Week 5 (ch. 17) Flashcards
Gut wall: Mucosa
Epithelium, including mucous producing cells
Gut wall: submucosa
CT - including blood vessels, nerves, lymphatics, secretory glands
Gut wall: serosa
visceral peritoneum
What are the structures of the gut wall
mucosa, submucosa, circular smooth muscle layer, longitudinal smooth muscle layer, serosa
What are the structures in the upper GI tract and accessory
Oral cavity Esophagus Stomach Liver Pancreas
salivary amylase
starts chemical breakdown of carbohydrates in oral cavity
Deglutition
swallowing
Esophagus
Closed except during swallowing, skeletal muscle at superior end - followed by smooth muscle
Describe what happens in the upper GI tract during swallowing
a. soft palate is pulled upward
b. vocal cords are approximated
c. epiglottis covers the larynx
d. respirations ceases
e. bolus is seized by the constricted pharynx
f. bolus of food moves into esophagus
how many muscle layers does stomach have
3
What are some functions of the stomach
a. Mixing and churning food
b. Initial digestion of proteins
c. production of intrinsic factor
d. formation of chyme
e. absorption of smell and lipid-soluble molecules
What chemical digests proteins and how is this chemical formed?
Pepsin (in the stomach)
– formed by combination of pepsinogen and HCl
Why is intrinsic factor important in stomach?
essential for absorption of vitamin B12 in ileum
Liver receives blood from where
hepatic portal vein
- from intestine to liver
What stores nutrients in the liver?
Hepatocytes
- play role in carbs, proteins, fat metabolism
What are some functions of the liver
a. production of plasma proteins and clotting factors
b. breakdown of old and damages erythrocytes
c. bile production
Pancreas is what
Exocrine pancreas arranged in lobules
Pancreas secretes digestive enzymes such as?
Trypsin Chymotrypsin carboxypeptidase ribonuclease pancreatic amylase bicarbonate ions
What does the pancreatic duct join to enter the duodenum
bile duct
What structures are in the lower GI tract?
Small intestine
Large intestine
What are the structures of the SI
Duodenum, jejunum and ileum
- villi / microvilli
villi and microvilli
villi = folds of mucosa microvilli = folds of cell membranes
Both increase surface area for absorption
SI is major site of what
absorption
SI is the site of what production?
mucus
enterokinase, peptidases, nucleosidases, lipase, sucrase, maltase, lactase, cholecystokinin (hormone)
SI is lacteal, meaning what?
lymphatic vessel
Large intestine functions
Fluid/electrolyte reabsorption
formation of solid feces
Large intestine has resident flora, which does what?
Breakdown of certain food material
Vitamin K synthesis by bacteria
Large intestine has Peyer patches, which are?
lymphatic tissue
PNS: stimulation and effect
Primarily though vagus nerve
- increased motility
- increased secretions
SNS stimulation and effects
Stimulated by factors such as fear, anger
- inhibits GI activity
- causes vasoconstriction
- reduced secretions and regeneration of epithelial cells
What do facial nerve and glossopharyngeal nerves do
maintain continuous flow of saliva in mouth
Effects of distention and stretching of stomach
- PNS activation
- increase peristalsis and gastric secretions
how often does stomach empty
2-6 hours after meal
Gastrin: formation
Secreted by mucosal cells (stomach) in response to distention of stomach or partially digested substances
gastrin: function
increase gastric motility, relaxes pyloric and ileocecal sphincters - promotes stomach emptying
Histamine
increased secretion of HCl acid
Secretin
Decreases gastric secretions
Cholecystokinin
inhibits gastric emptying; stimulates contraction of gall bladder
Digestion and Absorption: carbohydrates
Digestion starts in mouth followed by digestion in small intestine
Digestion and Absorption: proteins
digestions starts in stomach, continues in SI
Digestion and Absorption: lipids
Emulsified by bile prior to chemical breakdown. Action of enzymes form monoglycerides and free fatty acids.
