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Pathophysiology GI, Liver

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Dysphagia
Difficulty swallowing. can cause malnutrtion or aspiration
Dysphagia can be caused by
Fibrosis, Compression, Diverticulum, Congenital atresia, Congenital tracheoesophageal fistula, Neurologic damage, and Achalasia.
Fibrosis dysphagia
scar tissue in esophagus
Compression dysphagia
pressure caused by a tumor
Diverticulum
undigested food in pouch obstructs esophagus
Congenital atresia
developmental defect (esophagus is not connected)
Congenital tracheoesophageal fistula
Developmental defect (connection between esophagus and trachea)
Neurologic damage to cranial nerves _____ can cause dysphagia
CN V, VII,IX, X, and XII
Achalasia
loss of peristalsis in lower esophagus
Dysphagia treatments
"Thickener"
Aspiration precautions
Positioning (90 degrees)
Surgical correction
There are 2 types of Esophageal pain _______ and ________
Pyrosis (heartburn)
Pain in the middle of the chest
Mimics Angina Pectoris
May radiate
Pyrosis is caused by
Reflux of gastric contents (acid) into esophagus
Pain in the middle of the chest is caused by
Esophageal distention
Powerful esophageal muscle contraction
Clinical manifestation of esophageal pain
Chest pain
Shortness of breath
Retrosternal burning
Water brash
(regurgitation of sour fluid or tasteless saliva into the mouth-hypersalivation)
Nausea
Acute Diarrhea (Etiology)
Infection
Stress
Food allergy
Leakage of stool around an impaction
Chronic Diarrhea (Etiology)
Greater than 4 weeks
Malabsorption
Chronic infection
Diarrhea Motility disturbance
Decreased contact time of chyme with small intestine
Absorptive capacity in large intestine is exceeded
Diarrhea Exudative
Inflammatory processes
Mucous
Blood
Protein
Diarrhea Secretory
Toxins that stimulate intestinal fluid secretion and impair absorption
Staphylococcus aureus
Diarrhea Osmotic
Increased amounts of poorly absorbed solutes in the intestine cause sodium and water influx
Constipation
Small, infrequent, or difficult bowel movements
Fewer then 3 stools per week
Low fiber diet
Lack of exercise
Slow peristalsis (elderly)
Can lead to impaction
GastroEsophageal Reflux Disease (GERD)
Backward flow of gastric contents into esophagus
May or may not produce symptoms
GastroEsophageal Reflux Disease (GERD) Pathogenesis
Incomplete closure of lower esophageal sphincter (LES)
May be affected by:Fatty foods, Caffeine, ETOH, Smoking, Sleep position, Obesity
Increased abdominal pressure: Pregnancy, Hiatal hernias
Drugs: Birth control pills, Narcotics
GERD Clinical manifestations
Heartburn, Regurgitation, Dysphagia, Chest pain
Usually after a meal
GERD Complications
Esophageal strictures
Barrett esophagus
Pulmonary symptoms (from reflux into breathing passages)
Cough
Asthma
Laryngitis
GERD Treatment
Aimed at increasing function of LES
Sleep with HOB elevated
Sit up during meals
Hiatal Hernia
Cause not understood
Associated with conditions of increased intra abdominal pressure increases:
Ascites
Pregnancy
Obesity
Chronic straining/coughing
Hiatal Hernia Pathogenesis
Defect in the diaphragm that allows a portion of the stomach to pass into the thorax
Hiatal Hernia Clinical Manifestations
Ulcerations
Predisposed to GERD so:Heartburn, Chest pain, Dysphagia
Incarcerated hernia (rare):Life threatening
Portion of stomach caught above the diaphragm and occluded (slide 14)
Gastritis
Inflammation of stomach lining
May be acute or chronic
Acute Gastritis
Overuse of alcohol
Aspirin
NSAIDS
Tobacco use
Chronic Gastritis
Helicobacter pylori
Gastritis Pathogenesis
Acute-self limiting
Helicobacter pylori (chronic)
Causes chronic superficial gastritis in all infected persons
Promotes inflammation within the gastric mucosa
Interferes with prostaglandin which normally provides protection (see PUD)
Gastritis Clinical manifestations
Anorexia
Nausea
Vomiting
Postprandial discomfort (after meals)
Chronic gastritis is associated with _________ due to a loss of intrinsic factor
pernicious anemia
Gastritis Treatment
Removal of causative agent
Supportive care
Small meals
Lower gastric pH
Avoid irritants
Gastroenteritis
Irritation of stomach and small intestinal lining
Gastroenteritis Pathogenesis (acute)
Direct bacterial invasion of GI tract
Ingestion of bacteria
Imbalance of normal flora may predispose to "travelers" gastroenteritis
Gastroenteritis Pathogenesis (Chronic)
Usually the result of another GI disorder such as Ulcerative Colitis
Gastroenteritis Clinical Manifestations
Abdominal discomfort
Pain
Nausea
Vomiting
Diarrhea
Elevated temp and malaise may also be present
Gastroenteritis Treatment
Supportive care
Fluid replacement
Electrolyte replacement
Peptic Ulcer Disease (PUD)
Disorders of GI tract caused by the action of acid and pepsin.
