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The University of Alabama Capstone College of Nursing NUR 529 Exam 3 Blueprint Pages referred to below are from Porth’s Pathophysiology: Concepts of Altered States, 11th^ ed., and the current e-book on coursepoint. Older versions are not included, this course does not utilize older textbook versions. Format for page numbers below is Porth 10th^ ed “hard copy” book/ Course Point Porth E-Book. Example: p. 967/975. If the pages correlate between editions then only one will be listed.
Unit 11. Disorders of GI Function. Chapters 36-39. There are 10 questions from this unit.
- Chapter 36. Intestinal flora, roles. Essential vitamins in clotting, what are they and how are they made? Pg. 1067. a. Colonic (colon) microorganisms play a role in vitamin synthesis and in the absorption of calcium. The colonic flora synthesizes vitamin K.
- Chapter 37. Disorders of Gastrointestinal Function. Alterations in intestinal absorption. Celiac disease. What are the dietary recommendations for celiac disease? Pg. 1107. a. Malabsorption is the failure to transport dietary constituents, such as fats, carbohydrates, proteins, vitamins, and minerals, from the opening of the intestine into the ECF compartment for transport to the various parts of the body. b. Celiac Disease: An autoimmune disease that is triggered by dietary gluten- containing grains (wheat, barley, and rye). Removal of these results in resolution of symptoms. c. The primary treatment consists of removal of gluten and related proteins from the diet. Gluten is the primary protein in wheat, barley, and rye. Oat products may be contaminated with wheat during the process. Many gluten-free types of products are available. Meats, vegetables, fruits, and dairy products are free of gluten as long as they are not contaminated during the process. Complete exclusion of dietary gluten generally results in rapid and complete healing of the intestinal mucosa. (note: I am not expecting you to learn Table 37.2 but I do recommend printing this table and putting it in your notebook/clipboard for clinicals).
- Chapter 37. Disorders of the Stomach. Gastric mucosal layers. Which medications affect the mucosal layer? Which ones increase the risk for GI bleeding? Pg. 1083. a. NSAIDs (ex: aspirin) are commonly used for relieving pain and inflammation. Frequent usage is associated with GI lesions (peptic ulcers) because the drug
is able to cross the lipid bilayer and causes damage to the superficial cells, which can result in acute erosions. b. Gastric irritation and occult bleeding (d/t gastric irritation) occur in people who take aspirin on a regular basis.
- Chapter 38. Disorders of Hepatobiliary and Exocrine Pancreas Function. Bilirubin elimination and jaundice. How do we get rid of bilirubin? Pg. 1122. a. Bilirubin is the final product of the breakdown of heme and is contained in aged red blood cells. Bilirubin gives bile its color. In the process of degradation, the hemoglobin from the red blood cell is broken down to form biliverdin, which is quickly converted to free bilirubin. Free bilirubin, which is insoluble in plasma, is transported in the blood attached to plasma albumin. As it passes through the liver, free bilirubin is absorbed through the hepatocyte’s cell membrane and released from its albumin carrier molecule. Inside the hepatocytes, free bilirubin is converted to conjugated bilirubin, making it soluble in bile. Conjugated bilirubin is secreted as a part of bile, and in this form, it passes through the bile ducts into the small intestine. In the intestine, ½ of the bilirubin is converted into a highly soluble substance called, urobilinogen, by the intestinal flora. Some of the urobilinogen is absorbed into the portal circulation and remainder is excreted into the feces. Most of the urobilinogen that is absorbed is returned to the liver to be re-excreted into the bile. Only a small amount of bilirubin is found in the blood.
- Chapter 38. Disorders of Hepatobiliary and Exocrine Pancreas Function. Bile production and cholestasis. How does the body break down and digest fat? Pg. 1122. a. The secretion of bile and with the help of GI accessory organs such as the liver, pancreas and gallbladder.
- Chapter 38. Disorders of Hepatobiliary and Exocrine Pancreas Function. Bile production and cholestasis. What is the function/role of bile? Pg. 1122. a. The secretion of bile is essential for digestion of dietary fats, and absorption of fats and fat-soluble vitamins from the intestine.
