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Chapter 13 & 14 Clinical GuideNOTE: This clinical guide is intended to be used as a tool for study and may include 100% of the clinical material you will be responsible for on your exam. Please be sure to reference your notes and lecture material to ensure you aren’t overlooking any information. As always, I am available 3 times a week if you have any questions or difficulties concerning the material, my session times can be found here. Good luck studying!COPD (Chronic Obstructive Pulmonary Disease):-Reduced air flow in and out of the bronchi due to long term tissue damage, loss of elasticity in lumen and smooth muscle, inflammation, increased mucous secretions, infections, etc. This increases airway resistance, especially upon expiration/exhalation. -A combination of Chronic Bronchitis and Emphysema-is an Obstructive lung disease where lungs have increased compliance (ability to stretch and allow in more air) but does not have equal expiration resulting in “trapped air” and the indicative symptom of a barrel-shaped chest (thin = Emphysema, muscular = Bronchitis)-in Emphysema there is typically Hypoxemia but Normocapnia (normal arterial CO2 pressure)-In Chronic Bronchitis there is typically Hypoxemia but Hypercapnia (increased arterial CO2 pressure) >Emphysema: -causes destruction of alveolar wall, which decreases surface area (and therefore diffusion)-can be genetic, infectious, cancerous-a Restrictive lung disease-Pink Puffers: mild Hypoxemia causes heavy breathing (dyspnea) and pink discoloration in the skin, but patients also have Normocapnia (normal arterial CO2 pressure), difficulty exhaling, and possibly a thin, barrel-shaped chest. >Chronic Bronchitis:-narrow bronchial airways due to inflammation and tissue scarring (due to coughing), increased mucous secretions, increased susceptibility to chronic respiratory infections-people who smoke or are exposed to air-borne chemical irritants often may develop Chronic Bronchitis/COPD-Blue Bloaters: severe Hypoxemia, Cyanosis (blue tint to skin due to low O2 in the blood), and Hypercapnia (increased arterial CO2 pressure). Patients are susceptible to heart chamber failure in the right ventricle (which pumps deoxygenated blood into the lungs via Pulmonary artery for oxygenation), or edema somewhere in their Systemic circulation. An indicative symptom is a muscular barrel-shaped chestAsthma:-a chronic condition characterized by occasional airway constriction and inflammation with increased mucous production often as a response to an environmental trigger (similar to an allergic reaction) or illness -is an obstructive lung disease resulting in difficulties with exhalation, FEV1 decreases more than FVC, making their ratio (FEV1÷FVC) decrease-inflammation of bronchi, cause can be genetic, allergic (environmental), or auto-immune-decreases lung capacity and volume (less air inhaled) and also results in “trapped air” in the lungs above Residual Volume (RV, and FRC – Functional Residual Capacity) that is not exhaled when it should be.-Symptoms: wheezing, shortness of breath or in extreme cases suffocation, “tight” feeling in the chest, coughing.-Treatment: bronchi smooth muscles dilates with Albuterol (a Sympathetic β2 receptor Agonist)Fibrosis:-thickening or scarring of lung connective tissue as a result of damage, long-term irritation/inflammation, or excessive production of collagen & elastic fibers-a restrictive lung disease that destroys lung tissue, reducing FVC more than FEV1, making their ratio increase (or the ratio may not change from ~0.8)-thickening of the tissue membrane that decreases lung compliance (elasticity) and gas diffusion rate-the ability to inhale a normal Tidal Volume (TV) or Inspiratory Reserve Volume (IRV) is negatively impacted Pulmonary Edema:-occurs as a complication of Mitral Stenosis/Mitral Regurgitation, which causes Pulmonary Hypertension and Edema (an accumulation/retention of fluid in the lungs) resulting in swelling of lung and alveolar tissue.