Varies in severity from slight mucosal injury to ulcerations.
H. pylori major causative factor (90%)
Peptic Ulcer Disease (PUD) Pathogenesis (stomach)
break in the lining may be exacerbated by medications
Peptic Ulcer Disease (PUD) Pathogenesis (duodenum)
excessive secretion of acid
Thrives in acidic conditions
Slows rate of healing
High recurrence rate unless eradicated
H.pylori
PUD Clinical manifestations
Epigastric pain
Gastric-empty stomach
Duodenal- 2-3 hours post eating
Life threatening complication of PUD
GI bleeding
PUD Treatment
PPI
Eradication of H.pylori
"Coating agents"
Smoking cessation
Avoid Aspirin/NSAIDS
Avoid stress
Ulcerative colitis (UC)
Inflammatory disease of the mucosa of the rectum and colon
Characterized by remission/exacerbations (chronic)
Stress does NOT cause ______ but can increase severity of attack
Ulcerative colitis (UC)
Ulcerative colitis (UC) Pathogenesis
Sloughing occurs causing bloody, mucous-filled stools
Leukocytes invade the area and abscesses develop
Begins as inflammation at base of crypts of Lieberkuhn
Ulcerative colitis (UC) Manifestations
Abdominal pain
Bloody, mucous-filled diarrhea
Rectal bleeding
Weight loss
Anemia
Anorexia
Ulcerative colitis (UC) Treatment
Steroids
Side effects limit long term use
Immunosuppressive therapy
Broad spectrum antibiotics
Patients with signs of systemic toxicity
Megacolon
Colectomy
Crohn Disease (CD)
Inflammation of the GI tract that extends through all layers of the intestinal wall
Most commonly effects the proximal colon
Cause is unknown
Crohn Disease (CD) Pathogenesis
Lymph nodes of GI tract enlarge and flow is blocked
Engorgement and inflammation of the surrounding tissue leads to deep linear ulcer development
Affected portion becomes thickened with fibrous scarring and fissures
Bowel becomes incapable of adequately absorbing the intestinal contents
Crohn Disease (CD) Clinical manifestations
Constant abdominal pain concentrated in RLQ (Right Lower Quadrant)
Diarrhea
Perianal fissures
Fistulas
Abscesses
Weight loss
Nutrient deficiencies
Fluid imbalances
Crohn Disease (CD) Treatment
Diet changes
Limit fruits, veggies, high fiber, diary, spicy, fatty foods
Limit carbonated and caffeinated drinks
Antitumor necrosis factor INFLIXIMAB
Corticosteriods
Enterocolitis: Pseuomembranous Colitis
Inflammation and necrosis of large intestine. Clostridium difficile.