- Chapter 38. Disorders of Hepatobiliary and Exocrine Pancreas Function. Page 1127-
- Compare and contrast the transmission of hepatitis A, B, and C. a. Hepatitis is inflammation of the liver b. All can cause acute hepatitis c. Hepatitis A: transmitted primarily by the fecal-oral route. It has a brief incubation period of 14-28 days. The virus replicates in the liver, excreted in the bile, and shed in the stool. Drinking contaminated water or milk & eating shellfish from infected waters are fairly common routes of transmission. Children are asymptomatic, so they play an important role in the spread of the disease. Oral behavior and lack of toilet training promote viral infection. It is NOT transmitted by transfusion of blood or plasma derivatives.
certain cytokines (TNF, growth factors, and adiponectin-important in insulin resistance). The discovery of leptin, a peptide released from adipocytes, plays a role in energy homeostasis. Leptin decreases food intake and increases energy expenditure through an increase in thermogenesis and SNS activity. It is also involved in glucose metabolism. Leptin binds and activates with specific leptin receptors found in several peripheral tissues and in many areas of the brain, including specific regions of the hypothalamus. Receptors in these hypothalamic regions are known to be involved in appetite, food intake, SNS activity, temperature regulation, and insulin release by the pancreatic beta cells. Leptin levels tend to rise after food intake and fall during fasting. Adipose tissue signals the brain by leptin that sufficient storage of calories has been achieved and increased food intake in not necessary. Leptin resistance or a failure to respond to high levels of leptin may result in obesity.
- Chapter 39. Alterations in Nutritional Status. Page 1155. What is the main hormone involved in appetite regulation? a. Leptin Unit 12. Disorders of Endocrine Function. Chapters 40-41. There are 10 questions from this unit.
- Chapter 40. Mechanisms of Endocrine Control. Hypothalamic-Pituitary Regulation. Hypothalamic hormones. What hormones are released from the anterior pituitary gland? The FLAT PiG mnemonic is a great way to remember these. See the document under Module 8. a. FSH, LH, ACTH, TSH, PRL, I(IGNORE), GH
- Chapter 40. Mechanisms of Endocrine Control. Hypothalamic-Pituitary Regulation. Hypothalamic hormones. What hormones are released from the posterior pituitary gland? See FLAT Pig mnemonic. a. P.P.: ADH & Oxytocin
- Chapter 41. Disorders of Endocrine Control of Growth and Metabolism. Type 1 Diabetes. What is the etiology and pathophysiology of this disorder? a. Type 1 is characterized by destruction of the pancreatic beta cells and an ABSOLUTE deficiency of insulin, with most instances, immune mediated as reflected by the detection of specific autoantibodies. It is a catabolic disorder characterized by a lack of insulin production, elevation of blood glucose and breakdown of body fats and proteins as fuel for metabolic processes. The absolute lack of insulin in people with type 1 DM means that they are particularly prone to the development of ketoacidosis. One of the actions of insulin is the inhibition of lipolysis (fat breakdown). In the absence of insulin, these fatty acids are released from fat cells and converted to ketones in the liver, leading to ketosis. Because of the absolute insulin deficiency, people
with type 1 DM require exogenous insulin replacement to reverse the catabolic state, control blood glucose levels and prevent ketosis.
