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Study guide for NURS 320 Exam 2 Alterations of hormonal regulation 1. What is the function of the endocrine system?

- Differentiation of reproductive and CNS in fetus - Stimulation of growth and development - Coordination of the male and female reproductive system - Maintenance of internal environment - Adaptation to emergency demands of the body 2. What are the general characteristics of hormones...how do they operate...know the difference between water-soluble and lipid soluble hormones ...know the cellular mechanism of hormone action - Specific rates and rhythms of secretion. - diurnal, pulsatile and cyclic, and patterns depending on circulating substances - Operate with feedback systems - Affect only target cells with appropriate receptors. - The liver inactivates hormones, rendering the hormones more water soluble for renal excretion. - Lipid soluble hormones go inside the cell membrane. Water soluble has to have a carrier. Lipid are rapid and long lasting in response. Lipid soluble hormones usually go to nucleus. Water Soluble onset is short and response is short lived. 3. ADH is a posterior pituitary hormone--what is its function - Controls plasma osmolality; allowing reabsorption of water.

4. Table 17-5 pg 434 discusses the anterior pituitary hormones....

5. Diseases of posterior pituitary include SIADH and diabetes insipidus---what are these? Clinical manifestations and treatment...make sure you know the drug desmopressin Syndrome of inappropriate antidiuretic hormone secretion. - Hypersecretion of ADH - For diagnosis, normal adrenal and thyroid function must exist - Clinical manifestations are related to enhanced renal water retention, hyponatremia, and hypo-osmolality. Diabetes Insipidus - Insufficiency of ADH - Polyuria and polydipsia - Partial or total inability to concentrate urine - Neurogenic Insufficient amounts of ADH - Nephrogenic Inadequate esponse to ADH - Psychogenic - Pharm Treatment: Desmopressin. 6. What is the function of the thyroid gland...make sure you understand TRH, TSH, T3 and T4 - These hormones regulate the rate of cellular metabolism throughout the body. All the steps in synthesizing and releasing thyroid hormones are stimulated by thyroid- stimulating hormone (TSH) secreted by the pituitary gland. Another class of thyroid cells, the parafollicular or C cells, is found outside the follicles; C cells secrete calcitonin, a calcium-lowering hormone. - TRH - tropic, tripeptidal hormone that stimulates the release of TSH (thyroid-stimulating hormone) and

prolactin from the anterior pituitary. - TSH - Thyroid-stimulating hormone (also known as TSH or thyrotropin) is a hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates the metabolism of almost every tissue in the body. Affects growth and maturation of tissues, cell metabolism, heat production, and oxygen consumption. 7.Understand hyperthyroidism and hypothyroidism...clinical manifestations, and treatment...specifically: tapazole, lugol's solution, PTU, Armour, Synthroid - Hyperthyroidism - Thyrotoxicosis - Graves Disease - pretibial myxedema Hyperhyroidism resulting from nodular thyroid disease - goiter Thyrotoxic Crisis idism Hypothyro

Pr imary hypothyroidism ubacute thyroiditis utoimmune thyroiditis (Hashimoto disease) ainless thyroiditis ostpartum thyroiditis yxedema coma C ongenital hypothyroidism Thyroid carcinoma Pharm treatment: Desiccated thyroid (Armour) Levothyroxine (Synthroid) M P P A S

8. What is the function of the parathyroid-- understand hyperparathyroidism and hypoparathyroidism..clinical manifestations, and treatment - These glands secrete parathyroid hormone (parathormone), that regulates calcium and phosphorus metabolism. Hyperparathyroidism Primary hyperparathyroidism Excess secretion of PTH from one or more parathyroid glands Secondary hyperparathyroidism Increase in PTH secondary to a chronic disease Hypoparathyroidism Abnormally low PTH levels Usually caused by parathyroid damage in thyroid surgery 9. What is the function of the adrenal glands?