Formation of Chlyomicrons
Digestion and Absorption: Fat soluble vitamin
vitamins A, D, E K
– absorbed with fats
Digestion and Absorption: Water soluble vitamins
B and C
– diffuse into blood
Digestion and Absorption: electrolytes
absorbed by active transport or diffusion
Where are drugs primarily absorbed?
stomach
Where is aspirin usually absopbed?
stomach
How is water absorbed
primarily osmosis
how much water is secreted into digestive tract each day
about 700 mL
how much fluid is ingested in good and fluids each day
about 2300 mL
how much fluid leaves the body in feces
only 50-200mL
– vomiting and diarrhea disrupt this
Common manifestations of Digestive Disorders
Anorexia, nausea, vomiting and bulimia
where is the vomiting center located in the body
medulla
- coordinates activities involved in vomiting
- protects airway during vomiting
What is commonly effected from bulimia? Why?
Oral mucosa, teeth, esophagus
– damage is caused by recurrent vomiting
Vomiting Center Activation: what is effected?
a. distention / irritation of digestive tract
b. vestibular apparatus of inner ear (motion)
c. increased intracranial pressure
- - sudden projective vomiting without previous nausea
Vomiting Reflex Activities
Deep inspiration Closing glottis, raising soft palate Ceasing respiration Relaxation of gastroesophageal sphincter Contracting abdominal muscles Reversing peristaltic waves
Characteristics of Vomitus: Presence of blood
Hematemesis
- coffee grounds vomitus; brown glandular material indicates actions of HCl on hemoglobin
- hemorrhage - red blood may be in vomitus
Characteristics of Vomitus: yellow or green
bile from duodenum
Characteristics of Vomitus: deeper brown color
may indicate content from lower intestine
Characteristics of Vomitus: recurrent vomiting of undigested food
problem with gastric emptying or infection
Large volume diarrhea (secretory or osmotic)
Watery stool resulting from increased secretions into intestine from the plasma
Often related to infection
Limited reabsorption because of reversal of normal carriers for sodium and/or glucose
Small-volume diarrhea
Often caused by inflammatory bowel disease
- stool may contain blood, mucus and pus
- may be accompanied by abdominal cramps and tenesmus
Steatorrhea
“fatty diarrhea”
- frequently bulky, greasy, loos stools
- foul order
- characteristics of malabsorption syndromes
- fat usually the first dietary component affects
- abdomen often distended
What syndromes may have Steatorrhea
Celiac disease, cystic fibrosis
Why is fat usually the first dietary component affected leading to Steatorrhea ?
presence interferes with digestion of other nutrients
Blood in stool: Frank blood
Red blood - usually from lesions in rectum or anal canal
Blood in stool: Occult blood
Small hidden amounts, detectable with stool tests
may be caused by small bleeding ulcers
Blood in stool: Melena
Dark-colored, tarry stool
May result from significant bleeding in upper digestive tract
Causes of excessive gas
Eructation
Borborygmus
Abdominal distention and pain
Flatus
Gas results from
swallowed air (drinking through straw)
Bacterial action on food
foods or alterations in motility
Constipations
less frequent bowel movements than normal
- small or hard stools
- acute or chronic issue
Chronic constipation may cause what
hemorrhoids, anal fissures, diverticulitis
Causes of constipation
Weakness of smooth muscle fibers (age/illness) low fiber intake low fluid intake failure to response to defecation reflex immobility neurological disorders drugs some antacids, iron meds obstruction caused by tumors or strictures
Common complications of digestive tract disorders
dehydration and hypovolemia
Digestive tract disorders: Metabolic Alkalosis
Results from loss of hydrochloric acid with vomiting
Digestive tract disorders: metabolic acidosis
Severe vomiting causes a change to metabolic acidosis because of the loss of bicarbonate of duodenal secretions.
Diarrhea causes loss of bicarbonate.
