Exam 4- GI/Liver Flashcards
OSMOTIC DIARRHEA
ETIOLOGY: bacterial infection (e. coli), parasites, viral infection, drugs, celiac disease or UC, genetic d/o like congenital chloride diarrhea
- due to unabsorbed nutrients in the stool
- osmotic load causes fluid retention in the bowel
- seen with lactose intolerance and Zollinger Ellison syndrome and celiac disease
CLINICAL MANIFESTATION: stomach pain, bloating, nausea, watery bowel movement;
PATHOLOGY:occurs when too many solutes — the components of the food you eat — stay in your intestine and water can’t be absorbed properly. This excess water causes your bowel movements to be loose or more liquid than solid. Eating food that can’t be that can be absorbed and instead draw water into your intestine.
SECRETORY DIARRHEA
ETIOLOGY:
large volume: caused be excessive mucosal secretion of chloride- or bicarbonate rich fluid or inhibition of net sodium absorption. Usually caused by enterotoxins (E.coli), viruses (rotavirus), or exotoxins from overgrowth cdiff.
-increased water and electrolytes secretion by toxin or VIP in the intestinal lumen
Small volume: caused by IBD, UC, Crohns, colitis, fecal impaction
CLINICAL MANIFESTATIONS: stomach pain, bloating, nausea, watery bowel movement;
PATHOLOGY: large volume of feces caused by excessive amounts of water secretion. Occurs when your body secretes electrolytes into your intestine. This causes water to build up.
MOTILITY DIARRHEA
ETIOLOGY: diarrhea caused by resection of small intestine, surgical bypass of an area of the intestine, fistula formation between loops of intestine, irritable bowel syndrome, diabetic neuropathy, hyperthyroidism, and laxative abuse
CLINICAL MANIFESTATION: dehydration, electrolyte imbalance (hyponatremia, hypokalemia), metabolic acidosis, and weight loss, fever, cramping pain, and bloody stools, bloating, anal and perianal skin irritation.
PATHOLOGY: large volume of feces caused by excessive amounts of water secretion
DYSPHAGIA
Difficulty swallowing or perception of obstruction during swallowing
PATHOLOGY: mechanical obstruction of the esophagus or functional d/o that impairs esophageal motility.
- Functional dysphagia-caused by neural or muscular d/o that interfere with voluntary swallowing or peristalisis
- Mechanical dysphagia- can be intrinsic or extrinsic. Intrinsic is obstruction in wall of esophageal lumen. Extrinsic obstruction originate outside the esophageal lumen and narrow the esophagus by pressing inward on esophageal wall
EVALUATION: barium xray, swallow study, endoscopy, imaging scans, esophageal muscle test, fiber optic endoscopic evaluation of swallowing
TREATMENT:Medication, Swallowing retraining, Botulinum toxin, Dilation, Enteral feeding, Esophageal stent placement, Surgery, Treatment for specific swallowing disorders.
ACHALASIA
ETIOLOGY: It may be caused by an abnormal immune system response.
May be related to cell mediated and antibody mediated immune response against unknown antigen in myenteric neurons
-A motility d/or of esophagus d/t nerves fro swallowing being damanaged
CLINICAL MANIFESTATION: a backflow of food in the throat (regurgitation), chest pain, and weight loss, discomfort after swallowing, unpleasant taste, vomiting.
*discomfort 2-4 sec after eating=upper esophageal obstruction; discomfort 10-15 sec= lower obstruction
PATHOLOGY: Achalasia results from damage to nerves in the food tube (esophagus), preventing the esophagus from squeezing food into the stomach.
GERD
ETIOLOGY: reflux of acid and pepsin or bile salts from the stomach to the esophagus that causes esophagitis.