-May also occur as a complication of Pneumonia-increased volume of interstitial fluid retention and thickening of the cell membranes decreases gas diffusion capacity in the lungsAtelectasis:-partial or complete lung (or lung lobe) collapse as a result of Surfactant secretion deficiency in Pneumocyte Type II cells in the alveoli.Neonatal Respiratory Distress Syndrome:-Atelectasis (lung collapse) in premature newborns, symptoms typically arise within 24 hours of birth-more common in infants born premature by more than 2 months (~6 weeks) because of immature Pneumocyte Type II cells that are not yet capable of synthesizing & secreting Surfactant-Symptoms: difficulty breathing, decreased lung compliance (elasticity) resulting in difficulty inflating the lungs upon inhalation, Hypoxemia (due to a disordered ventilation/perfusion ratio, V/Q)-Treatment: Cortisol (steroid) injections given to the mother within a few days of anticipated premature birth can induce maturation/development of Pneumocyte Type II cells in order to reduce complications after birth, while Incubation or artificial O2 therapy can be used post-birth (though artificial oxygen use carries some possible side effects including Retinopathy or blindness later in life and scarring in the lungs)Gastric Reflux:-Can occur if the lower esophageal sphincter has weak muscle tone, causing gastric contents reflux into the esophagus from the stomach. This can be caused by a congenital condition, a neural disorder (weak innervation from Meissner & Auerbach plexuses), or it can be a muscle disorder. The mucus membrane of the esophagus becomes irritated and gives the patient a “burning” sensation (heart burn) and retrosternal pain. A differential diagnosis must be made to rule out a possible Myocardial Infarction (order an EKG). Achalasia (Cardiospasm):-A neuro-motor disease that occurs when the Myenteric plexus of Auerbach (a part of the Enteric (Intrinsic) Nervous System) fails to properly innervate the Lower Esophageal Sphincter, resulting in a decreased ability for the sphincter to relax when food or fluid in swallowed (called Dysphagia). There is NO Peristalsis in that area (Aperistalsis), so relaxation and dilation of that segment of the Lower portion of the esophagus does not occur. No contractions occur either, so there is an accumulation of food content in the upper part of lower esophageal sphincter, which increases Intra-esophageal pressure.-Symptoms: retrosternal pain (behind the sternum), dysphagia, lower esophageal aperistalsis, and a possible increase in Lower Esophageal Sphincter pressure (due to food material buildup)-Treatment: Calcium-channel blockers and Nitrate.Esophageal Atresia:-When the distal end of the esophagus is closed off. “Atresia” refers to tissue that is missing during fetal development because of a failure in recanalization of the esophageal tube (it doesn’t connect the upper and lower parts of the esophagus)-Symptoms: immediately after breastfeeding the newborn will have vomiting, nausea and coughing; an endoscopy tube will not be able to reach the stomach when insertedDysphagia: Difficulty in swallowing solids and fluids, any content ingested cannot pass through the lower esophageal sphincter.Tracheoesophageal fistula:-When there is an abnormality in development during embryogenesis that causes a hole connecting the esophagus to the trachea. This results from a failure in the separation of the esophagus (Digestive System) and trachea (Respiratory System) during embryogenic development of the Tracheoesophageal Septum, a membrane that separates the newly formed trachea and lung bud that branches off of the esophagus. When the newborn is breastfed, milk in the esophagus finds its way into the respiratory tract, causing severe respiratory problems. Air may also enter the esophagus from this hole, distending the esophagus.-Symptoms: coughing, vomiting & nausea during breastfeeding; recurring respiratory infections. 70-80% of fistulas here occur alongside Esophageal Atresia. Esophageal Stenosis:-“Stenosis” refers to the presence of layered esophageal tissues that connect the upper and lower parts of the esophagus in order to complete the connection to the stomach, but it does not fully form, resulting in an abnormally small esophageal diameter in that area.Esophageal Cancers:-Caused by long-tern irritation of the mucosal layer in the esophagus as a result of drug use (including Opium), smoking, alcohol consumption, hot fluids (black tea, common cause in Iran, China & India) over a long period of time. Hiatal Hernias:-Hernias around the Esophageal Hiatus (@ T10 vertebra) in the Thoracic