove caused by an arrest of the normal development of the brain and spinal cord during the first month of embryonic development.  Neural tube defects (NTDs), which include anencephaly, spina bifida, and encephalocele (as well as several other less common forms), are one of the most important classes of birth defects, and they are seen in 0.5 to 2 of 1000 pregnancies  Normally the neural tube closes at about the fourth week of gestation. A defect in closure, or a subsequent reopening of the neural tube, results in a neural tube defect 53. Types of hormones- ( google) Endocrine gland Hormone Main tissues acted on by hormone Main function of hormones Hypothalamus Thyrotrophin releasing hormone (TRH) Anterior pituitary Stimulates release of thyroid stimulating hormone (TSH) from the anterior pituitary Somatostatin Anterior pituitary Inhibitory hormone that prevents release of hormones such as growth hormone from the anterior pituitary Gonadotrophin releasing hormone (GnRH) Anterior pituitary Stimulates release of follicle stimulating hormone (FSH) and luteinising hormone (LH) from the anterior pituitary Corticotrophin releasing hormone (CRH) Anterior pituitary Stimulates adrenocorticotrophic hormone (ACTH) release from the anterior pituitary Growth Hormone Releasing Anterior pituitary Stimulates release of growth hormone (GH) form the anterior pituitary HORMONE TARGET TISSUE ACTION Thyrotropin-releasing horm one (TRH) Anterior pituita ry Stimulates release of thyroid- stimulating hormone(TSH) Modulates prolactin secretion Gonadotropin-releasing hor mone (GnRH) Anterior pituita ry Stimulates release of follicle- stimulating hormone (FSH) and luteinizing hormone(LH) Somatostatin Anterior pituita ry Inhibits release of growth hormone (GH) and TSH Growth hormone–releasing hormone (GHRH) Anterior pituita ry Stimulates release of GH Corticotropin-releasing hor mone (CRH) Anterior pituita ry Stimulates release of adrenocorticotropic hormone (ACTH) and β-endorphin Substance P Anterior pituita ry Inhibits synthesis and release of ACTH Stimulates secretion of GH, FSH, LH, and prolactin Dopamine Anterior pituita ry Inhibits synthesis and secretion of prolactin Prolactin-releasing factor (PRF) 58. Signs of breast cancer ( ch 24, pg 873) CLINICAL MANIFESTATION PATHOPHYSIOLOGY 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 59. Alzheimer’s disease- ( ch5, p 178)  a degenerative disease characterized by amyloid plaques and fibrillary tangles in the cortex and atrophy and widened sulci in the frontal and temporal lobes.  The plaques and tangles lead to progressive neuronal loss, and death usually occurs within 7 to 10 years after the first appearance of symptoms. 60. Guillain-Barre Syndrome (ch 17, p 622)  Guillain-Barré syndrome is an acquired, acute inflammatory demyelinating or axonal disorder caused by a humoral or cell-mediated immunologic response, or both, directed at peripheral nerves. Four subtypes have been identified and clinical manifestations depend on the subtype. SUBTYPES CLINICAL FEATURES PATHOLOGY PATHOGENESIS Acute inflammatory demyelinating polyneuropathy (AIDP accounts for most cases of GBS) Ascending paralysis with typically distant start Macrophages invade myelin sheaths and denude axons Lymphocytic inflammation Demyelination T-cell–mediated lymphocytic infiltration into nerves is common Early sensory symptoms Loss of DTRs Endoneurial edema Some degree of axon loss (all findings most prominent in the spinal roots and nerve terminals) Antibody-mediated pathogenesis not yet demonstrated CD4 and CD8 lymphocytes and macrophages are present Complement is deposited on the outermost Schwann cell plasmalemma Acute motor axonal neuropathy (AMAN) Acute progressive weakness with no sensory impairment Macrophages invade nodes of Ranvier, leaving the myelin sheath intact (absence of demyelination) Axonal degeneration in ventral root in severe cases Selective antibody-mediated attack on axon (presence of IgG and complement deposits on axolemma along