Enterocolitis: Pseuomembranous Colitis is also known as _______________
Also known as antibiotic associated colitis
Enterocolitis: Pseuomembranous Colitis Pathogenesis
Antibiotic exposure
Mediated by bacterial toxins
Colon develops "pseudomembrane" composed of leukocytes, mucous, fibrin, and inflammatory cells
Mucosal necrosis
Pseuomembranous Colitis Clinical manifestations
Diarrhea (often bloody)
Abdominal pain
Fever
Can lead to perforation
Major cause of fever among hospitalized patients receiving antibiotics
Pseuomembranous Colitis Treatment
Stop precipitating antibiotic
Oral Flagyl or Vancomycin
Supportive care
Appendicitis
Most common cause of emergent abdominal surgery
Inflammation of vermiform appendix
Twice as common before age 45 as after
Peak incidence between 10-19 years of age
More common in men
Appendicitis Pathogenesis
Caused by obstruction
May self limit if obstruction relieved
Inflammation can lead to necrosis of appendix
Infection
Perforation
Peritonitis
Inflammation of peritoneum produced by bacteria or irritating substances introduced into the abdominal cavity
Appendicitis Clinical manifestations
Generalized periumbilical pain
Nausea
Diarrhea
Fever
If someone has appendicitis, they usually complain of pain at __________
McBurney's point (Right Lower Quadrant)
Appendicitis Treatment
Surgical removal
open
laproscopic surgery (extremely small incisions)
Antibiotic therapy
Fluid replacement
Irritable Bowel Syndrome (IBS) Disorder of Motility
Alternating Diarrhea/Constipation
Abdominal pain
No other defined pathology identified
Irritable Bowel Syndrome (IBS) Disorder of Motility Pathogenesis
Poorly understood
Disorder of motility
Increased wave activity in the colon
Heightened sensory response to distention and stimulation
Irritable Bowel Syndrome Clinical manifestations
Variable
Minimal
Incapacitating
Alternating diarrhea/constipation
Mucous in stool
Irritable Bowel Syndrome Treatment
Anti-diarrheal agents
Antispasmodic agents
Increase fiber in diet
Hydration
Support groups
A polyp refers to a ________ or not yet malignant lesion
benign
Colon cancer Risk factors
Ulcerative colitis
Chron's Disease
Polyps of colon
The pathogenesis of colon cancer is _____________
largely unkown
Colon cancer Clinical manifestations are dependent on _________
location and size of the cancer
Colon cancer on the Right side of colon Clinical manifestations
Black, tarry stools
Colon cancer on the left side of the colon clinical manifestations
Obstruction
Abdominal cramping/fullness
Ribbon or pencil like stools
Blood or mucous in stool
Colon cancer on the rectum clinical manifestations
Change in bowel habits
Rectal fullness (late)
Colon cancer treatment
Surgical removal
Colostomy
at age __ you should be screened for colon cancer
50
Bile is formed in the ______ and then stored in the _______ and______.
liver/gallbladder/bile ducts
Cholelithiasis is another term for
gallstones
The majority of Cholelithiasis are composed of ________.
cholesterol
Cholelithiasis are 2x more common in ______.
females
Cholelithiasis Pathogenesis
Supersaturation of bile with cholesterol
Nucleation of cholesterol crystals
Hypomotility allowing for stone growth
Cholelithiasis Clinical manifestations
Persistent RUQ (right upper quadrant) abdominal pain (biliary colic)
Caused by intermittent obstruction of the cystic duct by a gallstone
Often precipitated by a meal
Most symptoms occur at night
Cholelithiasis Diagnosis/Treatment
Diagnosis ultrasound
Surgery
cholecystectomy
Lithrotripsy
Mechanical breaking of stones
Cholecystitis (acute) is inflammation of the __________.
gallbladder wall
Cholelithiasis are present in ___ of cases of Cholecystitis.
90%
Cholecystitis (acute) Pathogenesis
Obstruction of cystic duct
Cystic duct passes into common bile duct from gallbladder
Stasis of bile
Possible bacterial infection
If left untreated, the gangrene of the gallbladder wall with rupture may occur
Cholecystitis (acute) Clinical manifestations
Acute severe right upper abdominal pain
Fever
May have bacterial component
Nausea
Cholecystitis (acute)
Pre-treatment with antibiotics
Percutaneous catheter drainage or endoscopic drainage with stent placement may be performed to relieve obstruction
Surgical removal
Open
Laproscopic
4 small incisions
Cholecystitis (chronic)
Chronic inflammation of gallbladder
Diabetes and obesity are predisposing factors
Symptoms sporadic
Acute pancreatitis
Acute inflammation of pancreas
Predisposing factors
Biliary tract disease
Elevated triglycerides
Alcohol abuse (66%)
Acute pancreatitis Pathogenesis
The most prominent factor:
Obstruction of pancreatic duct by a stone or other cause
Digestive enzymes get released within the parenchyma of the pancreas
Autodigestion of pancreas itself
Acute pancreatitis Clinical manifestations
Increasing pain in LUQ
Radiates to back
Abdominal distension
Hypoactive bowel sounds
Acute pancreatitis Diagnosis/Treatment
Signs and symptoms
Serum lipase (most specific) and amylase
Ultrasound/CT
TREATMENT
NPO
Nasogastric suctioning
TPN
IV fluids
TPN means
total parenteral nutrition
Pancreatitis (chronic)
Chronic inflammatory lesions within the pancreas
The vast majoriy of Chronic pancreatitis cases are related to __________.