Diaphragm. Characterized by a protrusion of part of the stomach into the mediastinum (the chamber of the Thoracic Cavity between the lungs that contains the heart, trachea, and thoracic portion of the esophagus) through the Esophageal Hiatus. Hernias are painful and can present with upper abdominal pain and/or chest pains (including cardiac ischemia). Can be caused by a congenital condition, abnormal fetal development, neurological disorder (lack of neural plexus at lower esophageal sphincter or at esophageal hiatus), or a disorder of the muscles surrounding the lower esophageal sphincter or Esophageal Hiatus.2 main types:(A) Sliding Hiatal Hernia: occurs when the abdominal esophagus (lower part of esophagus beneath Thoracic Diaphragm), Cardia, and part of the Fundus slides up through the Esophageal Hiatus, herniating in the Thoracic Cavity. -Symptoms: gastric/acid reflux into the esophagus, gastric regurgitation and heart burn caused by irritation of the mucosal layer, retro-sternal pain, vomiting, nausea(B) Paraesophageal Hiatal Hernia: the Cardia and lower esophageal sphincter DO NOT move/herniate, but part of the Fundus passes through the Esophageal Hiatus and herniates.-Symptoms: NO gastric/acid reflux, NO regurgitation, ONLY retro-sternal pain & irritation in Thoracic Cavity.-Treatment: Surgery can help restore the barrier against gastric reflux from the stomach into the esophagus that is usually provided by the lower esophageal sphincter. The most common procedure performed to restore the barrier against gastro-esophageal reflux is a procedure called "fundoplication", where the Fundus is cut open and wrapped (“plicated”) around the lower (abdominal) portion of the esophagus, and then secured below the diaphragm to prevent possible recurrent herniations.Radiofrequency Treatment: A preventative procedure, artificial “burning” of the tissue surrounding the lower esophageal sphincter that toughens/thickens the tissue to prevent herniation and close off any defective/damaged part of the tissue that may become herniated. Uses an endoscope with electrodes that give off radiofrequency energy to make tiny burns at Gastro-Esophageal junction. The burned tissue heals, forming scar tissue that tightens the weak sphincter. Mumps:-An RNA viral disease (myxovirus) characterized by inflammation, pain and swelling of the Parotid salivary glands, spread via infected saliva and coughing. Vaccines exist but if it is contracted there is no cure so we can only treat the symptoms.-Symptoms: Swollen Parotid glands can be palpated (felt) in the cheeks, painful to touch, fever, headaches, fatigue, if contracted in childhood it can lead to infertility and hypogonadism as the virus causes severe inflammation in primary sexual organs which can suppress sex hormones (80-90% of people with Mumps are infertile).Vagotomy:-A surgical procedure that cuts the (typically Parasympathetic) branches of the Vagus Nerve (Cranial Nerve X) that innervate the stomach (especially the fundus) in order to decrease neural stimulation to Parietal cells that signals them to secrete HCl (or the branch innervating Pylorus, where G-cells are mostly found to inhibit Gastrin secretions). This is used to treat Gastric Ulcers, chronic Gastritis, Duodenal Ulcers, and Zollinger-Ellison Syndrome when there is no response to drug therapy. Side effects of this can be reduced motility in the stomach (since Parasympathetic branches also stimulate gastric contractions and sphincter contractions) which can result in impaired gastric emptying.Zollinger-Ellison Syndrome:-A gastrinoma/carcinoma (benign or, more often, malignant tumors) of pancreatic epithelial cells (non-β) that secrete excess Gastrin. This stimulates Parietal cells to increase HCl secretion with no inhibition/regulation (because the pancreatic tumor cells secreting Gastrin do NOT have the same negative feedback loop that G-cells have), leading to increased [H+] (or hyperacidity) in the stomach which may result in Gastritis, Gastric ulcers (in stomach), and Peptic ulcers (in esophagus, stomach, or small intestine). If a Gastric ulcer forms on the posterior wall of the stomach it may affect the Splenic artery and vein and can rupture, resulting in abdominal hemorrhage and internal bleeding (rapidly decreases blood volume and pressure) which can result in death if not treated immediately. -Symptoms: Pancreatic enzyme deficiency (therefore maldigestion), excess endocrine (Gastrin) secretion of pancreas, gastritis symptoms, severe abdominal pain, increased HCl, vomiting, nausea, abdominal inflammation, pain along the epigastric line, and in severe conditions hemorrhage.