WEEK+3+Alterations+of+GI+and+Immune+systems

__//**1. Review gastrointestinal and immune content from Nursing 138 (Nursing Care I). 2. Review the anatomy and physiology of gastrointestinal and immune systems.

3. Review the techniques for physical assessment of the gastrointestinal and immune systems.

4. Differentiate between the four types of hypersensitivity reactions, to include etiology, mechanisms of pathophysiology, related clinical manifestations and collaborative management.**//__ Type I, II, III are immediate reaction and are humoral immunity. Type IV is delayed reaction and is cell mediated. (Lewis 225 See table 14-9)

Type I: Ige - Mediated Reaction Occurs only in susceptible individuals who are highly sensitized to specific allergens. Etiology: IgE antibodies are produced in response to allergens and attach to mast cells and basophils. Mechanism of pathology: First exposure to allergen, IgE are produced and bind to mast cells and basophils. on subsequent exposures the allergen binds with the IgE bound to the mast cells or basophils and triggers degranulation of the cells and the release of chemical mediators. attacking target organs and causing clinical allergy symptoms. Clinical Manifestations: When mediators remain localized a cutaneous response termed wheal and flare reaction occurs. example is misquote bit or allergy skin test. occurs minutes to hours and is not usually a danger. Anaphylaxis: occur when mediators are released systemically. reaction occurs in minutes and can be life threatening. Causing bronchial constriction and subsequent airway obstruction and vascular collapse. rapid weak pulse, hypotension, dilated pupils, dyspnea, possibly cyanosis. death will occur if emergency treatment is not initiated. Atopic reaction: 20% of the population is atopic, an inherited tendency to become sensitive to environmental allergens. Allergic rhinitis or Hay fever is the most common example. target areas effected are conjunctiva of the eye and mucosa of the upper respiratory tract. symptoms include nasal discharge, sneezing, lacrimation, mucosal swelling with airway obstruction and pruritus around the eyes, nose, throat and mouth. Many people with asthma have an allergic component. inflammatory mediators produce a bronchial smooth muscle constriction and other asthmatic reactions. Atopic dermatitis: chronic inherited skin disorder characterized by exacerbation and remissions. skin lesions are generalized and involve vasodilation of blood vessels resulting in interstitial edema with vesicle formation. Urticaria (hives): cutaneous reaction against systemic allergens occurring in atopic persons. develops rapidly after exposure to an allergen and may last minutes to hours. Angioedema: localized cutaneous lesion similar to urticaria but involving deeper layers of the skin and submucosa. Type II: Cytotoxic reactions (Lewis pg 227) involving the direct binding of IgG and IgM to an antigen on the cell surface. cellular tissue is destroyed in one of two ways. activation of the complement cascade system resulting in cytolysis enhanced phagocytosis erythrocytes, platelets and leukocytes are cells frequently destroyed in Type II reactions. antigens involved are the ABO group, Rh factor and drugs. Hemolytic Transfusion Reactions: if the recipient is transfused with incompatible blood antibodies immediately coat the foreign erythrocytes causing agglutination (clumping) blocking small blood vessels in the body. Good pasture syndrome is a disorder involving lung and kidneys. Type III: Immune-Complex Reactions. (Lewis pg 228) complexes involving IgG and IgM that are to small to be removed by the mononuclear phagocyte system deposit in tissue or small blood vessels. they cause fixation of complement and the release of chemotactic factors that lead to inflammation and destruction of involved tissues. Examples are Lupus, Acute glomerulonenephritis and rheumatoid arthritis. Type IV: Delayed Hypersensitivity Reactions (lewis pg 228) sensitized T lymphocytes attack antigens or release cytokines. macrophages and enzymes released are responsible for most of the tissue destruction. it takes 24-48 hours for a response to occur. Contact Dermatitis: occurs when skin is exposed to substances that penetrate the skin to combine with epidermal proteins. poison ivy is an example. similar skin reaction to atopic dermatitis is contact more localized reaction to the area exposed to the allergen. Microbial hypersensitivity reaction: tuberculosis is classic example. organism itself does not damage the the lung tissue it is the antigenic material released from tubercle bacilli that reacts with the T lymphocytes that initiate the cell mediated immune response resulting in extensive caseous necrosis of the lung.