Visceral pain digestive tract: Burning sensation
inflammation and ulceration in upper digestive tract
Visceral pain digestive tract: dull, aching pain
typical result of stretching of liver capsule
Visceral pain digestive tract: cramping or diffuse pain
inflammation, distention, stretching of intestines
Visceral pain digestive tract: Colicky, often severe pain
Recurrent smooth muscle spasms or contraction
- response to severe inflammation or obstruction
Somatic pain receptors are directly linked to what
spinal nerves
rebound tenderness
Identified over area of inflammation when pressure is released
Somatic pain digestive tract:
Steady, intense, often localized
- may cause reflex spasms of overlying abdominal muscles
- involvement or inflammation of parietal peritoneum
referred pain
Pain is perceived at a site different from origin
referred pain results from what
when visceral and somatic nerves converse at one spinal cord level
- source of visceral pain is perceived as the same as that of the somatic nerve
Causes if limited malnutrition - specific problem
Vitamin B12 deficiency
Iron deficiency
Causes of generalized malnutrition
Chronic anorexia, vomiting, diarrhea Other systemic causes - chronic inflammatory bowel disorders - cancer treatment - wasting syndrome - lack of available nutrients
Sigmoidoscopy and colonoscopy
Diagnostic test
- biopsy and removal of polyps may be done
Laboratory analysis of stool specimens
check for infections, parasites and ova, blooding, tumors, malabsorption
Disorders of Oral cavity: Cleft lip / palate
Congenital abnormality
- arise 6-7 week of gestation
- multifactorial origin
- high risk of aspiration
- speech impaired (speech therapy)
- feeding problems in infant
- surgical repair asap
Disorders of Oral cavity: Herpes Simplex 1 infection
HSV-1
- kissing/close contact
- dormant virus on sensory ganglion
- cause: stress, trauma, infection
- antiviral medication
- can spread to eyes (conjunctivitis and keratitis)
Disorders of Oral cavity: Syphilis
Cause: Treponema pallidum
- oral lesions
- highly contagious during 1st and 2nd stages
- treated with long-acting penicillin
Primary Stage Syphilis
Chancre, a painless ulcer on tongue lip or palate
Secondary syphilis
Red macules or papules on palate - highly infections
heals spontaneously
Disorders of Oral cavity: Aphthous ulcers
Steptococcus sanguis may be involved
- part of oral resident flora
Small painful lesions on
- movable mucosa
- buccal mucosa
- floor or mouth
- soft palate
- lateral borders of tongue
usually heals spontaneously
Disorders of Oral cavity: Dental caries
Streptococcus mutans - initiating microbe
Lactobacillus follows in large numbers
–> bacteria break down sugards and produce large amount of lactic acid which dissolves mineral in tooth enamel which can lead to tooth erosion and formation of caries
anti-caries treatment
fluoride
what promotes the growth of dental caries
sugars and acids
Disorders of Oral cavity: Gingivities
Changes in Gingivae may lead to a local or systemic problems.
- inflammation of the gingiva –> tissue become red, soft, swollen, bleed easily. This may result from too much plaque, bad hygiene or toothbrush trauma
Disorders of Oral cavity: Periodontal disease
organisms enter the gingival blood vessels and travel to the connective tissues and bone of the dental arch.
Resorption of bone and loss of ligament fibers result in weakened attachment of teeth.
May result in total loss of tooth from socket
Periodontal disease treatment
Treated by antimicrobials, local surgery of gingiva, and improved dental hygiene
Disorders of Oral cavity: Hyperkeratosis
Whitish plaque or epidermal thickening of mucosa
Where does Hyperkeratosis occur
buccal mucosa, palate, lower lip
Hyperkeratosis may be related to what
smoking or chronic irritation
Why do Hyperkeratosis lesions require monitoring
Epithelial dysplasia beneath plaque may develop into squamous cell carcinoma
Hyperkeratosis example
Leukoplakia
common types of cancer of oral cavity
Squamous cell carcinoma Kaposi sarcoma (AIDs patients)
Oral cancer predisposing factors
smoking, alcohol abuse, preexisting leukoplakia
Sialadenitis
Inflammation of salivary glands
- infectious and non-infectious
- parotid gland most affected
Salivary gland disorders: Mumps
Infectious parotitis
- viral infection
- vaccine available
Salivary gland disorders: noninfectious parotitis
often seen in older adults who lack adequate fluid intake and mouth care
What are most malignant tumors of salivary glands?
mucoepidermoid carcinoma.