- Chapter 41. Disorders of Endocrine Control of Growth and Metabolism. Type 1 Diabetes. Describe the diagnostic criteria of Type 1 diabetes. a. Hemoglobin A1C, fasting blood sugar, ketones in the urine b. Hemoglobin A1C is a test that measures the quantity/ amount of hemoglobin that has been glycated, meaning glucose molecules have become bound to the hemoglobin molecule. When RBC’s are released from the bone marrow, hemoglobin does not contain glucose, however, during the 120-day lifespan of the RBC, hemoglobin normally becomes glycated. Glucose enters into the RBC by facilitated diffusion. The rate at which glucose becomes attached to the hemoglobin molecule reflects blood glucose levels. Glycation is essentially irreversible therefore the level of A1C present in the blood provides an index of blood glucose levels over the approximate 120-day lifespan of red blood cells. A1C level between 5.7-6.5 suggest pre-diabetes and greater than 6.5 indicates DM. c. Fasting Plasma glucose test measures plasma glucose after a period of at least 8 hours with no caloric intake. A diagnosis is not made from a single fasting plasma glucose test. Elevated levels would be followed up with repeat testing and some other additional tests. d. Urine tests: A positive urine glucose test indicates that the renal threshold for reabsorption of glucose has been exceeded which typically is accompanied by hyperglycemia. A urine test that is positive for ketones indicates that the body is producing excess ketone bodies, because the body is using non-glucose energy substrates (protein and fat) for fuel.
- & 17. Chapter 41. Chapter 41. Disorders of Endocrine Control of Growth and Metabolism. List the differences between Type 1 and Type 2 diabetes? How they similar? How are they different? (2 questions). a. In type 1, the age of onset is usually childhood, whereas in type 2, age of inset is usually adulthood. The type of onset in type 1 is abrupt, symptomatic (polyuria, polydipsia, and polyphagia) often with severe ketoacidosis. In type 2, type of onset is usually gradual and subtle, often asymptomatic. For body weight in type 1, it is normal, recent weight loss is common, but in type 2, they are usually overweight. Familial history occurs but is less common in type 1, where as it is very common in type 2. In type 1, beta cell mass is markedly reduced and in type 2, it is normal or slightly elevated. Circulating insulin level in type 1 is markedly reduced, and is elevated or normal in type 2. Clinical management for type 1 is requirement of insulin, whereas in type 2, insulin is usually not needed initially, but insulin supplement may be needed in later stages, and weight loss typically improves the condition.
Osteoporosis may develop because of destruction of bone proteins and alterations in calcium metabolism, resulting in back pain, compression fractures of the vertebrae and rib fractures. As calcium is mobilized from bone and renal calculi may develop. Glucocorticoids also possess mineralocorticoid properties; therefore, glucocorticoid excess can also cause hypokalemia (from excessive potassium excretion) and hypertension (excessive sodium retention). Glucocorticoid actions include inhibition of inflammatory and immune responses, therefore people with glucocorticoid excess have increased susceptibility to infection. Cortisol also increases gastric acid secretion, which may cause gastric ulceration and bleeding. Endogenous causes of hypercortisolism also may have an accompanying excess of adrenal androgens, leading to hirsutism, mild acne, and menstrual irregularities. Excess levels of glucocorticoids may also give rise to extreme emotional lability, ranging from mild euphoria and absence of normal fatigue to psychotic behavior.
- Chapter 41. Disorders of Endocrine Control of Growth and Metabolism. Describe the process of hyperosmolar hyperglycemic state and how it affects the body? How does it affect fluid balance? Pg. 1224. a. HHS is characterized by hyperglycemia, hyperosmolarity with dehydration, the absence of ketoacidosis, and depression of the sensorium. A partial or relative insulin deficiency may initiate HHS by reducing glucose utilization while increasing glucagon release and hepatic glucose output. The hyperglycemia leads to large volume water loss through osmotic diuresis. Dehydration is usually more severe in HHS than DKA. As the plasma volume contracts, renal insufficiency develops. The resultant decrease in renal elimination of glucose further elevates blood glucose levels, which increases the severity of the hyperosmolar state. In hyperosmolar states, the increased serum osmolarity has the effect of pulling water out of body cells, including brain cells. HHS may also be complicated by thromboembolic events related to the contraction of plasma volume with increased coagulability because of stasis. b. The most prominent manifestations of HHS are weakness, dehydration, polyuria, neurologic alterations, and excessive thirst. Neurologic alterations include hemiparesis, seizures, and coma, these symptoms may be mistaken for a stroke. Successful treatment of HHS involves careful patient monitoring and correction of dehydration, hyperglycemia, and electrolyte imbalance. Close observation and care is particularly important as water moves back into brain cells, posing a threat of cerebral edema.