__//**5. Describe how an individual becomes sensitized to an allergen in type I hypersensitivity reactions.**//__ First exposure to the allergen B cells create IgE and release them to go bind to mast cells and basophils. These antibodies remain on the cell waiting gor the next exposure. on subsequent exposures the allergen bind directly with the IgE bound to the mast cells or basophils and triggers degranulation of the cells and the release of chemical mediators. attacking target organs and causing clinical allergy symptoms.

__//**6. Discuss the different types of blood group antigens and the issues concerning blood type compatibility for blood transfusions. (Lewis pg 227)**//__ //this is a type II reaction. See table 30-10 on page 680 in Lewis.// O blood is the universal donor because these blood cells contain no Antigens to react with any of the antibodies although the donor has anti A and Anti B and can not receive any blood other then O. Persons with AB blood are the universal recipient their blood cell have both A and B antigens so they have no anti bodies to react with and can receive blood from any of the four types. People with A blood have antibodies that will react with any B antigens on either B or AB blood. then same goes for B blood types can not receive any blood with A antigens.

__//**7. Discuss the importance of the Rh antigen for women of childbearing age.**//__ A Rh Negative mother can have a child that is Rh positive. During birth blood can be released from the placenta or in amniotic sac when they rupture. In the first pregnancy of a Rh positive baby the mother will be exposed at birth or if there is a rupture during the pregnancy. This will cause here body to create anti-Rh Antibodies that will react at the next exposure. this process takes time and is not an issue for the first birth. However, any subsequent pregnancies the antibodies will react immediately and are a serious health risk to the mother that will have a severe hemolytic reaction. A Coombs test can evaluate the persons Rh status.

__//**8. List the hormones and the neurotransmitters responsible for the digestion and absorption of carbohydrates, fats, and proteins.**//__ __//**  Huether table 33-1 p 916. P. Point p. #2 (power point narrows this list down) ** Mucosa of the stomach   **-Gastrin; **secretion stimulated by presence of partially digested proteins in stomach. Action; stimulates gastric glands to secrete Hydrochloric acid & pepsinogen; growth of gastric mucosa - **Somatostatin; **secretion stimulated by acid in stomach; Action-Inhibits acid &pepsinogen secretion & release of gastrin. - **Acetylcholine; **secretion stimulated by Vagus &local nerves in stomach; Action-Stimulates release of pepsinogen &acid secretion - **Gastrin-releasing peptide (bombesin); **secretion stimulated by vagus nerve & local stomach nerves. Action- Stim. Release of pepsinogen &acid secretion.** Mucosa of small intestine -Motilin; **secretion stimulated by presence of acid &fat in duodenum; Action; Increases gastrointestinal motility. - **Secretin; **secretion stim by presence of chyme (acid, partially digested proteins &fats) in duodenum. Action: Stimulates pancreas to secrete alkaline pancreatic juice & liver to secrete bile; decreases gastric motility; inhibits gastrin & gastric acid secretion. - **Cholecystokinin; **secretion stim by presence of chyme in duodenum. Action-Stim gallbladder to eject bile & pancreas to secrete alkaline fluid; decreases gastric motility; constricts pyloric sphincter; inhibits gastrin - **Enteroglucagon; **secretion stim by intraluminal fats and carbs; Action- weakly inhibits gastric & pancreatic secretion & enhances insulin release, lipolysis, ketogenesis, & glycogenolysis. - **Gastric Inhibitory Peptide (GIP); **secretion stim by fat & glucose in small intestine. Action-Inhibits gastric secretion; stim insulin release <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">- **Peptide YY; **secretion stim by intraluminal fat & bile acids. Action- Inhibits postprandial gastric acid & pancreatic secretion & delays gastric & small bowel emptying.** <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">-Pancreatic polypeptide; **<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">secretion stim by protein, fat & glucose in sm Intestine. Action-decrease pancreatic HCO3- & enzyme secretion <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">- **Vasoactive Intestinal Peptide; **secretion stim by intestinal mucosa & muscle. Action-relaxes intestinal smooth muscle.**//__
 * <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">- **Histamine; **secretion stimulated by Gastrin; Action; stimulates acid secretion