-Treatment: specific receptor is unknown so we target other known receptors that also stimulate HCl secretion, or target proton pumps (with proton pump inhibitors) so that excess HCl cannot be formed. >Atropine – H+ (HCl) secretion inhibition by targeting Parasympathetic Cholinergic (muscarinic type) Acetylcholine receptors of the Parietal cells in the stomach. >Cimetidine – H2-receptor antagonist (blocker) which inhibits HCl secretion stimulation by Histidine (reduces HCl secretions by inhibiting some of the multiple stimulation signals the Parietal cells receive), in addition it reduces Histamine’s ability to perpetuate the Acetylcholine signal stimulating Parietal cells from Gastrin. >Omeprazole – a Proton Pump Inhibitor (of the H+/K+ antiport pump in Parietal cells) also called an antacid (brand name Prilosec) inhibits HCl formation in cells therefore decreasing secretions into the lumen of the stomach. -A Vagotomy of Parasympathetic fibers (from the Vagus nerve branches innervating the stomach) can also be severed to decrease Parasympathetic stimulation of Parietal cell secretion. (see Vagotomy for more info)Duodenal Ulcers:-More common than Gastric ulcers, most Duodenal ulcers form in the Duodenal Cap, within 5 cm of the Pylorus, and usually form on the anterior wall of the Duodenum. Gastrin secretions increase in response to eating, which increases HCl secretions (H+ acidity increases in stomach) and increases Parietal cell proliferation/growth. Increased HCl and Pepsin damage the gastric mucosa. Pain can wake the patient up at night and is relieved by eating. -Treatment: surgical treatment is difficult as the tissue can’t be removed without severely impacting the digestive system. Duodenum has many important specialized cells for digestion, so tissue removal has drastic negative impact on the functionality of the Stomach and small intestine.>Vagotomy (cuts Vagus nerve branch) & Pyloroplasty (widens Pylorus) combined>Vagotomy & Gastrojejunostomy (bypasses Duodenum by making a tube-like connection between the stomach and jejunum for food to pass through) combined>Parietal cell Vagotomy (cuts Parasympathetic fibers of Vagus nerve that stimulate HCl secretion)Gastric Ulcers:-If the mucosal layer (protective mucus barrier of the stomach) is damaged then any H+ (acid) and Pepsin present may injure the gastric mucosa (tissue layers of simple columnar epithelia, lamina propria, & muscularis mucosa). The most common cause is due to bacterial infection by Helicobacter pylori (H. pylori) which secretes large amounts of Urease enzyme that converts any Urea present in the stomach into acidic ammonium (NH4+) which damages gastric mucosa. Ulcers can also result from long-term Gastritis. The gastric mucosa has gastric folds containing Oxyntic glands (full of Parietal cells) so when the tissue is damaged HCl secretions decrease, which increases Gastrin secretion in response. Ulcers are most commonly found on the lesser curvature of the stomach and cause pain when eating. As mentioned in the section on “Zollinger-Ellison Syndrome” if ulcers form on the posterior wall they may penetrate the Splenic artery and vein (which passes outside the stomach) and rupture them, resulting in abdominal hemorrhage (which can be fatal). Gastric ulcers can (rarely) perforate the caudal (bottom) wall of the stomach (usually Pyloric ulcers) and irritate the Pancreas which results in referred pain to the back.-Treatment: >Vagotomy (cuts Vagus nerve branches) is used to treat Gastric ulcers that do not respond to drug therapy. >Hemigastrectomy, a removal of a portion of the stomach (Billroth I and II) can be used to resect portions of the stomach that cannot heal from the ulcer and do not respond to drug therapy. -Billroth I: Pylorus is removed and the rest of stomach is anastomosed (connected) to the Duodenum -Billroth II: Greater curvature of Stomach is anastomosed (connected) to the first part of the Jejunum>Antrectomy removes the Pyloric antrum portion of the stomach in the case of severe Pyloric ulcers that do not respond to drug therapy.