with macrophage recruitment) Associated with Campylobacter jejunienteritis Lymphocyte infiltration sparse GM1 autoantibodies play a direct pathogenic role through molecular mimicry Acute motor and sensory axonal neuropathy (AMSAN) Ascending paralysis Early sensory symptoms Similar to AMAN Absence of demyelination Evidence of axonal loss in dorsal and ventral roots Undetermined Lymphocytic infiltration sparse Extensive sensory nerve fiber degeneration Fisher syndrome (FS) (5% of cases of GBS) In purist form have ophthalmoparesis, areflexia, and ataxia Pathologic features similar to those in AIDP, but are atypical FS Antibodies to ganglioside GQ1b measured in serum in 90% of cases In atypical FS also have features of AIDP Deposition of antiganglioside antibodies initially causes reversible conduction block followed by axonal degeneration Anti-GQ1b antibodies cross- react with other gangliosides (typically GT1a, but in many cases with GD3, GD1b, and GT1b) Infections are common triggers for FS (Campylobacter jejunienteritis) 61. Sympathetic/parasympathetic nervous system ( ch 11 pg 344)  The parasympathetic system balances the sympathetic nervous system and, thus, also influences adaptation or maladaptation to stressful events. The parasympathetic system also has anti-inflammatory effects.  The parasympathetic system opposes the sympathetic (catecholamine) responses, for example, by slowing the heart rate. Researchers evaluate the relative balance of the parasympathetic and sympathetic nervous systems using a technique known as heart rate variability (the measurement of R wave variability from heartbeat to heartbeat).  Under conditions of allostatic overload, the parasympathetic system may decrease its restraint of the sympathetic system, resulting in increased or prolonged inflammatory responses 62. ACTH- (c 11,pg 339)  Adrenocorticotropic hormone;  the hypothalamus secretes corticotropin-releasing hormone (CRH), which binds to specific receptors on pituitary cells that, in turn, produce adrenocorticotropic hormone (ACTH). ACTH is then transported through the blood to the adrenal glands located on the top of the kidneys 63. Bartholin glands (C24,pg 920)  Bartholin glands]) near the urethra and vagina also are common. The external female genitalia are the mons pubis, labia majora, labia minora, clitoris, vestibule (urinary and vaginal openings), Bartholin glands, and Skene glands. 64. Gonococcal disease (c 26,pg 919)  a sexually transmitted disease caused by the bacteria gonococci that invade the mucous membranes of the genitals and urinary tract and in women the cervix, fallopian tubes, and ovaries, causing chronic pelvic pain or infertility.  Gonorrhea is caused by gonococci (singular, gonococcus), which are microorganisms of the species Neisseria gonorrhoeae. Neisser first identified gonococci in stained smears of vaginal, urethral, and conjunctival exudate in 1879. 65. Glomerulonephritis-( chap 38)  Glomerulonephritis is an inflammation of the glomerulus caused by primary glomerular injury, including immunologic responses, ischemia, free radicals, drugs, toxins, vascular disorders, and infection. 66. Small patent ductus arteriosus ( ch 33, pg 1202)  The patent ductus arteriosus (PDA) is a vessel located between the junction of the main and left pulmonary arteries and the lesser curvature of the descending aorta, usually just distal to the left subclavian artery  PDA closure in asymptomatic children with a murmur is recommended by 2 years of age because of the risk of subacute bacterial endocarditis. No treatment is recommended for small PDA in the absence of a murmur or other cardiac conditions 67. Risk factors for hypertension- ( ch 32, pg 1132-1140)  Risk factors associated with primary hypertension include: (1) family history of hypertension; (2) advancing age; (3) gender (men younger than 55 and women older than 70 years); (4) black race; (5) high dietary sodium intake; (6) glucose intolerance (diabetes mellitus); (7) cigarette smoking; (8)