Caused of dysphagia
neuro deficit - infection, stoke, brain damage, achalasia muscular disorder - impairment from muscular dystrophy) mechanical obstruction
achalasia
failure of the lower esophageal sphincter to relax because of lack of innervation
left off on slide 46
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Dysphagia: congenital atresia
developmental anomaly
upper and lower esophageal segments are separated
Dysphagia: stenosis
narrowing of esophagus
Dysphagia: esophageal diverticula
out-pouchings of esophageal wall
- congenital or acquired following inflammation
Dysphagia: tumors
may be internal or external
esophageal cancer: what kind of cells
primarily squamous cell carcinoma
esophageal cancer: location
usually distal esophagus
esophageal cancer is associated with chronic inflammation because?
- chronic esophagitis
- achalasia
- hiatal hernia
- alcohol abuse, smoking
hiatal hernia
part of stomach protrudes into thoracic cavity
sliding hernia
most common
- portions of the stomach and gastroesophageal junction slide up above the diaphragm
rolling or paraesophageal hernia
part of the fundus of the stomach moves up through the enlarged or weak hiatus in the diaphragm and may become trapped
what happens when food lodges and becomes trapped in hernia
inflammation of mucosa
reflux of food up esophagus
chronic esophagaitis
signs of hernia
heartburn pr pyrosis
belching
discomfort when lying down
substernal pain that radiates to should or jaw
gastroesophageal reflux disease (GERD)
Periodic reflux of gastric contents into distal esophagus causes erosion and inflammation
GERD often seen with with other disease
hiatal hernia
what may be a factor of GERD
delayed gastric emptying
GERD: avoid what
Caffeine, fatty and spicy foods, alcohol, smoking, certain drugs
Acute Gastritis: what
gastric mucosa is inflammed
- may be ulcerated and bleeding
Acute gastritis may result from?
Infection by microorganisms Allergies to foods Spicy or irritating foods Excessive alcohol intake Ingestion of aspirin or other NSAIDs Ingestion of corrosive or toxic substances Radiation or chemotherapy
Basic signs of gastrointestinal irritation
- Anorexia, nausea, vomiting may develop
- Hematemesis caused by bleeding
- Epigastric pain, cramps or general - discomfort
- With infection, diarrhea may develop.
Acute gastritis is usually self-limiting, meaning
Complete regeneration of gastric mucosa
Supportive treatment with prolonged vomiting
May require treatment with antimicrobial drugs
Chronic gastritis: what
Characterized by atrophy of stomach mucosa
- loss of secretory glands
- reduced production of intrinsic factor
What is often present in Chronic gastritis
Helicobacter pylori
sings of Chronic gastritis
may be vague
- Mild epigastric discomfort, anorexia, intolerance for certain foods
increased risk of what with Chronic gastritis
peptic ulcers and gastric carcinoma
gastroenteritis
inflammation of stomach and intestines
- usually caused by infection or allergic reactions to food or drugs
gastroenteritis: describe the effect that microbes have as they are transmitted by fecally contaminated food, soil or water
a. most infections self limiting
b. serious illness may result in compromised house or virulent organisms
c. may cause epidemic outbreaks in refugee or disaster settings
d. safe sanitation essential for prevention
Peptic ulcer (gastric and duodenal): cause
most caused by H. pylori infection
Where do peptic ulcers usually occur
proximal duodenum and antrum of stomach
Describe how the development of gastric ulcers begin
- breakdown of mucosal barrier
- decreased mucosal defense
- more common in gastric ulcer development
What is a predominant factor in duodenal ulcers
increased acid secretion
damage to mucosal barrier predisposes someone to the development of ulcers and is associated with what?