Adrenal cortex 80% of an adrenal glands total weight Zona glomerulosa Zona fasciculata Zona reticularis Adrenal medulla Innervated by the sympathetic and parasympathetic nervous systems Adrenal cortex Stimulated by adrenocorticotropic hormone (ACTH) Glucocorticoid hormones Direct effects on carbohydrate metabolism Anti-inflammatory and growth-suppressing effects Influence awareness and sleep habits Most potent naturally occurring glucocorticoid is cortisol Adrenal cortex Mineralocorticoid hormones Affect ion transport by epithelial cells Increase the activity of the sodium pump of the epithelial cells Cause sodium retention and potassium and hydrogen loss Most potent naturally occurring mineralocorticoid is aldosterone Regulated by the renin-angiotensin system Adrenal cortex Adrenal estrogens and androgens Estrogen secretion by the adrenal cortex is minimal The adrenal cortex secretes weak androgens Androgens are converted by peripheral tissues to stronger androgens such as testosterone Adrenal medulla Chromaffin cells (pheochromocytes) Chromaffin cells secrete the catecholamines epinephrine (majority) and norepinephrine Release of catecholamines has been characterized as a fight or flight response Catecholamines promote hyperglycemia

10. Disorders of the adrenal glands include Cushing's disease...what happens with this disorder, clinical manifestations and treatment...specifically Nizoral, and Mifeprex The symptoms from prolonged exposure to excessive glucocorticoid hormones. Glucocorticoids are naturally excreted by the adrenal glands; however, Cushing's syndrome is a side effect of the pharmacological use of steroids in the management of inflammatory illnesses (e.g., reactive airways disease or arthritis). Glucocorticoid excess from pituitary or adrenal adenomas or from the production of excess levels of adrenocorticotropic hormone by lung cancer is exceptionally rare (and is called Cushing's disease). The affected patient may complain of muscular weakness, thinning of the skin, easy bruising due to capillary fragility, weight gain, rounding of facial features (moon-like facies), cervicodorsal fat (buffalo hump) on the upper back, poor wound healing related to immunosuppression, decreased sexual drive and function, menstrual irregularities, insomnia, or psychological depression. 11. Addison's is a disorder of the adrenal cortex..what happens with this disease...clinical manifestations, and treatment...specifically the glucocorticoids..Cortef, Medrol, and dexamthasone
A rare illness marked by gradual and progressive failure of the adrenal glands and insufficient production of steroid hormones. Patients with Addison's disease make inadequate amounts of both glucocorticoids (e.g. cortisol) and mineralocorticoids. (e.g. aldosterone). Cortisol is important to glucose metabolism, affects protein, carbohydrate and fat metabolism, and helps to maintain blood pressure and cardiovascular function. Hypovolemia and hypotension may result from aldosterone deficiency. The patient may be symptom-free until the majority of adrenal tissue is destroyed. Early complaints are usually nonspecific, e.g., a feeling of weakness or fatigue. Subsequently, patients may notice lack of appetite, weight loss, nausea, vomiting, abdominal pain, craving for salt, and dizziness. Physical findings may include postural hypotension and increased skin pigmentation. Laboratory studies may reveal hyponatremia and hyperkalemia. If these findings are present, a cosyntropin stimulation test may be performed to establish the diagnosis.

Alterations in Urinary Tract Function 1. What can cause a urinary tract obstruction? Urinary tract obstruction is an interference with the flow of urine at any site along the urinary tract The obstruction can be caused by an anatomic or functional defect Obstructive uropathy

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What is hydroureter, what is hydronephrosis? -Hydroureter - The distention of the ureter with fluid owing to obstruction. - Hydronephrosis - Hydronephrosis is the distention of the pelvis and calyces of one or

both kidneys, resulting in thinning of the renal tubules because of obstructed urinary flow. When the obstruction is a stone or kink in one of the ureters, only one kidney is damaged. The obstruction causes backup, resulting in increased pressure in the kidneys. If the pressure is low to moderate, the kidney may dilate with no obvious loss of function.

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What causes kidney stones? What are clinical manifestations of kidney stones? Some kidney stones are treated with K+ citrate...know this drug..how else are kidney stones treated? Supersaturation of one or more salts Presence of a salt in a higher concentration than the volume able to dissolve the salt Precipitation of a salt from liquid to solid state Temperature and pH Growth into a stone via crystallization or aggregation What is a neurogenic bladder? Look at table 29-1 and table 29-2 on page 746 of patho book to understand types of in incontence and neuro bladder