RISK FACTORS: vomiting, coughing, lifting, bending, obesity, or pregnancy
CLINICAL MANIFESTATION: heartburn chronic cough, asthma attacks, laryngitis, sinusitis, and upper abdominal pain within 1 hr of eating. Symptoms worsen when person lays down
PATHOLOGY: abnormalities in lower esophageal sphincter function, esophageal motility, and gastric motility or emptying can cause GERD
UPPER GI BLEED
ETIOLOGY: bleeding from the esophagus, stomach, or duodenum
RISK FACTORS: helicobacter pylori infection, NSAIDs, aspirin, selective serotonin reuptake inhibitors, and other antiplatelet and anticoagulant medications
CLINICAL MANIFESTATION: frank red blood in emesis or coffee ground color stool
PATHOLOGY:cause by esophageal or gastric varices, tear eso-gastric junction, cancer, andiodysplasias, peptic ulcers, severe retching
LOWER GI BLEED
ETIOLOGY: bleeding from the small intestine, colon, or rectum
RISK FACTORS: age, overuse of NSAIDs, chronic constipation leading to hemmorhoids, family hx like IBD, bleeding d/o of family hx of bleeding d/o
CLINICAL MANIFESTATION: bright red blood in stool, abd cramps or pain, faintness/dizziness, paleness, SOB
PATHOLOGY: caused by polyps, inflammatory bowel disease, diverticulosis, cancer, vascular extasias, or hemorrhoids
PYOLRIC OBSTRUCTION
ETIOLOGY: is a result of any disease process that causes a mechanical impediment to gastric emptying. Can be due to a mechanical cause or motility d/o
RISK FACTORS: PUD, gastrointestinal tumors, pancreatitis
CLINICAL MANIFESTATION: nausea, nonbilious vomiting, epigastric pain, early satiety, abdominal distention, and weight loss
PATHOLOGY:
can be congenital or acquired. Acquired caused by peptic ulcer disease or tumor near the pylorus. Duodenal ulcers are more likely than gastric ulcers to obstruct the pylorus. Ulceration causes obstruction resulting from inflammation edema, spasm, fibrosis or scarring. Tumor caused obstruction by growing into the pylorus.
INTESTINAL OBSTRUCTION
ETIOLOGY: is a blockage that keeps food or liquid from passing through your small intestine or large intestine (colon). Can be SBO or LBO
RISK FACTORS: hernias, crohns, abd/joint/or spine surgery, swallowing a foreign body, decrease blood supply to small bowel, abnormal growth of tissue in or next to small intestine, tumors, cancer
CLINICAL MANIFESTATION:constipation, vomiting, inability to have a BM or pas gas, swelling of abd.
PATHOLOGY: Ingested fluid and food, digestive secretions, and gas accumulate above the obstruction.
ILEUS
ETIOLOGY:the motor activity of the bowel is impaired, usually without the presence of a physical obstruction.
RISK FACTORS: electrolyte imbalance involving potassium and calcium, hx of intestinal injury or trauma, hx of crohns or diverticulitis, sepsis, PAD, exposure to radiation near abd
CLINICAL MANIFESTATION: distended abd, fullness, gas, abd spasms, constipation, diarrhea, n/v
PATHOLOGY:Caused by Bacteria or viruses that cause intestinal infections (gastroenteritis)
3 ULCERATIVE DISEASE
- gastric ulcers
- duodenal ulcers
- stress r/t mucosal ulceration
DUODENAL ULCERS
ETIOLOGY:a peptic ulcer that develops in the first part of the small intestine (duodenum)
RISK FACTORS: alcohol abuse, H pylori infection (90%), hx radiation therapy, NSAIDs (ibuprofen, naproxen, or asprin), stress, severe illness, tobacco use
CLINICAL MANIFESTATION: belching, burning stomach or upper abd pain that may be severe, fullness, loss of appetite, n/v
PATHOLOGY:stomach acid damages the lining of the digestive tract: H pylori decrease mucosal protection and increases gastric acid secretion
STRESS RELATED MUCOSAL ULCERATION
ETIOLOGY: acute form of erosive, inflammatory peptic ulcer that tends to accompany the physiologic stress of severe illness; multisystem organ failure, or major trauma, including severe burns or head injury.