- Inadequate blood supply (vasoconstriction)
- excessive glucocorticoid secretion / meds
- ulcerogenic substances break down mucous layer (aspirin, NSAID, alcohol)
- atrophy of gastric mucosa
increase acid pepsin related to gastric ulcers may also lead to what?
- Increased gastrin secretion
- Increased vagal stimulation
- Increased sensitivity to vagal stimuli
- Increased number of acid pepsin secretory cells in the stomach (genetic anomaly)
- Increased stimulation of acid pepsin secretion d/t Alcohol, caffeine, certain foods
- Interference with normal feedback mechanisms
- Rapid gastric emptying
Complications of peptic ulcer: hemorrage
Caused by erosion of blood vessels
May be the first sign of a peptic ulcer
Complications of peptic ulcer: perforation
Ulcer erodes completely through the wall.
Chyme can enter the peritoneal cavity.
Results in chemical peritonitis
Complications of peptic ulcer: obstruction
may result later because the formation of scar tissue
peptic ulcer s/s
epigastric burning or localized pain, usually following stomach emptying
peptic ulcer diagnostic test
Fiberoptic endoscopy
Barium x-ray
Endoscopic biopsy
peptic ulcer treatment
Combination of antimicrobial and proton pump inhibitor to eliminate H. pylori
Reduction of exacerbating factors
Stress ulcers associated with
severe trauma or systemic problems
- burns, head injuries
- hemorrhage or sepsis
stress ulcers: rapid onset
multiple ulcer (usually gastric) may form within hours of precipitating event
first indicator of stress ulcer
hemorrhage and severe pain
Gastric cancer: where
mucous glands mostly in antrum or pyloric area
Gastric cancer: early carcinoma
confirmed to mucosa and submucosa
gastric cancer: later stages
involves muscularis
eventually invades serosa and spreads to lymph node
gastric cancer: prognosis
poor bc asymptomatic in early stages
key factor of gastric cancer
diet
- smoked foods, nitrates, nitrites
survival rate of gastric cancer
less than 20%
gastric cancer treatment
surgery and chemo
Dumping syndrome
Control gastric emptying is lost and gastric contents are “dumped” into duodenum without complete digestion
Dumping syndrome may follow
gastric resection
Dumping syndrome: Hyperosmolar chyme draws fluid from vascular compartment into intestine, which can cause
Intestinal distention
Increased intestinal motility
Decreased blood pressure → anxiety and syncope
Dumping syndrome occurs when
during or shortly after meals
Dumping syndrome s/s
adb. cramps, nausea, diarrhea
Dumping syndrome: hypoglycemia 2-3 hours after meals, why
High blood glucose levels in chyme stimulate increased insulin secretion → drop in blood glucose levels.
Dumping syndrome: treatment
dietary changes (frequent small meals high in protein, low in simple carbs)
often resolves over time
pyloric stenosis
Narrowing and obstruction of pyloric sphincter
pyloric stenosis signs / symptoms
Signs appear within several weeks after birth
- Projectile vomiting immediately after feeding
- Firm mass can be palpated at pylorus.