>If patient uses NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) commonly they must stop immediately, as NSAIDs are very irritating and damaging to the gastric mucosa (take NSAIDs with a meal and water to prevent irritation! Or take Tylenol instead, it is gentler on the stomach!)>If H. pylori infection is the cause then treat with antibiotics (Amoxicillin or Tetracycline) Gastritis:-The irritation and inflammation of the gastric mucosa, which can be erosive or nonerosive. It can occur suddenly (acute) or develop slowly (chronic). Acute Gastritis can be caused by a direct infection (Helicobacter pylori), which is more common in people that smoke or drink regularly. Gastritis can also be caused by direct toxicity due to alcohol or bile reflux (when bile refluxes into the stomach from the duodenum due to a malformed Pyloric sphincter), steroids and non-steroid drugs (NSAIDs & aspirin, which are acidic), Uremia, stress, chronic vomiting, smoking, viral infections, Pernicious Anemia (B12 deficiency), and other factors. Untreated gastritis may lead to ulcer formation, and even stomach cancer. -Symptoms: Gastritis may present with pain after eating (“early postprandial pain”), nausea, vomiting, upset stomach, abdominal bloating and pain, Indigestion, maldigestion and malabsorption, burning pain in stomach between meals and at night (usually with heartburn), hiccups, fever, loss of appetite, fresh blood in vomit (from ruptured capillaries) or coffee-ground looking material in vomit (gastric acid oxidized iron from Hemoglobin), black/tarry stool (oxidized old blood from stomach that gets into small intestine with Chyme and is excreted in feces). -Treatment: Excessive acids can be quickly controlled with Antacids (over-the-counter medications like Maalox or Tums), which neutralize acids in the stomach for quick relief. Prescription medications:>Cimetidine – H2-receptor antagonist (acid blocker) which inhibits HCl secretion stimulation by Histidine (reduces HCl secretions by inhibiting some of the multiple stimulation signals the Parietal cells receive), in addition it reduces Histamine’s ability to perpetuate the Acetylcholine signal stimulating Parietal cells from Gastrin. >Omeprazole – a Proton Pump Inhibitor (of the H+/K+ antiport pump in Parietal cells) also called an antacid (brand name Prilosec) inhibits HCl formation in cells therefore decreasing secretions into the lumen of the stomach. >If H. pylori infection is the cause then treat with antibiotic combo (Amoxicillin and Tetracycline) and a Proton-Pump Inhibitor like Omeprazole. >Vagotomy can also be preformed to control stimulation of secretionsHypertrophic Gastritis (Menetrier’s Disease):-Excessive growth of mucosal cells (Goblet cells) resulting in giant Rugal folds (gastric muscle folds that allow the stomach to expand when we eat or drink), simulating cancer. Mucosa is atrophic, meaning there is a loss of gastric glands, chronic inflammation, and an increase in epithelia that is less gastric-like and more intestinal-like, this is associated with protein loss in the gastric mucosa (muscularis mucosae layer).Jaundice:-Characterized by visible yellowing of the skin or the whites of the eyes due to Bilirubin accumulation in tissue fluid (interstitial fluid) and in the plasma. Skin begins to change color when Bilirubin levels in the blood plasma reach 1.5 mg/dL. -Newborn Jaundice: If baby is premature it could be due to a deficiency in Glucuronosyltransferase enzyme (which converts unconjugated Bilirubin + Glucuronic acid into Bilirubin glucuronide in the Liver, which is conjugated and water-soluble and can be removed from the body as Bile) which causes the newborn to build an accumulation of Unconjugated (non-soluble in water) Bilirubin in the Liver within a week after birth, resulting in yellowish skin. Within a few days-weeks the newborn Liver will continue to develop and will then be able to synthesize Glucuronosyltransferase enzyme and rid itself of the built-up Bilirubin. Light therapy (fresh sunlight or light use of Blue-Spectrum light lamps) can help treat Jaundice in addition to frequent feeding. Newborn jaundice is also be caused by underfeeding or blood-type incompatibility with the mother’s blood type.