RISK FACTORS: immense physical stress like those pts in ICU; stress-related ulcer, H, pylori infection, NSAIDs
CLINICAL MANIFESTATION: upper abd pain/n/v, anemia, bloated, pain that varies with food intake
PATHOLOGY: COME ON SUDDENLY, USUALLY AS RESULT OF PHYSIOLOGICAL STRESS; changes in body’s pH; caused by mucosal ischemia
2 INTESTINAL DISEASES
- ulcerative colitis
2. crohn’s disease
CROHN’S DISEASE
ETIOLOGY: an idiopathic inflammatory d/o that is distinguished from UC in that it affects any part of the GI track from the mouth the anus and involves “skip lesions” with inflamed areas mixed with un-inflamed areas, non-caseating granulomas, fistulas, and deep penetrating ulcers
RISK FACTORS: family hx, cigarette smoking, Jewish ethnicity, urban residency, age less than 40 years, slight predominance in women, and altered gut microbiome
CLINICAL MANIFESTATION: irritable bowel; diarrhea, sometimes rectal bleeding if colon is involved; abd pain, diarrhea, weight loss, anemia, and fatigue
PATHOLOGY: inflammatory lesions begin in the intestinal submucosa and spread with discontinuous transmural involvement (skip lesions), mutations in Toll-like receptor, gene name CARD15/NOD2. overreact to normal flora of bacteria
5 TYPES OF LIVER INJURY/FAILURE
- Hepatitis A
- Hepatitis B
- Hepatits C
- Hepatitis D
- Hepatitis E
HEPTITIS A
ROUTE: fecal oral route; 4-6 week incubation period
RISK FACTORS: poor sanitation, lack of safe water, sexual contact with infected person
CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice
PATHOLOGY: acute infection; is caused by a picornavirus usually transmitted by the fecal-oral route
IMMUNITY: antibodies to HAV (anti-HA) develop within 4 weeks after incubation
**IgM increases»_space; IgG increases for several years which leads to immunity
HEPATITIS B
ROUTE: sexual intercourse, blood, perinatal (mother to baby); 6-8 week incubation period
RISK FACTORS: unprotected sex, IV drug uses, men with men, mother to infant, job that exposes you to blood
CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice
PATHOLOGY: can be acute or chronic (>6 months)the interaction of the virus and the host immune system, which leads to liver injury and, potentially, cirrhosis and hepatocellular carcinoma
HEPATISIS C
ETIOLOGY:Serum, sexual contact; 6-8 week incubation
RISK FACTORS: IV drug use; HIV; Hep B infection
CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice
PATHOLOGY: can develop into cirrhosis and then hepatocellular carcinoma.
Antibody: anti HCV IgG
HEPATITIS D
ETIOLOGY: occurs in people who are also infected with the hepatitis B virus.
RISK FACTORS: IVDU
CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice
PATHOLOGY: Hepatitis D virus is hepatotropic. Replication within hepatocytes results in cytotoxicity and direct liver damage. The virus depends on the viral coat of HBsAg molecules on HBV for replication
Antibody used for dx: anti-HD
HEPATITIS E
ETIOLOGY: co-infection with HBV, HIV; transmitted fecal oral route; MOST COMMON IN ASIAN AND AFRICAN COUNTRIES
RISK FACTORS: contaminated water supplies, poor sanitation, ingestion of undercooked meat and shellfish
CLINICAL MANIFESTATION: usually asymptomatic and resemble Hep A or it can progress to liver failure or chronic hepatitis
PATHOLOGY:
ANTIBODY: anti-HEV IgM
CHOLELITHIASIS
ETIOLOGY: hardened deposit within the fluid in the gallbladder aka gallstones that are hardened deposits of digestive fluid (cholesterol, excess bilirubin) with impaired contractility
RISK FACTORS: female, obese, pregnant, sedentary, high fat diet
CLINICAL MANIFESTATION: RUQ pain, indegestion, n/v, abd cramping–may have no signs
PATHOLOGY:
- *Cholesterol gallstones due to over secretion of cholesterol by liver cells and hypomotility.
- *Pigmented gallstones, high heme turnover, bilirubin higher concentration which crystallize and become stones
CHOLECYSTITIS
ETIOLOGY: inflammation of gallbladder
RISK FACTORS: obese, pregnancy, hormone therapy, older age, diabetes, Native American or Hispanic
CLINICAL MANIFESTATION: severe pain in RUQ, pain that spreads to your right shoulder or back, tender abd, nausea
PATHOLOGY: gallstones that block the gallbladder preventing biliary outflow
CIRRHOSIS
ETIOLOGY: fibrosis of liver
RISK FACTORS: hepatitis, alcohol abuse
CLINICAL MANIFESTATION: jaundice, itchy skin, easy bruising, ascites, hepatic encephalopathy, weight, BLE edema, fatigue,
PATHOLOGY: a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism.