- Infant fails to gain weight, dehydration, persistent hunger
pyloric stenosis treatment
surgery
signs of pyloric stenosis if acquired lated in life
Persistent feeling of fullness
Increased incidence of vomiting
pyloric stenosis cause
developmental anomaly
Cholelithiasis
formation of gallstones
cholecystitis
inflammation of gall bladder and cystic duct
cholangitis
inflammation usually related to infection of bile ducts
Choledocholithiasis
Obstruction of the biliary tract by gallstones
gallstones may consist of
Cholesterol or bile pigment
Mixed content with calcium salts
small vs large gallstones
small: may be silent and excreted in bile
larger: obstruct flow of bile through gallbladder
possible locations of gallstones
Biliary Ducts & Pancreas
Gallstone risk factors / causes
Women High cholesterol in bile High cholesterol intake Obesity Multiparity Oral contraceptives or estrogen supplements Hemolytic anemia Alcoholic cirrhosis Biliary tract infection
Gallstones can cause obstruction of a duct by large calculi, which causes what
sudden, severe waves of radiating pain
gallstone treatment
laparoscopic surgery
low fat diet
why might jaundice develop from gallstones
bile backs up into liver and blood
pain related to gallstones decreases if gallstones move where
duodenum
Prehapatic jaundice
results of excessive destruction of RBC
What diseased might you see prehepatic jaundice
hemolytic anemias or transfusion reactions
intra-hepatic jaundice
occurs with disease or damage to hepatocytes
what disease might you see intra-hepatic jaundice
hepatitis or cirrhosis
Posthepatic jaundice
caused by obstruction of bile into gallbladder or duodenum
what disease might you see posthepatic jaunduce
tumor or cholelithiasis
bilirubin measurements: direct or conjugated bilirubin
cause be measured in blood
bilirubin measurements: total bilirubin
measured in blood
bilirubin measurements: how do you get indirect or unconjugated bilirubin
Total bilirubin - direct bilirubin
Type of jaundice indicated how ?
by increase in serum bilirubin level and changes in stools
bilirubin measurement for prehepatic jaundice?
Unconjugated bilirubin level elevated
bilirubin measurement for Intrahepatic jaundice
Both unconjugated and conjugated bilirubin levels may be elevated.
bilirubin measurement for posthepatic jaundice
increase conguated bilirubin level
- light colored stool caused by absense of bile
hepatitis
inflammation of liver
viral hepatitis
cell injury results in inflammation and necrosis in liver
- liver is edematous and tender
viral hepatitis: causative agents
Hepatitis A virus (HAV) Hepatitis B virus (HBV) Hepatitis C virus (HCV) Hepatitis D virus (HDV) Hepatitis E virus (HEV)
Hepatitis A virus (HAV): type is virus
small RNA virus
- acute but self-limiting infection
Hepatitis A virus (HAV): transmission
Fecal-oral route
- areas of bad sanitation / hygiene
- often from contaminated water or shellfish
- sexually transmitted (anal)
Hepatitis A virus (HAV): carrer or chronic state?
no
Hepatitis A virus (HAV): what happens before onset of signs
fecal shedding of virus
Hepatitis A virus (HAV): vaccine
available for travelers, food care workers, and health care workers
Hepatitis C virus (HCV): type of virus
single-stranded RNA virus
Hepatitis C virus (HCV): transmission
most common type transmitted by blood transfusion
Hepatitis C virus (HCV): carrier / chronic state
May exist in carrier state
about 50% of pt. enter chronic state
Hepatitis C virus (HCV): increased risk of what
hepatocellular carcinoma
Hepatitis C virus (HCV): treatment
interferon injections
Hepatitis D virus (HDV): virus type
incomplete RNA virus
Hepatitis D virus (HDV): requires what
HBV to replicate and produce active infection
Hepatitis D virus (HDV): effect on HBV
increases severity of HBV
Hepatitis D virus (HDV): transmission
blood
Hepatitis E virus (HEV): virus type
single-stranded RNA virus
Hepatitis E virus (HEV): transmission
oral-fecal
Hepatitis E virus (HEV): chronic or carrer state
no
Hepatitis: Preicteric stage s/s
Fatigue and malaise
Anorexia and nausea
General muscle aching
Hepatitis: Icteric stage s/s
Onset of jaundice
Stools light in color, urine becomes darker
Liver tender and enlarged, mild aching pain
Hepatitis: Posticteric stage - recovery stage s/s
Reductions in signs
Weakness persists for weeks
Viral hepatitis: bodies defense
only body defense is formation of antibodies via vaccination
Viral hepatitis: supportive measures
Rest, diet high in protein, carbohydrate, and vitamins
Chronic hepatitis can be treated with interferon: what does this do?