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What is interstitial cystitis? What are clinical manifestations and treatment? - Interstitial cystitis Nonbacterial infectious cystitis - Manifestations Most common in women 20 to 30 years old Bladder fullness, frequency, small urine volume, chronic pelvic pain urinary frequency and nocturia - Treatment No single treatment effective, symptom relief 6. Renal tumors account for about 3.8% of new cancers. What is a renal adenoma, renal cell carcinoma - Renal Adenoma - A benign tumor originating in the renal tubules of the cortex that is similar in appearance to a renal cell carcinoma - Renal Cell Carcinoma - A malignancy arising from the renal tubule that produces hematuria, flank pain, and an abdominal mass. 7. Bladder cancer is the 5th common malignancy...what are common clinical manifestations of bladder cancer 8. UTIs are inflammation of urinary epithelium caused by bacteria....ecoli most common bacteria. What are clinical manifestations of uti and pyelonephritis...they are usually treated with antimicrobial therapy such as amoxicillin (amoxil) and cephalexin (Keflex)--know these drugs. How else are they treated? - UTI - Frequency, dysuria, urgency, and lower abdominal and/or suprapubic pain - Pylenephritis. - The early symptoms of chronic pyelonephritis are often minimal and may include hypertension, frequency, dysuria, and flank pain. Progression leads to kidney failure, particularly in the presence of obstructive uropathy or diabetes mellitus.

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9. Look at table 29-5 on page 749 in patho book

10. Glomerular disorders are disorders that directly affect the glomerulus....what is the function of the glomerulus? What happens when the glomerulus is diseased...what is glomerulonephritis..what happens...what is treatment? - Glomerulus One of the capillary networks that are part of the renal corpuscles in the nephrons of the kidney. Each is surrounded by a Bowman's capsule, the site of renal (glomerular) filtration, which is the first step in the formation of urine. 11. What is nephrotic syndrome, clinical manifestations and treatment....know diuretic therapy such as LASIK Nephrotic syndrome is the excretion of 3.5 g or more of protein in the urine per day and is characteristic of glomerular injury. Primary causes of nephrotic syndrome include minimal change disease (lipoid nephrosis) (see Chapter 30), membranous glomerulonephritis, and focal segmental glomerulosclerosis.47 Secondary forms of nephrotic syndrome occur in systemic diseases, including diabetes mellitus, amyloidosis, systemic lupus erythematosus, and Henoch-Schnlein purpura (see Chapter 30). Nephrotic syndrome also is associated with certain drugs, infections, malignancies, and vascular disorders. When present as a secondary complication with renal diseases, nephrotic syndrome often signifies a more serious prognosis. 47 Nephrotic syndrome is more common in children than adults Many clinical manifestations of nephrotic syndrome are related to loss of serum proteins and associated sodium retention (Table 29-9). They include edema, hyperlipidemia, lipiduria, vitamin D deficiency, and hypothyroidism.48,49 Vitamin D deficiency is related to loss of serum transport proteins and decreased vitamin D activation by the kidney. Hypothyroidism can result from urinary loss of thyroid-binding protein and thyroxine. Alterations in coagulation factors can cause hypercoagulability and may lead to thromboembolic events. Nephrotic syndrome is commonly treated by adhering to a normal-protein (i.e., 1 g/kg body weight/day), low-fat, salt-restricted diet and by prescribing diuretics, immunosuppressive drugs, and heparinoids. When diuretics are used, care must be taken to observe for hypovolemia and hypokalemia or potassium toxicity in the presence of renal insufficiency. Aldactone may be combined with loop diuretics to suppress aldosterone activity to conserve potassium. Steroids or cyclophosphamide may be effective for the initial treatment of steroid-dependent nephrotic syndrome in children.51 Immunosuppressive drugs and angiotensin-converting enzyme (ACE) inhibitors are used with steroid-resistant nephrotic syndrome 12. If you understand the function of the kidney then you know more than half of what you need to know regarding renal failure...acute renal failure is a sudden decline in kidney function with decreased glomerular filtration, accumulation of nitrogenous waste and increased creatinine levels and increased BUN...they causes of acute renal failure are either pre, intra or post...know the difference of each...there are 3 phases of renal failure: oliguria, diuretic, and recovery phase. Understand the patho of each phase. 13. Chronic renal failure number one cause is diabetes....there are stages of chronic renal failure: stages 1-5...pg 757 table 75.7 of patho book..know them. Know the alterations in the body systems causes by renal failure ..pg 758, table 29-14