COMPLICATIONS OF CIRRHOSIS
- portal htn
- ascites
- hepatic encephalopathy
- jaundice
ACUTE PANCREATITIS
ETIOLOGY: a condition where the pancreas becomes inflamed (swollen) over a short period of time due to obstruction to the outflow of pancreatic digestive enzymes caused by bile duct or pancreatic duct obstruction. Enzymes become activated while still in the pancreas, irritating the cells of the pancreas causing inflammation
RISK FACTORS/CAUSES: alcohol abuse; gallstones; steroids; mumps virus, autoimmune, idiopathic, hypertriglyceridemia and hypercalcemia, drugs
CLINICAL MANIFESTATION: EPIGASTRIC PAIN, CULLEN SIGN (GREY AREA AROUND UMBILICAL AREA) , GREY TURNER SIGN (GREY SIGN ON FLANKS)abd pain, n/v, fever, bad pain may radiate to back, abd distention, jaundice
PATHOLOGY: is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes.
Dx: lipase and amylase levels, leukocytosis, c-reactive protein and lactate, enlarged pancreas, decreased ionized calcium levels
CHRONIC PANCREATITIS
ETIOLOGY: is a painful disease of the pancreas in which inflammation has resolved, but with resultant damage to the gland characterized by fibrosis, calcification and ductal inflammation.
RISK FACTORS/CAUSES: alcohol abuse, cigarette smoking, obesity, diabetes, family hx; gallstones, autoimmune d/o, hypertryglycerides, tumor, cystic fibrosis
CLINICAL MANIFESTATION: usually asymptomatic for awhile, epigastric pain that radiates to back, exocrine and endocrine insuffciency, steatorrhea
PATHOLOGY: relapsing episodes of pancreatitis which leads to pancreatic injury
Dx. : elevated bilirubin; 72 hour stool collection to dx fat malabsorption, CT scan
5 GI TRACK CANCERS
- Gastric cancer
- esophageal cancer
- colorectal cancer
- pancreatic cancer
- liver cancer
PYLORIC STENOSIS (babies)
ETIOLOGY: an uncommon condition in infants that blocks food from entering the small intestine
RISK FACTORS: boys, premature birth, smoking during pregnancy, family hx, early abx use
CLINICAL MANIFESTATIONS: vomiting after feeding; dehydration
PATHO: hallmark of pyloric stenosis is marked hypertrophy and hyperplasia of both the circular and longitudinal muscular layers of the pylorus.[3] This thickening leads to the narrowing of the lumen of the gastric antrum
CLEFT LIP/PALATE (babies)
ETIOLOGY: A cleft lip is an opening in the upper lip; a cleft palate is an opening in the roof of the mouth.
RISK FACTORS: smoking during pregnancy, diabetes, use of certain meds during first trimester
CLINICAL MANIFESTATIONS: difficult speaking and feeding
PATHO:
cleft lip- incomplete fusion of the nasomedial and intermaxillary process
cleft palate- failure of the primary palatal shelves, or processes, to fuse in the 3rd trimester; can occur with or without cleft lip
NEWBORN JAUNDICE (babies)
CAN BE CAUSED BY: infection, viral or bacterial infection, internal bleeding, enzyme deficiency, liver malfunciont
ETIOLOGY: excess bilirubin in blood
CLINICAL MANIFESTATIONS: yellow skin,
PATHO: baby’s liver isn’t mature enough to get rid of bilirubin in the bloodstream
Newborns produce more bilirubin than adults do because of greater production and faster breakdown of red blood cells in the first few days of life
MECONIUM ILEUS (babies)
ETIOLOGY: lack of contraction in muscles of intestines due to meconium
RISK FACTORS: cystic fibrosis
CLINICAL MANIFESTATIONS: abd distention, hyperactive peristalsis, but rectal ampulla empty; distended abd will show patterns of dilated intestinal loops
PATHO: intestinal obstruction in the neonatal period caused by meconium formed in utero that is abnormally sticky and accumulates and obstructs ileum
NECROTIZING ENTERCOLITIS
ETIOLOGY: necrotic bowel
RISK FACTORS: premature babies
CLINICAL MANIFESTATIONS: vomiting, diarrhea, feeding intolerance, and high gastric residuals after feeding
PATHO:
too little oxygen or blood flow to the intestine at birth or later. injury to the intestinal lining. heavy growth of bacteria in the intestine that erodes the intestinal wall. viral or bacterial infection of the intestine.