- Chapter 41. Disorders of Endocrine Control of Growth and Metabolism. What the microvascular complications of poorly controlled diabetes? Pg. 1225.
a. The microvascular complications of DM are related to the production of advanced glycation end products as reflected in the hemoglobin A1C measure. AGE’s induce vascular damage by stimulating an increased production of reactive oxygen species. These ROS are thought to damage endothelial cells by decreasing the production of the vascular endothelial relaxing factor, thus leading to endothelial dysfunction. b. In type 2 DM, this damage from AGE’s may be compounded by the increased oxidative stress, chronic systemic inflammation, and dyslipidemia associated with the metabolic syndrome. The types of microvascular complications that occur in DM include retinopathy, neuropathy, nephropathy, and disorders of GI motility.
- Chapter 41. Disorders of Endocrine Control of Growth and Metabolism. Effect of stress on clients with diabetes. Counter-regulatory hormones. Glucocorticoid hormones. What counter-regulatory hormones are released during a stress response? How does this affect the patient’s clinical status including labs? Pg. 1225. a. Epinephrine, a catecholamine from the adrenal medulla, helps to maintain blood glucose levels during periods of stress by stimulating glycogenolysis of the liver, thus causing large quantities of glucose to be released into the blood. Epinephrine also inhibits insulin release from pancreatic beta cells, which decreases movement of glucose into muscle cells and increases the breakdown of muscle glycogen stores. Although the glucose released from muscle glycogen does not enter the blood, the use of these internal energy stores by muscle conserves blood glucose for use by tissues such as the brain. Epinephrine also has a direct effect on adipose cells, increasing the availability of fatty acids for use as an energy source. The blood-glucose elevating effect of epinephrine is also an important homeostatic mechanism during periods of hypoglycemia. b. Various stresses can cause the secretion of growth factor. c. Stress increases the release of gluconeogenic hormones and predisposes the person to the development of ketoacidosis. DKA is often preceded by physical or emotional stress, such as infection, or inflammation, pregnancy or extreme anxiety. In clinical practice, ketoacidosis also occurs with the omission or inadequate use of insulin.
- Chapter 41. Disorders of Endocrine Control of Growth and Metabolism. Classifications and Pathophysiology. What is the connection between type 2 diabetes and metabolic syndrome? Pg. 1216. a. Central obesity, systemic hypertension and dyslipidemia
- Chapter 41. Disorders of Endocrine Control of Growth and Metabolism. Page 1175, Table 40.1 and/or Course Point Activity- Adrenal Gland. Describe the hormones produced by the adrenal gland.
a. Acute bacterial prostatitis is an acute infection of the prostate that results in pelvic pain & urinary tract symptoms, such as dysuria, fever, and chills. This condition requires immediate medical treatment. Most cases of acute bacterial prostatitis are caused by ascending urethral infection or intraprostatic reflux. Urogenital infection or anatomic malformations increase the risk for prostatitis. These infections may occur from direct inoculation after transrectal prostate biopsy and transurethral manipulations (e.g. catheterizations and cystoscopy). Direct or lymphatic spread from the rectum or hematogenous spread via bacterial sepsis, can cause acute bacterial prostatitis. Males with HIV are at higher risk, most likely due to immunosuppression. Many people with acute bacterial prostatitis have no risk factors. E. Coli is the most common cause. In addition to urinary infection symptoms, males may experience pain at the tip of the penis, dribbling, hesitancy, and poor stream. The physical exam should include an abdominal exam to detect a distended bladder, a genital exam, and a digital rectal exam. A digital rectal exam should be performed gently because vigorous prostatic massage can induce/cause bacteremia and subsequently sepsis. Urine may be cloudy and malodorous due to UTI. Rectal examination may reveal a firm, swollen, tender prostate. Because acute prostatitis is often associated with anatomic abnormalities, a thorough urologic exam is usually performed AFTER treatment is completed. Obtain blood cultures to assess for bacteremia if severe sepsis is suspected or if Staphylococcus is found in the urine culture. b. Chronic Prostatitis is an inflammation of the prostate with NO bacteria in the urinary system. Pain, which results from the nerves that supply this area or from the muscles in the pelvis, can last for weeks, months, or even years. Clinical manifestations include difficulty passing urine (which may be accompanied from pain), pain in the bladder, testes, and penis, and pain with ejaculation. If the patient is asymptomatic, treatment is not required. c. BPH: 1310
- Chapter 43. Disorders of the Prostate. Hyperplasia and Neoplasms. Annual wellness examinations. What should be included in diagnostics and physical exams? a.
