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

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