14. Know the following drug therapy for renal failure: Anemia- Epoetin Alfa (procrit, epogen) Hyperkalemia- (kayexalate) Hyperphospatemia - Phoslo, renagel Hypervolemia- lasix, diuril, aldactone, mannitol

Alterations of MS function 1.What is the role of Calcium and vit d in bone formation - Ca+ is the primary mineral for bone formation & for bone health - Critical for nervous, muscular and cardiovascular function. - It is regulated by the PTH, calcitonin and Vit D. - Vit D-inactive form is cholecalciferol, becomes calcifediolactive form of Vit D-- by an enzymes in the kidneys Vitamin D allows for calcium to be absorbed in the intestines. 2. What are the signs and symptoms of hypocalcemia and treatmentlook at table 47.1 on page 734 of pharm book. - Signs and Symptoms Nerve and muscle excitability Numbness and tingling of the extremities

3. What is Osteomalaciaclinical manifestations and treatment - Osteomalacia is a metabolic bone disease characterized by softening of bone due to demineralization. - Osteomalacia causes varying degrees of diffuse muscular and skeletal pain and tenderness. Pain is noted particularly in the hips, and the individual may be hesitant to walk. Muscular weakness is common and may contribute to a waddling gait. Facial deformities and bowed legs or knock-knees may be present. Bone fractures and vertebral collapse occur with minimal trauma. Low back pain may be an early complaint, but pain may also involve ribs, feet, other areas of the vertebral column, and other sites. Fragility fractures may occur. Uremia may be present in renal osteodystrophy. - 1. Adjustment of serum calcium and phosphorus levels to normal - 2. Suppression of secondary hyperthyroidism - 3. Chelation of bone aluminum if needed - 4. Administration of calcium carbonate to decrease hyperphosphatemia - 5. Administration of vitamin D supplements (oral or infusion) - 6. Administration of bisphosphonate - 7. Implementation of renal dialysis, if indicated 4. What is osteoporosis, causes, clinical manifestations, treatment, specifically bisphosphonates and calcitonintable 47.2, page 736 in pharm book. In osteoporosis, old bone is being resorbed faster than new bone is being made, causing the bones to lose density, becoming thinner and more porous. A progressive loss of bone mass may continue until the skeleton is no longer strong enough to support itself. Eventually, bones can fracture spontaneously. The specific clinical manifestations of osteoporosis depend on the bones involved. The most common manifestations, however, are pain and bone deformity. Unfortunately, these manifestations occur only in an advanced disease state. Fractures are likely to occur because the trabeculae of spongy bone become thin and sparse, and compact bone becomes porous. As the bones lose volume, they become brittle and weak and may collapse or become misshapen. Vertebral collapse causes kyphosis (hunchback) and diminishes height The goals of osteoporosis treatment are to slow the rate of calcium and bone loss and to stop the disease. Bisphosphonates are first-line medications for treating osteoporosis; they primarily work by inhibiting hydroxyapatite breakdown, reducing bone resorption