- Chapter 43. Disorders of the prostate. Hypertrophy. What are the clinical manifestations and complications? a.
- Chapter 45. Acute cervicitis. What is this disorder? Most common causes? a. Acute cervicitis may result from the direct infection of the cervix or may be secondary to a vaginal or uterine infection. b. It may be caused by a variety of infective agents, including streptococcus, Staphylococcus, Enterococcus, C. Albicans, T. Vaginalis, N.
Gonorrhoeae, Chlamydia trachomatis, and HSV type 2, Gardnerella Vaginalis, and UU.
- Chapter 45. Acute cervicitis. What are the clinical manifestations? a. With acute cervicitis, the cervix becomes red and swollen. Irritation from the infection results in copious mucopurulent drainage and leukorrhea (whitish or yellowish discharge of mucus from the vagina).
- Chapter 45. Disorders of the Fallopian Tubes and Ovaries. Ovarian Cysts and Tumors. Describe important considerations regarding ovarian cancer (intro paragraph) and Diagnosis & Treatment. a. X b. No good screening tests or other early methods of detection exists for ovarian cancer. Transvaginal sonography has been used to evaluate ovarian masses for malignant potential. The serum tumor marker is a cell surface antigen. Most ovarian tumors do not secrete hormones, but the cancer antigen is detectable in the serum of about half of the epithelial tumors that are confined to the ovary and of those that spread. The specificity of this test is highest when combined with TVS. Screening with serum tumor markers can be used in monitoring therapy and reoccurrences when preoperative levels have been elevated. Treatment depends on the stage and type of ovarian cancer, but it most often includes surgery and chemotherapy. Systemic treatment includes chemotherapy and hormone therapy. A more localized treatment includes radiation therapy but is rarely used except to treat areas where the cancer has metastasized. Examples include external beam radiation therapy and brachytherapy. Stage 1 is treated by surgically removing the tumor and most often a hysterectomy is performed. Stage 2 may also be treated with chemotherapy. Stage 3 & 4 are usually treated the same as stage 2. Maintenance therapy may be recommended to keep cancer from returning.
- Chapter 45. Disorders of the Cervix and Uterus. Disorders of the Uterine Cervix. (2 questions from this section). Prevention of cervical cancer. Testing and interpretation of Papanicolaou smear. a.
- Chapter 45. Disorders of the Cervix and Uterus. Disorders of the Uterine Cervix. (2 questions from this section). Prevention of cervical cancer. Testing and interpretation of Papanicolaou smear. What type of test is this? What specifically is collected during the sampling process? (This question was on the midterm blueprint but the class performed poorly on it). a. Tissue from the squamocolumnar junction
- Chapter 45. Disorders of the Fallopian Tubes and Ovaries. Ectopic Pregnancy. How is this condition diagnosed?. a. Diagnostic tests for ectopic pregnancy include a urine pregnancy test, transvaginal ultrasound, and HCG levels. Definitive diagnosis may require laparoscopy.
frequently hypertrophies and becomes red, swollen and extremely crumbled. This can lead to greater fallopian tube damage and increase the reservoir for further chlamydial infections.