Cause of large volume diarrhea
excessive amounts of water or secretions, or both, in the intestines
Cause of small volume diarrhea
volume of feces is not increase, usually results from extensive intestinal motility
Evaluation and treatment of GERD
EVALUATION: upper endoscopy, ambulatory acid probe test, esophageal manometry, xray of upper GI
TREATMENT: meds (antacids, proton pump inhibitor, antidiarrheal), lose weight, stay up after eating, avoid large meals, avoid foods that increase acid (caffeine), decrease fatty foods and alcohol
What is digestion
Digestion is the breakdown of large insoluble food molecules into small water-soluble food molecules so that they can be absorbed into the watery blood plasma
Absorption
is the process of transferring small absorbable units with water, electrolytes, vitamins from GI lumen into the blood and lymph.
Motility
means muscular contractions. When we eat, the food need to be broken down to small pieces and mixed, stored and moved forward, the food we eat can be digested and absorbed. Motility refers to the muscular contractions that mix and move forward of the contents in the GI tract.
Secretion
secretes water mucus, electrolytes (such as HCl), enzymes, and bile salts which are all important for digestion
4 primary functions of GI
- digestion
- absorption
- motility
- secretion
Mouth and salivary gland
Motility: chewing
Secretion: amylase, mucus, lysozyme mucus
Digestion: carbohydrate digestion begins
Pharynx and esophagus
Motility: swallowing
SECRETION: mucus
DIGESTION: none
ABSORPTION: none
Exocrine Pancrease
MOTILITY: not applicable
SECRETION:
-pancreatic digestive enzymes: trypsin, chymotrypsin, amylase, lipase
-Pancreatic aqueous
-NaHCO3 secretion
DIGESTION: These pancreatic enzymes accomplish digestion in duodenal lumen
ABSORPTION: not applicable
Liver
MOTILITY: Not applicable
SECRETION: Bile: bile salts, alkaline secretion bilirubin
DIGESTION: bile does not digest anything, but bile salts facilitate fat digestion and absorption in duodenal lumen
ABSORPTION: not applicable
Small Intestine
MOTILITY: segmentation, migrating motility complex
SECRETION: Succus entericus (aka intestinal fluid): mucus and salt (small intestine enzymes are not secreted but function intracellularly in the brush border-disaccharidases and amniopeptidases
DIGESTION: in lumen under influence of pancreatic enzymes and bile, carbs and protein digestion continue and fat digestion is completely accomplished; in brush border, carb and protein digestion completed
ABSORPTION: all nutrients, most electrolytes, and water
Large Intestine
MOTILITY: mass movements
SECRETION: mucus
DIGESTION: none
ABSORPTION: salt and water converting contents to feces
What makes up the digestive tube?
mucosa, submucosa, and the muscularis externa, and the serosa
What do exocrine cells in the mucous membrane do?
secretion of digestive juice
-secrete mucus to facilitate the movement of particles along the body’s various tubes, such as the throat and the intestines.
Endocrine cells in the mucous membrane secrete what
gastrointestinal hormones, and cells specialized for absorbing digestive nutrients
What are the 2 intrinsic nerve plexuses in the GI tract
- the submucous plexus located in the submucosa
2. myenteric plexus located between the smooth muscle layers
Portan vein
carries blood from one capillary network to another
Hepatic portal vein
- formation by union of splenic and superior mesenteric veins
- receives blood from digestive organ capillaries and delivers it to the liver capillaries
The hepatic portal vein receives _____________ blood from the inferior, superior, and splenic veins
deoxygenated
The hepatic portal vein delivers 70% of the blood supply to the liver which is rich in nutrients from where
the digestive tract
Splenic vein gets blood from where
portions o the stomach, pancreas and portions of large intestine
Superior mesenteric vein gets blood from where?
small intestines and portions of large intestine, stomach and pancreas
Effects of aging on the GI system
- starts <50 years old
- taste buds decline in number, salivary secretion decreases
- decreases in the stomach volume and the lining’s capacity to resist damage decrease
- in small intestine, decreased in lactase levels and excessive growth of certain bacteria–lactose intolerance, pain and/or bloating, decreased absorption of certain nutrients, such as vitamin B12, iron, and calcium
- decrease motility in large intestines and rectum-constipation
- rate of liver regeneration decreases
- decrease secretion of HCl-, intrinsic factor
- altered mucous barrier, intestinal flora
Three mechanisms of diarrhea
- osmotic diarrhea
- secretory diarrhea
- motility diarrhea
Acute bleeding includes:
- hematemesis-throwing up blood
- melena-dark stool; partly digest blood
- hematochezia-blood in stool
Intestinal obstruction can be caused by what?