5. What is osteomyelitisclinical manifestations and treatment - Osteomyelitis is a bone infection most often caused by bacteria; however, fungi, parasites, and viruses also can cause bone infection (Figure 37-14). It is further categorized according to the pathogen's mode of entry into bone tissue. The most common type is exogenous osteomyelitis, an infection that enters from outside the body, for example, through open fractures, penetrating wounds, or surgical procedures. In exogenous osteomyelitis, the infection also can spread from soft tissue into adjacent bone. An example of this is a diabetic foot infection. Endogenous osteomyelitis is caused by pathogens carried in the blood from sites of infection elsewhere in the body; the infection can then spread to adjacent soft tissue. Hematogenous osteomyelitis (a common form of osteomyelitis) is usually found in infants, children, and elderly persons. (Osteomyelitis in children is discussed in Chapter 38.) In infants, incidence rates among males and females are approximately equal. In children and older adults, however, males are most commonly affected. Osteomyelitis is a common complication of sickle cell anemia and low oxygen tension. - Acute osteomyelitis causes abrupt onset of inflammation - If an acute infection is not completely eliminated, the disease may become subacute or chronic. In subacute osteomyelitis, signs and symptoms are usually vague. In the chronic stage, infection is indolent or silent between exacerbations. The microorganisms persist in small abscesses or fragments of necrotic bone and produce occasional exacerbations of acute osteomyelitis. The progression from acute to subacute osteomyelitis may be the result of inadequate or inappropriate therapy, or the development of drug-resistant microorganisms. - In the adult, hematogenous osteomyelitis has an insidious onset. The symptoms are usually vague and include fever, malaise, anorexia, weight loss, and pain in and around the infected areas. Edema may or may not be evident. Recent infection (urinary, respiratory, cutaneous) or instrumentation (catheterization, cystoscopy, myelography, diskography) usually precedes onset of symptoms. - Single or multiple abscesses (Brodie abscesses) characterize subacute or chronic osteomyelitis. Brodie abscesses are circumscribed lesions 1 to 4 cm in diameter, usually in the ends of long bones and surrounded by dense ossified bone matrix. The abscesses are thought to develop when the infectious microorganism has become less virulent or the individual's immune system is resisting the infection somewhat successfully. - In exogenous osteomyelitis, signs and symptoms of soft tissue infection predominate. Inflammatory exudate in the soft tissues disrupts muscles and supporting structures and forms abscesses. Low-grade fever, lymphadenopathy, local pain, and swelling usually occur within days of contamination by a puncture wound. - Treatment of osteomyelitis includes bone biopsy to identify the causative organism, use of antimicrobial agents, and dbridement of infected bone. 6. What is the difference between inflammatory vs noninflammatory joint disease - Traditionally, noninflammatory joint disease was differentiated from inflammatory joint disease by (1) the absence of synovial membrane inflammation, (2) the lack of systemic signs and symptoms, and (3) the presence of normal synovial fluid. 7. What is osteoarthritis- clinical manifestations and treatment - Osteoarthritis (OA) is a common, age-related disorder of synovial joints. It is characterized by local areas of loss and damage of articular cartilage, new bone formation of joint margins (osteophytosis), subchondral bone changes, variable degrees of mild synovitis, and thickening of the joint capsule (Figure 37-16). Pathology centers on load-bearing areas. Advancing disease shows narrowing of the joint space attributable to cartilage loss, bone spurs (osteophytes), and sometimes changes in the subchondral bone. OA can arise in any synovial joint but is commonly found in the hands, hips, and spine. It is less common in people younger than 40 years of age and its prevalence increases with age. Although the exact causes of OA are unclear, they involve low-grade inflammation, calcification of articular cartilage, genetic alterations, and metabolic disorders. - Clinical manifestations of OA typically appear during the fifth or sixth decade of life, although asymptomatic, articular surface changes are common after the age of 40 years. Pain in one or more jointsusually with weight bearing, use of the joint, or load bearingis the first and most predominant symptom of the disease. Resting the joint often relieves pain. If present, nocturnal pain is usually not relieved by rest and may be accompanied by paresthesias (numbness, tingling, or prickling sensations). Sometimes pain is referred to another part of the body. For example, osteoarthritis of the lumbosacral spine may mimic sciatica, causing severe pain in the back of the thigh along the course of the sciatic nerve. OA in the lower cervical spine may cause brachial neuralgia (pain in the arm) and is aggravated by movement of the neck. Osteoarthritic conditions in the hip cause pain that may be referred to the lower thigh and knee area. Sleep deprivation adds to the stress of the chronic pain of OA. Physical examination of the person with OA usually shows general involvement of both peripheral and central joints. Peripheral joints most often involved are in the hands, wrists, knees, and feet. Central joints most often afflicted are in the lower cervical spine, lumbosacral spine, shoulders, and hips. - Joint structures are capable of generating a limited number of signs and symptoms. The primary signs and symptoms of osteoarthritic joint disease are pain, stiffness, enlargement or swelling, tenderness, limited range of motion, muscle wasting, partial dislocation, and deformity - Conservative treatment includes rest of the involved joint until inflammation (if present) subsides; implementation of rangeof-motion exercises to prevent joint capsule contraction; use of a cane, crutches, or walker to decrease weight bearing; loss of