- Chapter 47. Vaginal-Urogenital –Systemic Infections. Describe diagnostic lab tests for chlamydia. What are the benefits of using NAAT? a. Diagnosis of chlamydial infections takes several forms. The identification of polymorphonuclear leukocytes on gram stain of penile discharge or cervical discharge in the female provides presumptive evidence. The direct fluorescent antibody test and the enzyme-linked immunosorbent assay that use antibodies against an antigen in the chlamydia cell wall are quick tests that are highly sensitive and specific. b. One of the newest sets of nonculture techniques, the NAATs does NOT require viable/living organisms for detection and can produce a positive signal from as little as a single copy of the target DNA or RNA. c. NAATs can be performed on urine or self-collected swab specimens from the distal vagina as well as the traditional endocervical and urethral specimens. Most NAATs in use today detect both C. trachomatis and Neisseria Gonorrhoeae.
- Chapter 47. Vaginal-Urogenital –Systemic Infections. Why is it essential to identify chlamydial and gonorrheal infections in women of child-bearing age? a. To prevent infertility and other complications associated with STI’s
- Chapter 47. Vaginal-Urogenital –Systemic Infections. How does syphilis affect a fetus if untreated in the mother? a. Congenital syphilis (syphilis passed from pregnant people to babies) continues to be a problem in the U.S. b. T. pallidum (causes syphilis) is spread by direct contact with an infectious moist lesion, usually through intercourse. Bacterial secretions may transfer the organism during any type of intimate contact. Skin abrasions provide another possible portal of entry. c. Untreated syphilis can cause prematurity, stillbirth, and congenital defects and active infection in the infant. d. Because the manifestations of syphilis may be subtle, testing for syphilis is mandatory in all pregnancies.
- Chapter 47. Vaginal-Urogenital –Systemic Infections. What the three stages of syphilis? Describe the clinical manifestation characterizes the primary stage. a. The three stages of syphilis are: primary, secondary and tertiary. b. Primary syphilis is characterized by the appearance of a chancre at the site of exposure, such as on the penis, vulva, anus, or mouth. Chancres typically appear within an average of 3 weeks of exposure but may incubate up to 3 months. The primary chancre begins as a single, indurated (hardened) papule that erodes (wears away) to create a clean-based ulcerated lesion on an elevated base. Lesions are usually painless and located at the site of sexual contact. Primary syphilis is readily apparent in
the male, where the lesion is on the scrotum or penis. Although chancres can develop on the external genitalia in females, they are more common on the vagina or cervix and therefore may go untreated since they are not visible without a speculum exam. Often there is accompanying inguinal lymphadenopathy. Syphilis infection is highly contagious at this stage, because symptoms are mild, it frequently goes unnoticed. The chancre usually heals within 3-12 weeks, with or without treatment. Unit 14. Disorders of Musculoskeletal Function. Chapters 47-50. There are 7 questions from this unit.
- Chapter 47. Geriatric Considerations. Changes related to aging. What happens to the muscles during the aging process? a. Sarcopenia, a decrease in muscle strength/mass and physical performance associated with normal aging, is a leading cause of loss of independence and can lead to falls, physical disability, fractures, and mortality b. Sarcopenia differs from frailty, but the two are related, as conditions that lead to frailty also lead to the development of sarcopenia and can worsen functionality and quality of life. c. Degenerative pain in tendons associated with aging is a common cause of musculoskeletal pain. Drying of joints due to biochemical changes causes decreased movement and increased pain. d. Posture changes and a loss in height associated with aging are due to the thinning of vertebral disks and curving of the cervical vertebrae. e. Bone mineral density reduces with age causing bones to become brittle and fracture.
- Chapter 48. Injury and Trauma of Musculoskeletal Structures. Fractures. What complications can occur from impaired/poor healing of fracture? a. Delayed union: manifests by failure of fracture to heal within predicted time as determined by x-ray/ failure of the fracture to unit within the normal period. b. Malunion: healing with deformity or rotation that is visible on x-ray films. Early, aggressive treatment can prevent this and result in earlier alignment and return of function. It is caused by inadequate reduction or alignment of the fracture. c. Non-union: failure to produce union and cessation of the process of bone repair. It is most often seen in the tibia, especially with open fractures or crushing injuries. It is characterized by mobility of the fracture site and pain on weight bearing. Muscle atrophy and loss of range of motion may occur. It is failure of the bone to heal before the process of bone repair stops.