-Hemolytic Jaundice: Excessive lysis (cell degradation) of erythrocytes (red blood cells) results in increased plasma levels of Bilirubin. Bilirubin conversion into Bile is not inhibited just excessive, resulting in excessive amounts converted into Urobilinogen in the small intestine (via bacteria), some of which is diverted to the Kidneys for excretion in the urine as Urobilin in larger amounts than normal (results in dark yellow, foamy urine), while the rest is excreted in feces as Stercobilin. -Obstructive Jaundice: Obstruction or damage to the Biliary system/Bile ducts or Liver that inhibits Bilirubin/Bile secretion to the GI tract, resulting in an accumulation in the Liver. Bilirubin in this case is conjugated and build up may rupture obstructed bile ducts (canaliculi) resulting in increased conjugated Bilirubin levels in the blood (can test plasma). Acute Cholecystitis:-Acute inflammation of the Gallbladder walls, usually due to Cystic Duct obstruction, Gallstones, infection, duct malformation, or a congenital issue.-Symptoms: Bile accumulation in the Gallbladder, enlarged Gallbladder, severe pain along Epigastric line and abdomen, pain in Right Hypochondriac regions (under ribs) along Transpyloric line (horizontal line across abdomen at the level of the Pylorus), pain radiates to the right side of the back, vomiting, nausea and a positive Murphy’s Sign (determined if sharply painful respiration occurs if “palpated” or physical pressure is applied to the Right Upper Quadrant during deep inspiration, which indicate an issue with the Gallbladder or Liver), “involuntary muscle guarding” (involuntarily tightened or spasming muscle over inflamed areas)-Treatment: Cholecystectomy, the surgical removal of the Gallbladder due to “Biliary colic” (sudden pain in Biliary System) caused by Cystic Duct obstruction or Cholecystitis (inflammation of Biliary System).Gallstones (cholelithiasis):-Gallstones form due to an imbalance between the concentration of Cholesterol & Bile salts in the bile. As a result of this imbalance, Bile salts are no longer in suspension (in fluid) and can precipitate along with Cholesterol, leading to gallstone formation. Excessive Bilirubin in the Gallbladder can also accumulate into stones, giving them a green color (pigment stones), while excessive Cholesterol can give stones a yellow color. Therefore, a greenish-yellow pigment to the stone indicates high levels of both Cholesterol and Bile salts (and Bilirubin). Types of gallstones include Cholesterol stones, Pigment (bilirubin) stones, and Calcium bilirubinate stones. Hemolytic anemia (like sickle cell anemia) can cause gallstones due to the excessive amount of destroyed red blood cells. Liver Cirrhosis or Biliary tract infections can also cause Gallstones due to the buildup of Bilirubin, disorder in the mechanism for Bile formation/secretion, or Hepatocyte damage.-Symptoms: pain in the upper right quadrant of abdominal cavity immediately after eating (especially if the food ingested is high in fat) due to CCK stimulation of Gallbladder contraction), vomiting, nausea, severe abdominal pain in general that is variable (dull or sharp, comes and goes, can radiate to the back or right shoulder as “referred pain”), jaundice as a symptom (yellowing of the eyes), fever, and light clay-colored stools (due to lack of Bilirubin pigment in converted Stercobilin form that is usually excreted in feces)Hepatitis:-A disease marked by inflammation of the Liver, which can be caused by various viruses and/or poisons, long term drug or alcohol use, certain autoimmune conditions, or hereditary conditions. The damage caused by either type of Hepatitis can lead to Liver Cirrhosis or Liver Cancer. Typical symptoms abdominal pain, nausea, vomiting, diarrhea, fatigue, fever, loss of appetite, dark colored urine and light-colored feces, jaundice. Treatment varies depending on type of Hepatitis, as some types can clear up within months (Hep. A), and other types can last a lifetime and only have their symptoms controlled.Hemochromatosis:-A hereditary condition that causes a metabolic disorder of Iron, resulting in Iron deposits that accumulate in the Liver. Toxic Iron buildup causes free radical damage to the tissues which can cause Liver Cirrhosis.Wilson’s Disease:-A hereditary condition that causes a metabolic disorder of Copper, resulting in Copper deposits that accumulate in the