<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">  9. Describe the major nutrients absorbed in the small intestine. __//** Huether Box-33-2 p.922, 918-922 ** Water & Electrolytes; p. 922  ** <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> -Sm intestine absorbs 85%-90% water that enters GI Tract ** -  **<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> Na+ passes through tight junctions   & is actively transported across sm intestine cell membranes; Na+ is exchanged for bicarbonate to maintain electroneutrality in ileum. Na+ absorption is enhanced by glucose transport <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> -Potassiummoves passively across tight junctions w/ changes in the electrochemical gradient ** Carbohydrates  **  ; p.921, 922 -Only monosaccharides are absorbed by intestinal mucosa; so complex carbs must be hydrolyzed to simplest form - Starches are broken down by salivary & pancreatic amylases into oligosaccharides. Stomach and duodenum brush border enzymes hydrolyze them in intestine for absorption ** //__//Proteins; p921,922 __**  90%-95% protein is absorbed; most hydrolysis in sm intestine by pancreatic enzymes -Brush border enzymes then break them down into smaller peptides, -Finally broken down into amino acids that can cross sm intestine cell membranes ** Fats; p 921, 922 <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> 4 phases of digestion & absorption; <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic; mso-fareast-font-family: Arial;">    __//__  1)   Emulsification & lypolysis; cover sm fat particles so they won’t reform into fat droplets; then lypolysis breaks them into diglycerides, monoglycerides, free fatty acids, & glycerol.     2)    Micelle formation; products made H2o soluble 3)   Fat absorption; diffuse through intestinal epithelium by resynthesis     4)    Triglycerides & phospholipids enter systemic circulation. Minerals p. 922 Calcium  -absorbed primarily in ileum by passive diffusion & active transport Magnesium-  50% absorbed in jejunum & ileum (active trans.& passive) Phosphate-  absorbed in sm intestine (active trans. & passive) Iron-  absorbed by epithelial cell in duodenum &jejunum; Vit C facilitates Vitamins p.922 Absorbed mainly by Na+-dependent active transport w/ vit B12 bound to intrinsic factor & absorbed in terminal ileum. __ <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">  10. Examine the functions of the liver and related clinical manifestations to altered liver function. __//**<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Lewis table 39-4 p.932; Huether p.960-964, p.925-930 ** <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Major functions of the liver; **<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Lewis 932, p.point p.7 (p.p. narrows list down) <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Performs over 400 fx-all body systems in danger if not working ** <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Metabolic Functions; //__ <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Protein metabolism ////__<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">; <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Synthesis of plasma proteins (incl albumin), <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Synthesis of clotting factors, <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Synthesis of nonessential amino acids, <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Urea formation from NH3 (ammonia) which is formed from deamination of amino acids byaction of bact. On proteins in colon-liver deactivates A.acids and removes ammonia (p.p.) __ <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Fat metabolism; ////__<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Synthesis of lipoproteins <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Breakdown of tryglycerides into fatty acids &glycerol. <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Formation of keytone bodies <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Synthesis of fatty acids from a.acids and glucose <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Synthesis & breakdown of cholesterol __ <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Detoxification; __<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Inactivation of drugs & harmful substances & excretion or their breakdown products __ <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Steroid metabolism; __<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Conjugation & excretion of gonadal & adrena corticosteroid hormones __//** __//<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Bile Synthesis; <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Bile excretion; __<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> liver excretes about 1L/day of bile __**// __//<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Storage; // //**<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Glucose in form of glycogen <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Vitamins; fat soluble (A,D,E, K) &H2O soluble(B1, B2, colbalamin, folic acid) <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">--Fatty