Herniation, adhesions; volvulus (torsion), intussusception
What is gastritis
inflammation or break in gastric mucosa
peptic ulcer is
a break or ulceration in the mucosal lining of the lower esophagus, stomach or duodenum caused by excessive secretion of gastric acid, disruption of the protective mucosal barrier or both.
Risk factors for Peptic ulcer
- genetic predisposition, H.pylori infection, habitual use of NSAIDs.Alcohol, smoking, acute pancreatitis, chronic obstructive pulmonary disease, obesity, cirrhosis, age >65y, stress…
- Can be acute or chronic.
- Chronic use of NSAIDs suppresses mucosal prostaglandin synthesis, resulting in decreased bicarbonate secretion and mucin production, increased secretion of hydrochloric acid
Curling’s ulcer
A stress‐induced ulcer of the stomach or duodenum that occurs in relation to extreme physical stress.
Stress‐related mucosal disease can cause mucosal erosions and superficial hemorrhages in patients who are critically ill or in those who are under extreme physiologic stress, resulting in minimal‐to‐severe gastrointestinal blood loss and leading to blood transfusion if not addressed in time.
Zollinger‐Ellison Syndrome
Rare digestive disorder that results in too much gastric acid neuroendocrine tumor or multiple tumors (gastrinoma) of the pancreas or duodenum that can cause the formation of ulcers
Causes: abd pain, acid reflux, and diarrhea, weight loss
Key characteristics of UC
- increased risk of obstruction and colon cancer
- intermittent periods of remission and exacerbation
- loss off absorptive mucosal surface, bleeding, cramping pain, and urge to defecate, frequent bloody diarrhea with passage of purulent mucus, frequent diarrhea (more than 6 a day), anemia, weight loss
complications: anal fissures, hemorrhoids, and perirectal abscess
Irritable bowel disease
is a group of symptoms that occur together, including repeated pain in your abdomen and changes in your bowel movements, which may be diarrhea, constipation, or both.
- functional disorder-no specific altered structures or biochemical processes
- several hypotheses - visceral hypersensitivity, abnormal GI motility and/or secretion, food allergy/intolerance, psychosocial
Ex: UC and Crohn’s
What is a common cause of acute liver failure
acetaminophen overdose
Chronic liver failure is associated with
liver metabolism and extra liver abnormalities
What is diarrhea?
- > or =3 loose or liquid stools/day
- osmotic (water drawn into the intestine)
- secretory (Increase Cl- or HCO3- secretion or low Na+ absorption)
- infection
- endotoxin (c diff)
- inflammatory bowel disease
- motility
- intestine shortened, neuropathy, hyperthyroidism
- negative effects on fluid, electrolyte, acid-base balance
Phases of hepatitis infection: **
Incubation-HAV 30 days: HBV up to 6 mo.; HCV 1-2 mo
Prodromal-2 wks after exposure to jaundice; likelikhood infectious very high
Icteric- may or may not be jaundiced (HBV, HCV); symptoms of specific illness; increased bilirubin, increased PT
Recovery - posticteric; livery enzymes within norms; chronic active hepatitis (carrier)
What happens in cholelithiasis?
-“supersaturated” cholesterol form crystals»_space; aggregate»_space; + mucin»_space; matrix within the gallbladder that lodge in the cyst or common duct
What is cirrhosis
inflammatory, fibrotic disease related to alcohol or hepatitis
How does ethanol effect liver dysfunction?
Alcohol changes the chemicals that break down and remove scar tissue. This means that scar tissue builds up in the liver. Scar tissue replaces normal healthy cells. This means that the liver can’t work properly and can fail, leading to death.How does ethanol effect liver dysfunction?
ethanol metabolizes to acetaldehyde via 3 enzymes»_space; alcohol dehydrogenases, cytochrome P-450, catalase - forms NADH
What are toxic effects of alcohol
GI bacteria endotoxins translocate»_space; injury, inflammation»_space; necrosis»_space; collagen formation»_space; fibrosis, scarring
Complications of cirrhosis
- portal htn
- ascites
- hepatic encephalopathy
- jaundice
Cirrhosis portal hypertension
Your body carries blood to your liver through a large blood vessel called the portal vein. Cirrhosis slows your blood flow and puts stress on the portal vein. This causes high blood pressure known as portal hypertension.