body fat if obesity is present (obese persons are five times more likely to have OA of the knees and twice as likely to have OA of the hips as persons of ideal body weight) (see Health Alert: Body Weight and Osteoarthritis); and use of analgesic and anti-inflammatory drug therapy to reduce swelling and pain. Glucosamine and possibly chondroitin, so-called nutraceuticals, have shown some success in reducing the pain and progression of OA. Intra-articular injection of high-molecular-weight viscose supplements, such as hyaluronic acid, also has been successful in decreasing knee pain with OA. Newer agents, including inhibitors of cytokines, matrix metalloproteinases (MMPs), and leptin, are under investigation and may prove more effective in treating OA. Surgery is used to improve joint movement, correct deformity or malalignment, or create a new joint with artificial implants. It has been estimated by some researchers that one in four individuals has a lifetime risk of developing symptomatic OA of the hip.68 More than 250,000 total hip replacement surgeries are performed yearly in the United States, most of which are related to OA. It is estimated that by 2015, almost 600,000 hip replacements and 1.4 million knee replacements will be performed in the United States. 8. What is rheumatoid arthritis- clinical manifestations and treatment: Humira, Enbrel, Imuran, Plaquenil, and Methotrexate - Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory autoimmune disease distinguished by joint swelling and tenderness and destruction of synovial joints leading to disability and premature death - Systemic autoimmune damage to connective tissue, primarily in the joints (synovial membrane) - Similar symptoms to osteoarthritis - Presence of rheumatoid factors (RA or RF test) - Antibodies (IgG and IgM) against antibodies - Joint fluid presents with inflammatory exudate - Early treatment of RA begins with disease-modifying antirheumatic drugs (DMARDs), such as methotrexate (MTX), azathioprine, sulfasalazine, hydroxychloroquine, leflunomide, and cyclosporine. These agents have been shown to slow the progression of RA and may prevent complications such as joint deformities and extra-articular complications. MTX remains the first line of treatment. 9. What is gout? Clinical manifestations, and treatment-Allopurinol and colchicine - Gout is a syndrome caused by incomplete purine metabolism, resulting in excess serum uric acid levels (hyperuricemia). It is characterized by inflammation and pain of the joints. Either excessive uric acid production or underexcretion of uric acid by the kidneys will cause hyperuricemia. - . Gout is manifested by (1) an increase in serum urate concentration (hyperuricemia); (2) recurrent attacks of monoarticular arthritis (inflammation of a single joint); (3) deposits of monosodium urate monohydrate (tophi) in and around the joints; (4) renal disease involving glomerular, tubular, and interstitial tissues and blood vessels; and (5) the formation of renal stones. These manifestations appear in three clinical stages: - 1. Asymptomatic hyperuricemia. The serum urate level is elevated but arthritic symptoms, tophi, and renal stones are not present; this stage may persist throughout life. - 2. Acute gouty arthritis. Attacks develop with increased serum urate concentrations; tends to occur with sudden or sustained increases of hyperuricemia but also can be triggered by trauma, drugs, and alcohol. - 3. Tophaceous gout. The third and chronic stage of the disease; can begin as early as 3 years or as late as 40 years after the initial attack of gouty arthritis. Progressive inability to excrete uric acid expands the urate pool until monosodium urate crystal deposits (tophi) appear in cartilage, synovial membranes, tendons, and soft tissue Alterations in Digestive function 1. What is the function of the liver? - The liver is one of the most metabolically active organs of the body. Amino acid metabolism: It synthesizes
nonessential amino acids, deaminates excess amino acids for use in energy production, and forms urea, which the kidneys excrete. Bile production: It is responsible for the production of bile salts, which emulsify fats in the small intestine; 800 to 1000 ml of bile is secreted in 24 hr, and the secretion rate is increased greatly during digestion of meals rich in fats. Carbohydrate metabolism: It converts monosaccharides other than glucose to glucose, and stores excess glucose as the starch glycogen, until such energy is needed. Detoxification: It produces enzymes to metabolize potentially harmful substances found in the portal circulation (e.g., alcohol, ammonia, indole, many medications, and skatole) into less toxic ones. Endocrine functions: It facilitates the conversion of levothyroxine to the more metabolically active thyroid hormone, triiodothyronine. Excretion: It discharges the breakdown products of hemoglobin (bilirubin and biliverdin) into the bile; these are eliminated in feces. Fat metabolism: It synthesizes cholesterol as well as lipoproteins for the transport of fat to other body tissues; it converts fatty acids to acetyl groups or ketones, so they may be used as energy sources.Phagocytosis: Its macrophages (Kupffer cells) scavenge bacteria, other pathogens, and senescent red blood cells from the portal circulation. Protein synthesis: It manufactures albumin, alphaglobulins and beta-globulins, complement components, and clotting factors, some of which are dependent on vitamin K. Storage: It stores copper, iron, vitamin B12, and the fat-soluble vitamins A, D, E, and K.