alcohol abuse
Pancreatitis (chronic) Clinical manifestations
Intermittent bouts of acute pancreatitis
Diabetes mellitus
Malabsorption
Fats
Fat soluble vitamins
Wasting
Insidious onset of pain
Pancreatitis (chronic) Treatment
Pain control
Endocrine and exocrine insufficiency management
Oral hypoglycemics
Insulin
Low fat diet
Pancreatic enzyme replacement
Abstain from alcohol
Pancreatic cancer Risk factors
Smoking
Alcohol abuse
Diabetes
High fat diet
Excessive salt intake
More common in older people
Pancreatic cancer Clinical manifestations
Insidious onset
Dull epigastric pain that radiates to the back
Jaundice
Weight loss
Nausea/vomiting
Pancreatic cancer has a mortality rate of ___.
99%
The liver receives ___ of blood from the hepatic artery, and ___ of blood from the portal vein that drains the capillary bed of the alimentary canal and pancreas.
25%/75%
The following manifestations are attributable to hepatocellular failure:
Jaundice
Decreased clotting factors
Hypoalbuminemia
Glucose imbalance
Decreased absorption of vitamins D and K
Feminization
Hepatic encephalopathy
The following manifestations are attributable to portal hypertension (disruption of blood flow):
GI congestion
Esophageal varices
Gastric varices
Hemorrhoids
Splenomegaly
Ascites
Jaundice is impaired _______ metabolism.
bilirubin
Jaundice Pathogenesis has 3 stages ____________, ____________, and ___________.
Pre-hepatic, Hepatic, Post-hepatic
Jaundice Pre-hepatic (Pathogenesis)
Hemolysis
Ineffective erythropoiesis
Jaundice Hepatic (Pathogenesis)
Impaired liver function
Jaundice Post-hepatic (Pathogenesis)
Defective transport of bile salts
Obstruction
Jaundice Clinical manifestations
Yellowish cast to skin
Yellowish cast to sclera
Dry, itching skin
Portal hypertension
Elevated pressure in the portal system
Sluggish or obstructed flow through the portal vein/system
Venous drainage of much of the GI tract is congested
Usually the result of alcoholic or post hepatic cirrhosis (in Western society)
Portal hypertension Clinical manifestations
Caput medusae (head of Medusa)
Superficial periumbilical varices
Varices
Esophageal
Gastric
Rectal
Varices is another term for
varicose veins
Gastroesophageal varices is the main cause of death in people who have ____________.
chronic cirrhosis
Gastroesophageal varices
Collateral venous pathway that occurs due to portal hypertension
As portal pressure elevates, becomes vulnerable to rupture
Gastroesophageal varices Clinical manifestations
Major upper GI bleed
Hematemesis
Melena
Rapid intestinal transit and vigorous bleeding
Mortality up to 50%
Profound anemia
Shock
Gastroesophageal varices Treatment
Fluid resuscitation
Normal saline
Medications to lower portal pressure or reduce flow to susceptible organs
Vasopressin
Nitroglycerin
Somatostatin
Endoscopic sclerosis
Hepatic encephalopathy
Exact cause unclear
Asterixis (classic physical finding): liver flap
Spastic jerking of hands when in forced extended position
_____________ is Associated with elevated ammonia levels
Hepatic encephalopathy
Grade 1 Hepatic encephalopathy
Mild confusion, no flap
Grade 2 Hepatic encephalopathy
Mild confusion, no flap
Grade 3 Hepatic encephalopathy
Stuporous, marked confusion, flap present
Grade 4 Hepatic encephalopathy
Coma, no flap
Hepatic encephalopathy Treatment
Identify precipitating factors
GI bleeding
Reduce dietary protein intake
Diuretics
Enhance elimination of nitrogenous wastes
Osmotic cathartic
Lactulose
Antibiotics
Reduce normal flora to reduce protein breakdown
Ascites
Accumulation of fluid in peritoneal cavity
Advanced liver disease
Portal hypertension
Hypoalbuminemia
Intraabdominal accumulation of sodium, water, and protein
Ascites Clinical manifestations
Abdominal distention
Difficulty breathing
Abdominal or umbilical herniation
Ascites Treatment
Reduce dietary sodium
Diuretics
Bedrest
Therapeutic paracentesis
Cirrhosis
Irreversible end stage of multiple liver diseases
Severe acute hepatitis
Chronic hepatitis
Alcoholism
Toxic hepatitis
Cirrhosis Pathogenesis
Fibrosis and wide spread scarring secondary to inflammation
Results in permanent alteration of hepatic blood flow
Decreased liver function results
Cirrhosis Clinical manifestations
Jaundice
Portal hypertension
Esophageal varices
Ascites
Hepatic encephalopathy
Alcoholic liver disease (Alcoholic fatty liver)
Abnormal deposits of fat in liver cells
More fat than liver can metabolize
Most from ETOH but also:
Diabetes
Obesity
TPN
Drugs
if Alcoholic liver disease (Alcoholic fatty liver) is left untreated, it may progress to _________ and ______.