- Chapter 48. What is compartment syndrome? How is it diagnosed?
d. Treatment: There is no definitive treatment for correction of the defective collagen synthesis that is characteristic of OI; however, bisphosphonates have been shown to produce an increase in cortical bone width and cancellous bone volume, as well as increased bone strength and mineral content. Prevention and treatment of fractures is important. Precise alignment is necessary to prevent deformities. Surgical intervention is often needed to stabilize fractures and correct deformities.
- & 49. Chapter 50. Crystal-Induced Arthropathies. Gout. (2 questions from this section). What are the possible causes of gout? Describe the basic pathophysiology of gout. a. Increased serum uric acid and urate crystal deposits in kidneys and joints b. It is an elevation of serum uric acid levels. Uric acid is the end product of purine metabolism. Two pathways are involved in making purine. 1: Purines are made from non-purine precursors. 2: The salvage pathway in which purine bases are recaptured from the breakdown of nucleic acids that are derived from exogenous (dietary) or endogenous sources. The elevation of uric acid and the development of gout results from overproduction of purines, decreased salvage of free purine bases, increased breakdown of nucleic acids due to increased cell turnover, or decreased urinary excretion of uric acid. Primary gout may be a consequence of enzyme defects that results in the overproduction of uric acid or inadequate elimination of uric acid by the kidney. In secondary gout, high levels of uric acid may be caused by the increased breakdown of nucleic acids. Other cases of secondary gout result from chronic renal disease. Some diuretics, including thiazides, can interfere with the excretion of uric acid. An attack of gout happens when monosodium urate crystals precipitate in the joint and start an inflammatory response. Crystal deposition usually occurs in peripheral areas of the body, such as the great toe, where the temperatures are cooler than in other parts of the body. Synovial fluid is a poorer solvent for uric acid than plasma, and uric acid crystals are even less soluble at temperatures below 37 degrees. Unit 15. Infection, Inflammation, and Immunity, Chapter 9; and Disorders of Integumentary Function. Chapters 51-52. There are 9 questions from this unit.
- Chapter 9. Infection, Inflammation, and Immunity. Acute inflammation. What happens in the vascular phase? a. The vascular phase of acute inflammation is characterized by changes in the small blood vessels at the site of injury, which is marked by tissue edema. It begins with momentary vasoconstriction followed quickly by vasodilation and vascular permeability mediated in part by lipid mediators and vasoactive products. Vasodilation includes the arterioles and venules with an increase in capillary blood flow, causing heat and redness, which are two
of the cardinal signs of inflammation. This is accompanied by an increase in vascular permeability with outpouring of protein-rich fluid (exudate) into the extravascular spaces. The loss of proteins reduces the capillary osmotic pressure and increases the interstitial osmotic pressure. This, along with an increase in capillary pressure, causes a marked outflow of fluid and its accumulation in the tissue spaces, producing swelling, pain, and impaired function. As fluid moves out of the vessels, stagnation of flow and clotting of blood occur. This helps in localizing the spread of infectious microorganisms.
- Chapter 9. Infection, Inflammation, and Immunity. Describe the requirements of the body for optimal wound healing to occur. a. Blood flow, nutrients, immune response, approximation of wound edges.
- Chapter 52. Disorders of Integumentary Function. Impetigo. Cause and clinical manifestations (how would you recognize it?). a. Impetigo is a common, superficial BACTERIAL infection caused by staphylococci or group A beta-hemolytic streptococci or both. Its occurrence is highest during warm, summer months or in warm, moist climates. b. It initially appears as a small vesicle or pustule or as a large bulla on the face or elsewhere on the body. As the primary lesion ruptures, it leaves a denuded area that discharges a honey-colored serous liquid that hardens on the skin surface and dries as a honey-colored crust. New vesicles erupt within hours. Pruritis often accompanies the lesions, and skin excoriations that result from scratching multiply the infection sites. Although very low, a possible complication of untreated streptococcal impetigo is post- streptococcal glomerulonephritis. c. It is highly contagious.