2.why does the following occur: portal hypertension, varcies, ascites, hepatic encephalopathy, jaundice, hepatorenal syndrome. Know clinical manifestations of each and treatment. - Portal Hypertension

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Portal hypertension is caused by disorders that obstruct or impede blood flow through any component of the portal venous system or vena cava. Intrahepatic causes result from vascular remodeling with shunts, thrombosis, inflammation, or fibrosis of the sinusoids, as occurs in cirrhosis of the liver, biliary cirrhosis, viral hepatitis, or schistosomiasis (a parasitic infection). Posthepatic causes occur from hepatic vein thrombosis or cardiac disorders that impair the pumping ability of the right heart. This causes blood to collect and increases pressure in the veins of the portal system. The most common cause of portal hypertension is fibrosis and obstruction caused by cirrhosis of the liver97 (see p. 921). Long-term portal hypertension causes several pathophysiologic problems that are difficult to treat and can be fatal. These problems include varices, splenomegaly, ascites, hepatic encephalopathy, and hepatopulmonary syndrome. Vomiting of blood (hematemesis) from bleeding esophageal varices is the most common clinical manifestation of portal hypertension. Slow, chronic bleeding from varices causes anemia and the presence of digested blood in the stools. Usually the bleeding is from varices that have developed slowly over a period of years. emergency management of bleeding varices includes use of vasopressors and compression of the varices with an inflatable tube or balloon, sclerotherapy, variceal ligation or portacaval shunt. Surgical shunts may decompress the varices, but this treatment can precipitate encephalopathy or liver failure and require liver transplant in selected cases.

Ascites o Ascites is the accumulation of fluid in the peritoneal cavity. Ascites traps body fluid in a third space o Portal hypertension usually is the cause. o The accumulation of ascitic fluid causes weight gain, abdominal distention, and increased abdominal girth (Figure 34-13). Large volumes of fluid (10 to 20 L) displace the diaphragm and cause dyspnea by decreasing lung capacity. Respiratory rate increases, and the individual assumes a semi-Fowler position to relieve the dyspnea. Approximately 10% of individuals with ascites develop bacterial peritonitis, which causes fever, chills, abdominal pain, decreased bowel sounds, and cloudy ascitic fluid. o The goal of treatment is to relieve discomfort. If the restoration of liver function is possible, the ascites diminishes spontaneously. In the meantime, dietary salt restriction and use of potassium-sparing diuretics can reduce ascites. Levels of serum electrolytes are monitored carefully because the individual is at risk for hyponatremia and hypokalemia. Hepatic Encephalopathy Hepatocyte Dysfunction o Hepatic encephalopathy results from a combination of biochemical alterations that affect neurotransmission. Liver dysfunction and the development of collateral vessels that shunt blood around the liver to the systemic circulation permit toxins absorbed from the gastrointestinal tract to accumulate and circulate freely to the brain. The accumulated toxins alter cerebral energy metabolism, interfere with neurotransmission, and cause edema. The most hazardous substances are end products of intestinal protein digestion, particularly ammonia, which cannot be converted to urea by the diseased liver. Other substances include inflammatory cytokines, short-chain fatty acids, serotonin, tryptophan, and manganese. Infection, hemorrhage, and electrolyte imbalance (including zinc deficiency) as well as the use of sedatives and analgesics can precipitate hepatic encephalopathy in the presence of liver disease o Subtle changes in personality, memory loss, irritability, lethargy, and sleep disturbances are common initial manifestations of hepatic encephalopathy. Symptoms then can progress to confusion, flapping tremor of the hands (asterixis), stupor, convulsions, and coma. Coma is usually a sign of liver failure and ultimately results in death. o Correction of fluid and electrolyte imbalances and withdrawal of depressant drugs metabolized by the liver are the first steps in the treatment of hepatic encephalopathy. Restricting dietary protein intake and eliminating intestinal bacteria with antibiotics reduce blood ammonia levels. Lactulose or nonabsorbable antibiotics may be administered to prevent ammonia absorption in the colon. Jaundice o Jaundice, or icterus, is a yellow or greenish pigmentation of the skin caused by hyperbilirubinemia (plasma bilirubin concentrations greater than 2.5 to 3.0 mg/dl). Hyperbilirubinemia and jaundice can result from (1) extrahepatic (posthepatic) obstruction to bile flow, (2) intrahepatic obstruction, or (3) prehepatic excessive production of unconjugated bilirubin (i.e., excessive hemolysis of red blood cells) o fever, chills, and pain often accompany jaundice resulting from viral or bacterial inflammation of the liver (e.g., viral hepatitis). Yellow discoloration may first occur in the sclera of the eye and then progress to the skin as bilirubin attaches to elastic fibers. Pruritus (itching) often accompanies jaundice because bilirubin accumulates in the skin. o The treatment for jaundice consists of correcting the cause. Heptorenal Syndrome o Hepatorenal syndrome is functional renal failure that develops as a complication of advanced liver disease. The renal failure is not caused by primary renal disease or other extrinsic factors but rather by portal hypertension and other circulatory alterations associated with advanced liver disease, such as alcoholic cirrhosis or fulminant hepatitis with portal hypertension and functional renal failure including oliguria, sodium and water retention (with or without ascites and peripheral edema), hypotension, and peripheral vasodilation.106 The kidney usually has a normal structure. o The onset of hepatorenal manifestations may be gradual or acute. Oliguria and complications of advanced liver disease, including jaundice, ascites, and gastrointestinal bleeding, are usually present. Systolic blood pressure is