Liver fibrosis, and cirrhosis
Alcoholic liver disease (Alcoholic hepatitis) is associated with ________.
Binges
Alcoholic liver disease (Alcoholic hepatitis) Treatment
Stop alcohol intake
Nutritional support
Steroids
Complicated by DTs
_________ is Usually a metastatic process because of vascularity
Liver cancer
Liver cancer Clinical manifestations
Hepatomegaly
Nausea
Weight loss
Abdominal pain
Advanced:
Jaundice
Ascites
Hepatitis A virus (enteric)
Transmission
Fecal-oral
Sexual (oral-anal contact)
Common in areas of overcrowding
Day care centers
Institutional settings
Despite the cause, changes to the liver are usually similar in each type of _________.
viral hepatitis
Hepatitis A virus (enteric) Clinical Manifestations
ACUTE onset
Malaise
Anorexia
Low-grade fever
RUQ pain
Jaundice
Clinical course usually self limiting
Hepatitis A virus (enteric) Treatment
Vaccination
Added to routine childhood vaccines in 2006
May be vaccinated after exposure
Prevention
Handwashing
Prognosis good
Hepatitis B virus (serum)
Transmission by parenteral contact with
blood
blood products
contaminated needles
sexual contact
Perinatal
Hepatitis B virus (serum) Clinical Manifestations
More insidious onset
Similar to Hepatitis A but may involve:
Urticaria & other rashes
Arthralgia
Angioedema
Glomerulonephritis
Hepatitis B virus (serum) Treatment
Supportive
Hepatitis B immune globulin
May be given within 7 days of exposure
Recommended as part of childhood vaccination regimen
Recommended for high-risk individuals
Multiple sex partners
Male homosexuals
Illicit drug users
Hemodialysis patients
Health care workers
Hepatitis C virus (non-A, non-B)
Important occupational risk for health care workers
Transmission similar to Hepatitis B
IV drug use
Blood transfusions prior to availability of screening test
Intranasal cocaine use
Hepatitis C virus (non-A, non-B) Clinical Manifestations
Acute phase usually asymptomatic
Insidious onset
Most progress to chronic active infection
Advanced liver disease
Hepatitis C virus (non-A, non-B) Treatment
Interferon alfa
No specific drug therapy
Supportive
Rest
Nutritional support
Prognosis moderate
Hepatitis D virus
Requires an infection with Hepatitis B to survive
Transmission by parenteral routes
Exposure to blood and blood products
IV drug users
Hemophiliacs
Hepatitis D virus Clinical Manifestations
Tends to accelerate the progress of liver disease associated with Hepatitis B infection
Hepatitis D virus Treatment
No specific treatment for Hepatitis D
Prognosis fair, worsens with chronic disease
Hepatitis E virus
Transmission fecal-oral (especially contaminated water)
Most common cause of acute hepatitis in developing countries
Cases in the US typically follow travel
India
Africa
Asia
Central America
Hepatitis E virus Clinical Manifestations
Similar to Hepatitis A
Usually lasts only 2 weeks
Hepatitis E virus Treatment
Supportive
No vaccine
Prevention
Avoid undercooked foods
Careful handwashing
Drink safe water and beverages
Canned
Bottled
Purified