acids <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Minerals (iron, copper) <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Amino acids in form of albumin & B-globulins ** <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Mononuclear Phagocyte System; //__ __//<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-breakdown of old RBCs, WBCs, bacteria, &other particles <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Breakdown of hemoglobin from old RBCs to billirubin to biliverdin //__** __//<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Converts bilirubin to bile; <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Filter blood of portal system- **<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">kupffer cells (p.Point) ** <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Thiamine deficiency ////**<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">- (p.point) <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> **Clinical Manifestations of Liver Disorders Huether p960-961, p.point <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">-Portal Hypertension; ////**<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">abnormally high blood pressure in the portal venous system. Caused by disorders that obstruct or impede blood flow through the portal venous system or vena cava. <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Long-term portal hypertension can lead cause many issues including; <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic; mso-fareast-font-family: Arial;"> 1) **<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Esophageal, Stomach, and Rectum Varices ////**<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">; Vomiting of blood from esoph.varice is most common clin manifestation of potal hypertension. Slow chronic bleeding from varices causes anemia and blood in stools. Rupture causes usually painless hemorrhage & vomiting of dark-colored blood. High mortality <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic; mso-fareast-font-family: Arial;"> 2)  **<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Splenomegaly; ////**<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">enlargement of spleen from increased pressure in splenic vein <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic; mso-fareast-font-family: Arial;"> 3) **<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Ascites **<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">; Caused by portal hypertension and reduced serum albumin. Accumulation of fluid in peritoneal cavity. The effect is to reduce amt of fluid available for normal physiologic fx. Causes wt gain, abdominal distension, dilated upper abd veins, inverted umbilicus. Lg volumes of fluid displace diaphragm and cause dyspnea by decreasing lung capacity. Resp increases, semi-fowlers ** <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic; mso-fareast-font-family: Arial;"> 4)  <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">Hepatic encephalopathy; **<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Liver dysfx & vesels that shunt blood around liver to the systemic circulation permits toxins absorbed from GI tract to circulate freely in brain; Includes ammonia-alters cerebral metabolism & interfere w/ neurotransmitters. CNS disturbances; partially reversible alterations of consciousness. In beginning-subtle changes in personality, memory loss, irritability, lethargy, sleep disturbances. Later-confusion, asterix; flapping tremor of hands, stupor, convulsions, coma ** <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">-Jaundice- **<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">yellow, greenish pigmentation of skin caused by hyperbilirubinemia-anorexia, malaise, fatique, yellowdiscoloration inschlera first then in skin ** <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-style: italic;">-Hepatorenal: //**//<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">advanced liver disease; manifestations include oliguria, jaundice, ascites, GI bleeding. Systolic BP usually below100mm Hg, anorexia, weakness, fatigue //**__**//11. Relate changes in the gastrointestinal system to aging. (MS p 933, Table 39-5)
 * //<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">-Carbohydrate metabolism __<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">; Glycogenesis (conversion of glucose to glycogen) &Glycogenolysis (process of breaking down glycogen to glucose) &Gluconeogenesis (forms glucose from a. acids & fatty acids); used in flight or fight when not enough glucose is available __
 * <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">- **//__//**Bile production; __Formation of bile; containing bile salts, bile pigments (mainly bilirubin), and cholesterol__
 * //<span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Kupffer Cells; //
 * <span style="font-size: 10pt; font-family: Arial; mso-bidi-font-size: 13.0pt; mso-bidi-font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">In Liver unconjugated bilirubin is conjugated w/ glucuronic acid. The conjugated bilirubin is H2O soluble and can be excreted in bile. **