Liver. Toxic Copper buildup causes free radical damage to the tissues which can cause Liver Cirrhosis. Liver Cancer:-Cancer of the liver is most commonly Hepatocellular carcinoma (a “primary” liver cancer) which targets Liver Hepatocyte stem cells and may be caused by chronic Hepatitis B or C. Secondary Liver Cancers include Cholangiocarcinoma (cancer of Biliary System Bile ducts and tubes) and Metastatic Cancers (cancers that originate from other cancerous tissues that produce cancerous cells that can break off and move to spread cancer to new tissue; usually originate from other cancerous tissues of the GI tract)Cirrhosis:-The formation of fibrous liver tissue (scar tissue) to replace dead cells, resulting in a nodular and rough texture pattern on the Liver surface. Cell death can be caused by viral Hepatitis (B & C), Autoimmune disease, Primary Biliary System disorders, Alcoholism, drug use, long-term exposure to other chemical toxins, or caused by Iron (Hemochromatosis) or Copper (Wilson’s Disease) metabolic disorders.-Cirrhosis is a chronic liver disease where cell death is progressive and expansive, often including inflammatory responses, and “compensatory Hyperplasia” (quickly regenerating cells that are enlarged and abnormal).-There is also an increased risk of Hepatocellular Carcinoma (see section on Liver Cancer) with Cirrhosis.-The Liver hardens as a result of the buildup of fibrotic scar tissue, making it difficult for blood to get in and out of the Liver vessels/Portal vein. Fibrosis causes obstructions to these blood vessels, leading to Portal Hypertension, where incoming blood is pushed back through the Portal Vein System and back into the digestive tract (Retro-flow), causing an accumulation of blood in the abdominal cavity, and bleeding in the esophagus or other GI areas. Ascites can also occur due to Cirrhosis. -Ascites: The peritoneum (a double-layered tissue membrane that lines abdominal cavity and wraps around different abdominal organs and intestines to secure them to the abdominal wall and protect them from damaging each other with friction), normally secretes a small amount of peritoneal fluid to lubricate the membrane and organ surfaces. In Ascites, excessive peritoneal fluid is secreted in response to injury or infection (most commonly Cirrhosis), leading to a bloated appearance and increased intra-abdominal pressure due to increased retained fluid taking up space in the abdominal cavity and pressing in on the organs.-Other Symptoms: Indigestion, pain, nausea, vomiting, Edema (fluid retention) in the legs, blood in feces or vomit, weakness and fatigue, weight loss, jaundice, anemia and malabsorption of nutrients (due to Portal Vein obstruction, which brings nutrients from GI to Liver to be distributed to the body), hormone deficiencies, weakened immune system-Treatment: It’s possible to surgically create shunts (bypass vessels) between areas of Portal system vessels and Systemic circulation vessels to relieve the symptoms of Portal Hypertension and restore blood flow. A Liver transplant is needed in some patients with advanced Cirrhosis that may go into organ failure (which can result in multiple organ failure and death). To treat malabsorption of nutrients, supplemental solutes like Iron, proteins, dietary amino acids, ions, glucose, vitamins, and others are given. To treat Ascites a decrease in salt in the diet is recommended, diuretics can be used to increase water output in urine which can relieve some fluid accumulation. In cases of more severe fluid accumulation, a Paracentesis (syringe puncture procedure) must be used to manually drain fluid from the abdominal cavity.Abetalipoproteinemia:-A lipid metabolism disorder characterized by a deficiency in the Apoprotein-β protein, which results in a decreased ability to absorb and utilize fats and fat-soluble vitamins (A, D, E, K). Apoprotein-β is responsible for taking up digested cholesterol esters, triglycerides, phospholipids and fat-soluble vitamins and forming the lipoprotein Chylomicron, which allows the fat-soluble nutrients to travel through the body’s aqueous (water-based) environment in the bloodstream to bring those nutrients for absorption in target tissues. Without Apoprotein-β fat remains unabsorbed in the GI and is seen as “Steatorrhea” fat deposits in the feces.