- intrahepatic (ex cirrhosis) or extrahepatic (right side heart failure)
- may result in varices: esophageal»_space; increased risk rupture
Cirrhosis ascites
- fluid in peritoneal cavity; complication of portal htn, right side heart failure, nephrotic syndrome, hypoalbuninemia
- post likely “cause” is splanchnic vasodilation»_space; decrease systemic vascular resistance»_space; Na retention (stimulated by RAAS)»_space; increase ADH»_space; fluid retention and transudation
What is peritonitis?
Fluid in the peritoneal cavity that is infected
Cirrhosis - Hepatic encephalopathy
- neurologic impairment from accumulated “un-detoxified” gi toxins-cytokines, serotonin, tryptophan, ammonia
- ammonia is especially challenging -metabolizes to glutamine in brain and interferes with neurotransmitters
- ammonica is broken down in liver to urea and sent kidneys for excretion, but with cirrhosis the liver cann’t break it down and it builds up
- look for :impaired cognitive function, asterixis, EEG changes
Cirrhosis - Jaundice
- due to hyperbilirubinemia
- portal blood flow is distorted accompanied by a decrease in hepatic clearance of bilirubin.
- obstruction to outflow-conjugated bilirubin in urine; none in stool
- obstruction within liver-both conjugated and unconjugated bilirubin increase
Nonalcoholic fatty liver disease
- hepatocytes infiltrated with triglycerides (primarily)
- associated with obesity, metabolic syndrome, DM2
- risk=cirrhosis, liver failure, cancer
Biliary cirrhosis
**When bile ducts become damaged, bile can back up into the liver, causing damage to liver cells. This damage can lead to liver failure
- process begins in bile duct and canaliculi
- primary-due to antigen antibody mediated destruction; antinuclear, antimitochondrial antibodies present
- secondary-d/t prolonged obstruction of common bile duct which lead to necrosis
Pancreatitis
- acute, chronic, mild to severe
- alcohol or obstructive (bile or pancreatic ducts); adverse drug reaction less common
- elevation of pancreatic enzymes-amylase, lipase»_space; proteolytic enzymes cause autodigestion»_space; inflammation»_space; proinflammatory cytokines + vasoactive peptides
What systemic effects can pancreatitis have?
pleural effusion, acute lung injury, abscess formation, sepsis, systemic inflammatory response syndrome
Chronic pancreatitis
pancreatic tissue gradually replaced by fibrotic and/or calcified tissue, formation cysts, strictures, obstruction
GI disorders in children
- pyloric stenosis
- cleft lip/cleft palate
- neonatal jaundice
- GI effects cystic fibrosis
GI effets of cystic fibrosis
- fibrocystic disease of pancreas-leading to pancreatic enzyme deficiencies
- pancreatic ducts obstructed by thick mucus»_space; degeneration, fibrotic changes»_space; potentially affetcs beta cells
- enzyme deficiencies»_space; protein, fat, CHO digestion»_space; failure absorb fat soluble vitamins, growth failure, decreased bone mineral deposits
GI disorders in neonates
- esophageal atresia
- meconium ileus
- necrotizing enterocolitis
Esophageal atresia
- trachea/esophagus fails to differentiate during 4-6 wk fatal development
- esophagus ends in blind pouch, may occur with esophageal fistula
necrotizing enterocolitis
- newborns, especially low birth weight; d/t immature mucosal barrier
- ischemic, inflammatory process that leads to bowel necrosis, perforation
If pt is Hep A IgM neg and IgG pos, what is their status?
***
Negative for Hep A and immune due to previous illness or received vaccine
if pt is Hep A IgM neg and IgG neg, what is their status?
***
Negative for Hep A, but susceptible to Hep A infection (never vaccinated or did not maintain antibody response
Diverticulosis
- condition in which there are small pouches or pockets in the wall or lining of any portion of the digestive tract.