//** //** related to gastrointestinal and hepatic function and examine the abnormalities specific to **
 * __ //12. Discuss the diagnostic evaluations (laboratory & radiological tests) and special procedures// __****__
 * various alterations in gastrointestinal function. **

GI ** diagnostic evaluations (laboratory & radiological tests): **// __** ** MedSurg Table 39-12 p 941-945 ** **__ //GI special procedures:// __** ** Med Surg Table 39-7 p 934 ** **__ //Hepatic ** diagnostic evaluations (laboratory & radiological tests): **// __** ** MedSurg Table 39-13 p 946 ** **__ //Hepatic special procedures// __****<span style="font-weight: normal; font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">: (MS p1107) ** __ //For Acites:// __**<span style="font-weight: normal; font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> __ //Peritoneovenous shunt// __ is a surgical procedure that provides continuous reinfusion of ascitic fluid into the venous system. ** __ //Transjugular intrahepatic portosystemic shunt (TIPS)// __ is a nonsurgical procedure in which a tract (shunt) between the systemic and portal venous systems is created to redirect portal blood flow (__ Fig. 44-11 __). A catheter is placed in the jugular vein and then threaded through the superior and inferior vena cava to the hepatic vein. The wall of the hepatic vein is punctured and the catheter is directed to the portal vein. Stents are positioned along the passageway, overlapping in the liver tissue and extending into both veins. __ //abnormalities specific to// // various alterations in gastrointestinal function: //

__//MedSurg Table// 39-11, p 939-940 __ //13. Examine the etiology, pathophysiology, clinical manifestations, potential complications,// // diagnostic evaluation, and collaborative management of the client with gastroesophageal reflux (GERD). // __** (MedSurg p 1003-1007) (Patho 991-992) **__