- Chapter 52. Disorders of Integumentary Function. What is cellulitis? What is the treatment of cellulitis? a. This is a deeper infection that affects the dermis and subcutaneous tissues. Pre-existing wounds (e.g. ulcers, erosions) and tinea pedis are often portals of entry. b. Legs are the most common sites, followed by the hands and pinnae of the ear, but cellulitis may be seen on many body parts. c. It involves the lymph system, and once compromised, repeat infections may impair lymphatic drainage, leading to chronically swollen legs, and eventually dermal scarring and lymphedema. d. Treatment measures (oral and IV antibiotics) are aimed at the invasive organisms and the extent of the infection. 53. Chapter 52. Disorders of Integumentary Function. What is herpes zoster? Describe the clinical manifestations a. Herpes Zoster (Shingles) is an acute, localized vesicular (small, fluid-filled sacs) eruption distributed over a dermatomal segment of the skin.
these burns maintain their softness and elasticity, but there may be the loss of some sensation. Scar formation is usual. These burns heal with supportive medical care aimed at preventing further tissue damage, providing adequate hydration and ensuring that the granular bed is adequate to support re- epithelialization. d. Third-degree, full-thickness burns extend into the subcutaneous tissue and may involve BONE and MUSCLE. Thrombosed vessels can be seen under the burned skin, indicating that the underlying vasculature is involved. These can vary in color from waxy white or yellow to tan, brown, deep red or black. These burns are hard, dry, and leathery. Edema is extensive in the burn area and surrounding tissues. There is NO pain because nerve sensors have been destroyed. These burns are almost always surrounded by second- degree burns which are an area surrounded by first-degree e. Table 52.
- Chapter 52. Disorders of Integumentary Function. Skin cancer assessment. What are the characteristics you look for in a suspicious lesion? Also be sure to read detection and diagnosis under this section. a. ABCDE of lesions, asymmetry, border, color, diameter and whether or not they are evolving
- Chapter 52. Disorders of Integumentary Function. Fungal infections. Candida Infections. Risk factors and associated systemic disorders. Who is at the highest risk for fungal infection? a. Some people are pre-disposed to candidal infections by conditions such as DM, antibiotic therapy, pregnancy, oral contraceptive use, poor nutrition, and immunosuppressive diseases. Oral candidiasis may be the first sign of infection with HIV.
- Chapter 52. Atopic Dermatitis (Eczema). Management/Care. Describe recommendations you would make to a client living with Eczema. a. Treatment of atopic dermatitis (atopic eczema) is designed to target the underlying abnormalities: dryness, itching, infection and inflammation. Underlying all treatment measures is a comprehensive education program regarding the cause of the disorder, treatment measures, and avoidance of temperature changes and stress to minimize vascular and sweat responses. Basic therapy begins with optimal skin care, addressing the skin barrier defect with continuous use of skin hydration, along with avoiding exposure to environmental irritants and foods that cause exacerbations of the symptoms. The person should bathe with warm water and mild soap. Bathing dries the skin, yet it is important to maintain a low level of microorganisms to prevent infection. Application of moisturizers increases hydration of the skin. Topical corticosteroids remain an important treatment for acute flare-ups but can cause local and systemic side effects. Potency of topical corticosteroids is classified by the potential for vasoconstriction. In general, the face and genital areas receive only preparations that have weak
or moderate potency, whereas other areas of the body tolerate preparations that have moderate or high potency. One of the main concerns of topical corticosteroid use is skin thinning. Another concern is secondary adrenal suppression and the suppression of growth in children resulting from systemic absorption. Wet-wrap therapy, in which a wet dressing is applied over emollients in combination with topical antiseptics (e.g., triclosan, chlorhexidine) or topical corticosteroids, has been shown to be beneficial in some cases of severe atopic dermatitis. Antihistamines are useful for their sedative effects and may be helpful during severe pruritus episodes. Phototherapy alone or in combination with corticosteroids during acute flares is often practiced, with beneficial results. Probiotics reduce the severity of atopic dermatitis. Probiotic preparations are available to the consumer in the form of powders, tablets, drinks, and fermented dairy products