-Symptoms: Hypocholesterolemia (decreased lipid absorption decreases blood levels), Retinitis pigmentosa (due to vitamin A “Retinol” deficiency, causes decreased sight, nighttime blindness, does not result in total blindness), irritation and maldevelopment of Central Nervous System which results in mental disabilities, diarrhea, muscle weakness and disordered motor coordination, issues with balance and slurred speech, possible Scoliosis (due to vitamin D deficiency)Osteomalacia(adults)/Rickets(children):-Osteomalacia is a condition characterized by the softening of bones in adults due to severe deficiency of vitamin D, which calcium (Ca2+) requires for absorption in the small intestine. In adults this can usually be treated within 6 months with the use of vitamin D supplements. Vitamin D deficiency may be congenital, disordered vitamin D synthesis in skin/kidneys/liver, or dietary.-Symptoms: fragile bones are more susceptible to fractures and breaks, bone pain especially in hips, muscle weakness, increased cavities or tooth defects-Rickets: In children this condition is called Rickets and in addition to the above symptoms children may also have malformed bone formation in the legs (bow legged, waddling walk), skull and rib cage (malformed ribs or sternum may cause a protruding “Pigeon Chest” and respiratory problems), short stature due to impaired bone growth, delayed tooth formation, and delayed walking in infants and toddlersChron’s Disease:-An autoimmune disease presenting with chronic inflammation in any part of the GI (from oral cavity to anal cavity) due to an overactive immune response (antibodies) to the patient’s own GI tissues. This can result in irritation and tissue damage, decreases in digestion and absorption of nutrients, and a thickened (fibrotic) tissue wall in the GI. -Chron’s is a form of Inflammatory Bowel Disease (IBD) and can also include Irritable Bowel Syndrome (IBS, “spastic colon”). -Chron’s can affect some GI regions and skip others, but usually affects the ileum (3rd part of small intestine) and the colon (1st part of large intestine). -Symptoms: Cramping pain in Right Lower Quadrant of the abdomen, fever, watery diarrhea, rectal bleeding and cramping rectal pain associated defecation and a quickly recurring feeling of needing to defecate again ( called “Tenesmus”), fatigue, appetite loss, maldigestion and malabsorption of food, anemia, dehydration (due to diarrhea and decreased absorption of water in GI), increased risk of bacterial infection (damaged GI tissue creates infection opportunities to bacteria normally found in GI), weight loss, vertigo, Hypotension, electrolyte imbalance (Na+ from NaCl, and K+ deficiency especially), muscle weakness, cardiovascular disorders (Na+ deficiency decreases Action Potentials)-Treatment: Dietary changes can be made, including smaller meals eaten more frequently throughout the day, increased hydration and electrolyte consumption, avoidance of high-fiber foods (whole wheat products and fibrous fruits and vegetables), avoidance of fatty/greasy/fried food (can increase diarrhea), avoidance of caffeine (soda, teas and coffee increase Peristalsis, which decreases digestion/absorption), avoidance of alcohol, and introduction of vitamin supplements (D and B12 especially), Iron supplements, and Calcium supplements.-Anti-diarrheal drugs: “Loperamide” (Brand name: Imodium) diarrhea can increase irritation, inflammation and tissue damage, and increase dehydration.-Corticosteroids: Prednisone, Methylprednisolone, Hydrocortisone, and Cortisone can be administered orally or anally to suppress inflammation by blocking B-Lymphocytes (B-cells, they make antibodies) to inhibit the release of autoimmune antibodies attacking GI tissue.-Immunomodulators: “Azathioprine” an immunosuppressant that helps control symptoms caused by autoimmune responses, Taken orally or subcutaneously (injection).-Antibiotics: prescribed when fistulas (swollen fusions between tissues of two different parts of the GI that can make holes and cause infection) or abscesses (painful swollen pockets within tissue layers that are filled with fluid pus as a result of infection) form in the GI as a result of the chronic inflammation and irritation, since they may be possible sites of bacterial infection ................
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