//etiology://  __ It results when the defenses of the lower esophagus are overwhelmed by the reflux of acidic gastric contents into the esophagus. The lower esophageal sphincter (LES) is the antireflux barrier. Predisposing conditions include hiatal hernia, incompetent LES, decreased esophageal clearance (ability to clear liquids or food from the esophagus into the stomach) resulting from impaired esophageal motility, and decreased gastric emptying. __ //Pathophysiology:// __ The acidic gastric secretions that reflux up into the lower esophagus can result in esophageal irritation and inflammation (esophagitis). The gastric enzyme pepsin and intestinal enzymes (e.g., trypsin) and bile salts are also corrosive to the esophageal mucosa. The degree of inflammation depends on the amount and composition of gastric reflux and on the ability of the esophagus to clear the acidic contents. One of the primary factors in GERD is an incompetent LES. An incompetent LES results in a decrease in pressure in the distal portion of the esophagus. As a result, gastric contents are able to move from an area of higher pressure (stomach) to an area of lower pressure (esophagus) when the patient is in a supine position or has an increase in intraabdominal pressure. Decreased LES pressure can be due to certain foods (e.g., caffeine, chocolate) and drugs (e.g., anticholinergics). Obesity is a risk factor for GERD although the mechanism remains to be determined.__ 11 __ Pregnant women are also at greater risk for GERD. Cigarette and cigar smoking can also contribute to GERD. A common cause of GERD is a hiatal hernia, which is discussed in the next section. __ //clinical manifestations:// __ __ Heartburn __ //(pyrosis)// from gastroesophageal reflux of acidic gastric secretions is the most common clinical manifestation. Patients may also complain of dyspepsia. __//Dyspepsia//__ is defined as pain or discomfort centered in the upper abdomen (mainly in or around the midline as opposed to the right or left hypochondrium). Episodes of __hypersalivation__ (water brash) are another common complaint. Complaints of __noncardiac chest pain__ are more common in older adults with GERD. __Nocturnal coughing__ can awaken the patient, resulting in disturbed sleep patterns. Otolaryngologic symptoms include __hoarseness, sore throat, a //globus sensation// (sense of a lump in the throat), and choking.__ __//Regurgitation//__ (effortless return of food or gastric contents from the stomach into esophagus or mouth) is a fairly common manifestation of GERD. It is often described as hot, bitter, or sour liquid coming into the throat or mouth. Gastric symptoms including __early satiety, postmeal bloating, nausea, and vomiting are related to delayed gastric emptying.__ __ //potential complications:// __ Complications of GERD are related to the direct local effects of gastric acid on the esophageal mucosa. Esophagitis (inflammation of the esophagus) is a frequent complication of GERD. Other risk factors for esophagitis include hiatal hernia, chemical irritation from lye or physical irritants such as smoking, cold or hot liquids, and excessive alcohol intake. Trauma to the esophagus can produce inflammation. Esophagitis with esophageal ulcerations is shown in __ Fig. 42-4 __. Repeated exposure may cause scar tissue formation and decreased distensibility //(esophageal stricture)// of the esophagus. This may result in dysphagia. Another complication of GERD is Barrett's esophagus (esophageal metaplasia). Barrett's esophagus is considered a precancerous lesion that increases the patient's risk for esophageal cancer. Approximately 10% to 15% of patients with chronic reflux have Barrett's esophagus. In Barrett's esophagus there is replacement of the normal squamous epithelium with columnar epithelium. These cell changes are thought to be due to GERD. However, patients with no history of reflux can still develop Barrett's esophagus. __ //diagnostic evaluation:// __**<span style="font-weight: normal; font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> Barium swallow can detect if there is protrusion of the upper part of the stomach //(gastric fundus)//. Endoscopy is useful in assessing the LES competence and the degree of inflammation (if present), potential scarring, and strictures. Biopsy and cytologic specimens can be taken to differentiate stomach or esophageal carcinoma from Barrett's esophagus. Manometric studies may be performed to measure pressure in the esophagus and LES. The determination of pH using specially designed probes can be used in the laboratory or as ambulatory monitoring systems to determine esophageal pH. With reflux there is acid in the normally alkaline esophagus. Radionuclide tests may also be performed to detect reflux of gastric contents and the rate of esophageal clearance.Because of the cost and discomfort of diagnostic procedures, it has been suggested that high-dose proton pump inhibitor (PPI) treatment (explained under Drug Therapy) for a short period (2 weeks) can be used as a first step in the diagnosis of GERD.__ 13 __ In patients with GERD, PPI treatment should result in a marked reduction or elimination of symptoms. <span style="font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> ** __ //collaborative management:// __ **<span style="font-weight: normal; font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Most can be managed with lifestyle modifications and drug therapy. **  **__ Lifestyle __****<span style="font-weight: normal; font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> Avoid foods that aggravate symptoms. Avoid eating close to bedtime. Weight reduction if overweight. **  __ //Drugs // __ <span style="font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Cholinergics(bethanechol)-Increase LES pressure <span style="font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Prokinetic(Reglan)-Increases motility <span style="font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Antacids-Acid Neutalizing <span style="font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">H2 receptor blockers(Tagamet,Pepcid,Zantac)-antisecretory <span style="font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">proton pump inhibitors(PPI)(Nexium,Prilosec)-antisecretoty <span style="font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Cytoprotective(gaviscon, sucralfate) <span style="font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> __ Surgery __ <span style="font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Antireflux surgery-most are laparoscopic <span style="font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">Fundus of stomach is wrapped around lower portion of esophagus to reinforce and repair the defective barrier. <span style="font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;"> __ Endoscopic therapy (MS p1006) __ __ //14. Discuss the reasons for an infant’s increased susceptibility to gastroesophageal reflux.// __**<span style="font-weight: normal; font-size: 10pt; color: black; font-family: Arial; mso-bidi-font-weight: bold; mso-bidi-font-style: italic;">(patho p992, pilli p 1423) ** A neuromuscular disturbance in which the gastroesophogeal sphincter and the lower portions of the esophagus are lax and thus allow easy regurgitation of gastric contents into the esophagus. Usually starts within one week and could be assoc. hiatal hernia. Children with cerebral palsy or other neurological involvement are at particular risk. <span style="font-size: 12pt; font-family: 'Thorndale for VST'; mso-bidi-font-family: 'Thorndale for VST'; mso-fareast-font-family: 'Times New Roman'; mso-ansi-language: EN-US; mso-fareast-language: EN-US; mso-bidi-language: AR-SA;"> Delayed maturation of the lower esophageal sphincter or impaired hormonal response mechanisms are possible causes. Factors that maintain lower esophageal sphincter integrity in children include the location of the gastroesophageal junction in a high-pressure zone within the abdomen, mucosal gathering within the sphincter, and the angle at which the esophagus is inserted into the stomach. Reflux persists if any one of these pressure-maintaining factors is altered. Irritation of the mucosa by acidic gastric contents results in inflammation of the esophageal epithelium and stimulation of the vomiting reflex.