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usually below 100 mm Hg. Nonspecific symptoms of hepatorenal syndrome include anorexia, weakness, and fatigue. Renal function improves with improvement in liver function. Secondary complications, including fluid and electrolyte disorders, bleeding, infections, and encephalopathy, also are vigorously treated.

3. what is hepatitis...clinical manifestations and treatment..refer to table in pharm book as mentioned in voice over power point. - Hepatitis is the inflammation of the liver o Can lead to cirrhosis 4.What happens with cirrhosis...clinical manifestations and treatment...hint if you can answer question #2 you know this answer..as it is the same Irreversible inflammatory disease that disrupts liver function and even structure Decreased hepatic function caused by nodular and fibrotic tissue synthesis (fibrosis) Biliary channels become obstructed and cause portal hypertension. Because of the hypertension, blood can be shunted away from the liver, and a hypoxic necrosis develops 5. What is cholecystitis and cholelithiasis...clinical manifestations and treatment - Cholelithiasis (gallstones) is a prevalent disorder in developed countries, where the incidence is 10% to 15% in white adults and 60% to 70% in Native Americans. Risk factors include obesity, middle age, female gender, use of oral contraceptives, rapid weight loss, Native American ancestry, genetic predisposition, and gallbladder, pancreatic, or ileal disease. - Cholelithiasis is often asymptomatic. Abdominal pain and jaundice are the cardinal manifestations of cholelithiasis. Vague symptoms include heartburn, flatulence, epigastric discomfort, and food intolerances, particularly to fats and cabbage. The pain (biliary colic) occurs 30 minutes to several hours after eating a fatty meal. It is caused by the lodging of one or more gallstones in the cystic or common duct. It can be intermittent or steady and usually occurs in the right upper quadrant, radiating to the mid-upper area of the back. Jaundice indicates that the stone is located in the common bile duct. - Endoscopic removal of gallstones by sphincterotomy or endoscopic papillary balloon dilation is the preferred treatment for uncomplicated gallstones causing obstruction of the bile ducts. 6. What happens in pancreatitis....what are the clinical manifestations and treatment.. - Pancreatitis Inflammation of the pancreas o Associated with several other clinical disorders o Caused by an injury or damage to pancreatic cells and ducts, causing a leakage of pancreatic enzymes into the pancreatic tissue o These enzymes cause autodigestion of pancreatic tissue and leak into the bloodstream to cause injury to blood vessels and other organs - Manifestations and evaluation o Epigastric pain radiating to the back o Fever and leukocytosis o Hypotension and hypovolemia o Enzymes increase vascular permeability o Characterized by an increase in a patients serum amylase level o Chronic pancreatitis o Related to chronic alcohol abuse -