- mucosa herniates through smooth muscle layer colon wall
GASTRIC ULCER
ETIOLOGY: 70% usually cause by H.Pylori which induces local inflammation
RISK FACTORS: long term use NSAIDs use (arise due to decrease in mucosal protection against gastric acid
CLINICAL MANIFESTATION: epigastric pain that worsens after eating, loss of appetite, and weight loss
PATHOLOGY:are a break in the mucosa of the stomach lining that penetrates through the muscularis mucosa and extends more than 5 mm in diameter. When alterations occur to the defense mechanisms of the stomach, it can cause changes in the gastric mucosa which will eventually result in erosion and then ulceration.
How does NSAID cause ulcers?
it blocks cyclooxygenase from making prostaglandins that increase gastric mucous that decrease gastric acid
ZOLLINGER-ELLSION SYNDROME
- type of peptic ulcer
- rare digestive disorder that results in too much gastric acid. This excess gastric acid can cause peptic ulcers in your stomach and intestine.
- s/s: PAIN THAT IMPROVES WITH EATING AND PRESENT WITH WEIGHT GAIN: diarrhea,
Ulcerative cholitis
- effects more of the rectum and large bowel
- inflammation and ulcer formation that is continuous
- faulty immune system causing an overdrive, environment, stress, bacteria, viral, NSAIDs, genetic
- affects more of the inner lining of intestinal wall
S/S: Urgent BM Loss of weight, low RBCs Cramps abd Electrolyte imbalance Rectal bleeding Severe diarrhea
CURE: is surgery; colectomy and may have ostomy, anastamosis and pouch is created to the ilium so that ostomy is not needed
COMPLICATIONS: rupture of bowel, toxic magacolon (leads to rupture), weight loss, dehydration (inflammation doesn’t allow for water absorption), anemia (bleeding ulcers)l inflammation of joints, eyes, skin, and liver
If you have UC or Crohn’s what foods do you want to avoid
hard to digest foods (popcorn, nuts), high fiber foods, fatty food, dairy, spicy food
Crohns
- scattered patches throughout the GI tract
- affects entire lining of intestinal wall
- commonly found in terminal ileum and start of colon
S/S: RLQ pain, ulcers in mouth, anal fissures, weight loss
CURE: none; bowel resection, ileostomy
COMPICATIONS:
Abscessing Fistulas May Form Sepsis; malnutrition, fissures (anal), strictures (obstructions)
What happens in pancreatitis
- leads to digestion of the pancreas by its own enzymes and/or irreversible structure damage to the organ
- enzymes are activated inside pancreas instead of the duodenum
- CBGs can be elevated because Islet of Langerhans don’t work properly
- pancreas will swell and leak the digestive enzymes out into surrounding tissues and organs
- comes on suddenly (acute form)
Complications: ascites, malabsorption, fibrosis, cysts, abscesses, GI pain, internal bleeding, shock
What does bicarb do?
neutralizes stomach acid
What causes ACUTE pancreatitis?
- gallstones and alcohol
- high amount of amylase and lipase produce by acinar cells of pancreas
- reversible of treated quickly
What causes CHRONIC pancreatitis
- repeated episodes of acute pancreatitis and YEARS OF ALCOHOL ABUSE
- damage is irreversible
How does alcohol effect the pancreas
pancreatic acinar cells metabolize alcohol into toxic byproducts that damage pancreatic ducts, and enzymes that are normally released into the digestive tract build up and begin to digest the pancreas itself. The damaged pancreatic tissue promotes inflammation, which leads to further damage of the pancreas.
Test for pancreatitis
ERCP–procedure to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas
Treatment for pancreatitis
NPO IV fluids Diet Minitor I/Os Meds: PPI, antacids, H2 blockers
stomach
Motility: receptive relaxation peristalsis
SECRETION: gastric juice: HCL, pepsin, mucus, intrinsic factor
DIGESTION: carb digestion continues in body of stomach; protein digestion begins in antrum of stomach
ABSORPTION:
- none
- no food stuffs; a few lipid soluble substances, such as alcohol and aspirin
Liver gets oxygenated blood from where?
the hepatic ARTERY
Patient is HBAb core is neg and HBAb surface is positive, what is their status?
They are immune protected. Surface antibodies are present due to natural infection. Has recovered from a prior Hep B infection. Cannot infect others.
If HBAg surface is neg, HBaB is core neg and HBAb surface is pos, what is their status?
immunity d/t vaccine
Patient is HBAg surface pos and HBIgG core pos and HBAb surface neg, what is their status?
no immunity, chronically infected