//15. Compare and contrast between ulcerative colitis and Crohn’s disease specific to their etiology, pathophysiology, clinical manifestations, and collaborative management.// Certain criteria are used to differentiate ulcerative colitis from Crohn’s disease, but the diseases have much in common, and a clear differentiation between the two cannot be made in about a third of the cases. The fact that people with ulcerative colitis commonly have a relative with Crohn’s disease and vice versa supports the existence of a common gene. (See TABLE 43-17 Lewis 1051)

**//16. Describe the etiology, pathophysiology, clinical manifestations, and collaborative//** **//management relative to the child with a pyloric stenosis.//** .  (Pillitteri 1424)     Pyloric Stenosis is caused by a stenosed or hypertrophied pyloric valve. This prevents any food from passing from the stomach to the intestine and causes vomiting immediately after each feeding. Vomiting grows increasingly forceful until it is projectile, possibly projecting 3-4 feet. Pyloric stenosis tends to occur more frequently in first born white males usually at 4-6 weeks of age. Vomitus smells sour b/c it has reached the stomach and has been in contact w/ stomach enzymes. There is never bile in the vomit of pyloric stenosis b/c feeding doesn’t reach the duodenum to become mixed w/bile. The infant is usually hungry directly after vomiting b/c nausea is usually not present. If nausea is present infant may show disinterest in feeding, drool excessively, or chew on its tongue. Dx is made from the hx according to what the parents say. Ask ?’s like these: What is the duration? What is the intensity? What is the frequency? What is the description of the vomitus? Is the infant ill in any other way? Dehydration is seen with pyloric stenosis by assessing for tears, sunken fontanels, dry warm skin, dry mucous membranes, fever, poor skin turgor, weight loss. Alkalosis may be present b/c excessive loss of Cl- ions from stomach fluid, along w/hypochloremia, hypokalemia, and starvation. Hypopnea occurs as the body attempts to compensate for the alkalosis. Tetany may occur w/alkalosis b/c the increased HCO3 ions may bind w/Ca+ ions, trying to effect homeostasis and thereby lowering the level of ionized calcium. Low serum calcium levels lead to tetany. A definite dx is made by watching the infant drink. Palpate for an olive-size lump in the RUQ before the infant drinks. If one is present it will become more pronounced as the child drinks and projectile emesis will follow soon after. If the dx is still in doubt a sonogram will show the hypertrophied sphincter. Endoscopy may also be used for dx by directly visualizing the hypertrophied sphincter. Rx is surgical/laparoscopic correction (a pyloromyotomy), performed before electrolyte imbalance from vomiting or hypoglycemia from the lack of food occurs. Before surgery, electrolyte imbalance, dehydration, and starvation must be corrected by admin. of IV fluid, usually isotonic saline or 5% glucose in saline b/c this contains an excess of Cl- ions. NPO status held to prevent further electrolyte depletion. An infant who is receiving only IV fluid needs a pacifier to fulfill sucking needs. If tetany is present, IV calcium must be admin. The infant usually needs K+, but as a rule this must not be admin. until it is determined that the child’s kidneys fxn. (child is voiding). Otherwise K+ buildup could cause arrhythmias. This surgery is a difficult one and has a high risk for infection afterward b/c the abdomen incision is near the diaper area. The prognosis for infants w/pyloric stenosis is excellent if the condition is discovered before an electrolyte imbalance occurs. **//17. Analyze the etiology, pathophysiology, clinical manifestations, potential complications, and//** **//collaborative management of the client with cirrhosis.//** (Lewis 1101) Cirrhosis is a chronic progressive disease of the liver characterized by extensive degeneration & destruction of the liver parenchymal cells. Eventually, irregular, disorganized regeneration; poor cellular nutrition; and hypoxia caused by inadequate blood flow and scar tissue result in decreased fxn of the liver. Cirrhosis may have an insidious, prolonged course. Cirrhosis is ranked as the 9 th leading cause of death in the U.S. and the 4 th leading cause of death in persons 35-54 yrs of age. Highest incidence occurs 40-60 and usually in men. 4 types of cirrhosis: Alcoholic, Postnecrotic, Biliary, and Cardiac. Excessive alcohol consumption is the single most common cause of cirrhosis b/c alcohol has a hepatotoxic effect. Controversy of whether it’s the alcohol or malnutrition that accompanies excessive alcohol intake that causes cirrhosis, probably a combination of both. Approx. 20% of pts w/chronic Hep C & 10% of pts w/chronic Hep B will develop cirrhosis. The combo of chronic hep & ETOH ingestion is synergistic in terms of accelerating liver damage. Biliary causes of cirrhosis include primary biliary cirrhosis and primary sclerosing cholangitis. Clinical Manifestations:  See FIG. 44-6 Lewis 1104 Potential Complications:  Portal HTN & Esophageal & Gastric Varices, Peripheral Edema & Ascites, Hepatic Ecephalopathy, Hepatorenal Syndrome. Collaborative Management of Cirrhosis:  See TABLE 44-15 Lewis 1107 ***Note:** **  Cirrhosis in children has a short explanation in Patho 999 and Pillitteri 1430

18. Examine the progressive degeneration of a client with cirrhosis to include of the following: (Lewis, 1104-1106)(Heuther, 960-961)** a. Portal hypertension b. Esophageal varices c. Ascites **(Abdominal distention) caused by:** d. Hepatic encephalopathy **(Neuropsychiatric manifestations)** e. Hepatorenal syndrome
 * Increased venous pressure in the portal circulation(from 3 to 10) from any obstuction theat impedes blood flow through the portal(thrombosis, infammation, fibrosis from cirrhosis) that leads to collateral circulation to reduce this high portal pressure. The common areas of collateral circulation are formed in the lower esophagus and the rectum (Hemorrhoids)**
 * Are a complex of tortuous veins at the lower end of the esophagus, enlarged and swollen as a result of portal hypertension. Bleeding varices are the most life threatening complication of cirrhosis. They can rupture and bleed from alcohol ingestion, acid regurg, Increased intraabdominal pressure lifting, vomiting, swallowing hard foods**
 * Accumulation of serous fluid in the peritoneal or abdominal cavity
 * When portal pressure is elevated proteins and water leak through the liver capsule into the peri cavity. The osmotic pressure of these proteins pulls in additional fluid
 * Hypoalbuminemia resulting from the inability of the liver to produce it resulting in decreased colloidal oncotic pressure.
 * Hyperaldosteronism resulting in increased sodium reabsorption and water retention.
 * Liver damage causes a build up of ammonia, major source of AM is deamination of amino acids in the intestines that usually goes to the liver via portal circulation and converted to urea. AM crosses the blood brain barrier


 * Complication of advanced liver disease, the kidneys usually have no structural damage
 * Renal failure with oliguria and ascites, Portal hypertension causes systemic vasodilatation and decreased arterial Blood volume. Leads to renal vasodilation and renal failure.

__//19. Examine the etiology, pathophysiology, and clinical manifestations of fulminant hepatic failure.//__ • Etiology 2. isoniazid, halothane, sulfa drugs, nSAIDS, 3. Viral hepatitis 2nd most common cause 4. Mushroom poisening “death caps”** • Patho 2. Rapid onset of severe lover dysfunction in someone with no prior history of liver disease** • Clinical manifestations
 * 1. most common cause is drugs, usually acetaminophen in combo with ETOH
 * 1. Drugs cause liver cell failure by disrupting essential intra cellular process or causing an accumulation of toxic metabolic products
 * 1. Jaundice, coagulations, abnormalities, encephalopathy (changes in mentation are the first clinical signs)**

__//20. Analyze the etiology, pathophysiology, clinical manifestations, potential complications, and collaborative management related to the client with acute pancreatitis(Lewis, 1118-1120) (Heuther, 970-971).//__ • Etiology 2. Most common-gallbladder disease followed by chronic ETOH intake 3. Trauma, viral infections, ulcer, cysts, abscesses, Kaposi sarcoma, drugs** • Patho • Clinical manifestations 2. Sudden onset, severe, deep, piercing, flushing, cyanosis, dyspnea, nausea, vomiting decreased bowel sounds 3. Lung are involved, crackles, cyanosis from circulation enzymes 4. Ecchymosis on the flanks (Turner’s spots) & periumbilical area (cullen’s)** • Complications 2. Pancreatic abscess-fluid filled cavity within the pancreas that may become infected or perforated into other organs. 3. Systemic complication include pulmonary (pneumonia, pleural effusion, atelectasis) and cardio (hypotension) Tetany caused by hypocalcemia (sign of severe disease)** • Collaborative 2. Surgical removal of gallstones (laparoscopic cholecystectomy) 3. Drug therapy (table 44-21 1121 Lewis) 4. Nutritional therapy-NPO initially to reduce pancreatic secretions**
 * 1. Biliary tract disease (women), Alcoholism (men) Primary factors
 * 1. Obstuction by gallstones causes the outflow of enzymes to backup causing autodigestion of the pancreas- activation of the pancreatic enzymes in the pancreas instead of the intestines due to reflux of bile acids into the pancreatic ducts through an open or distended sphincter of Oddi.**
 * 1. Abdominal pain in the left upper quadrant radiating to the back because of the retroperitoneal location of the pancreas
 * 1. Pseudocysts- a cavity surrounding the outside of the pancreas filled with necrotic products and enzymes. When these enzymes escape the surface becomes inflamed.
 * 1. Pain relief, prevention of shock, reduction of secretions, control of f&E’s prevention of infections

__//21. Compare and contrast acute and chronic pancreatitis (Lewis 1124).**//__ Chronic pancreatitis is a structural or functional impairment of the pancreas where acute is a blockage by gallstones Major manifestation is the same as acute-PAIN; in chronic it may be constant pain. Pain is located in the same area but in chronic it is usually described as heavy gnawing or sometimes as burning and cramp like. Food or antacids do not relieve the pain in chronic but may in acute Malabsorption is associated with chronic with weight loss, steatorrhea, DM, In Acute serum amylase and lipase are elevated but not in chronic