Decrease viral replication
- effective 30-40% ind.
- drug combination (slow-acting interferon plus antiviral drugs) more effective
Toxic or nonviral Hepatitis
Variety of hepatotoxins can cause inflammation and necrosis of the liver.
May result from sudden exposure to large amounts or from lower dose and long-term exposure
drugs and chemicals that can cause Toxic or nonviral Hepatitis
Drugs include:
Acetaminophen, halothane, phenothiazines, tetracycline
Chemicals include: Carbon tetrachloride (not used currently), toluene, ethanol
Cirrhosis
Progressive destruction of liver
Cirrhosis causes
alcoholism
biliary cirrhosis
postnectrotic cirrhosis
metabolic abnormalities
biliary cirrhosis associated with
associated with immune disorders
Postnectrotic cirrhosis
Linked with chronic hepatitis or long-term exposure to toxic materials
Cirrhosis leads to
Extensive diffuse fibrosis
- Interferes with blood supply
- Bile may back up.
Loss of lobular organization
Degenerative changes may be asymptomatic until disease is well advanced.
Cirrhosis diagnosis
Liver biopsy and serologic test to determine cause and extent of damage
Cirrhosis (Alcoholic Liver Disease): initial stage
Fatty liver
- enlargement of liver
- Asymptomatic and reversible with reduced alcohol intake
Cirrhosis (Alcoholic Liver Disease): second stage
Alcoholic Hepatitis
a. inflammation / cell necrosis
b. fibrous tissue formation (irreversible)
Cirrhosis (Alcoholic Liver Disease): third stage
End stage cirrhosis
a. fibrotic tissue replaces normal tissue
b. little normal function remains
slide 80: functional loss with cirrhosis
go look
Cirrhosis: initial manifestations
Mild and vague
- chronic infection s/s
- dull aching pain may be present in upper right abdominal quadrant
Advanced cirrhosis s/s
Ascites and peripheral edema increased bruising esophageal varies jaundice encephalopathy
Cirrhosis treatment
Avoidance of alcohol Supportive or symptomatic treatment Dietary restriction Balancing serum electrolytes Paracentesis Antibiotics Liver transplant
Hepatocelluar carcinoma
most common primary tumor of liver
- more common in cirrhotic livers
Liver cancer: secondary or metastatic cancer
Arises from areas served by the hepatic vein or spread along the peritoneal membranes
liver cancer: initial signs and diagnosis
signs: mild and general
Diagnosis: usually occurs with advanced stages
liver cancer treatment
possible lobectomy, radio-frequency ablation (RFA) procedure
Acute pancreatitis
Inflammation of pancreas; results in auto-digestion of tissue
causes of acute pancreatitis
- gallstones
- alc abuse
- sudden onset may follow large meal or large amount of alcohol
pancreatitis can be acute or chronic, what is acute consider?
medical emergency
describe patho of pancreatitis
Pancreas lacks capsule
- substances released by necrotic tissue lead to widespread inflammation
- destruction may progress into tissue surrounding pancreas
Acute pancreatitis
Severe epigastric/abdominal pain radiating to back
signs of shock
low grade fever until infection develops
abdominal distention (decreased peristalsis and paralytic ileus)
Acute pancreatitis Diagnostic tests
Serum amylase levels—first rise, then fall after 48 hours
Serum lipid levels are elevated.
Hypocalcemia
Leukocytosis
Acute pancreatitis treatment
Oral intake is stopped.
Treatment of shock and electrolyte imbalances
Analgesics for pain relief
Pancreatic cancer risk factors
smoking
pancreatitis and dietary factors
Adenocarcinoma
most common type of Pancreatic cancer
- arises in ducts
Pancreatic cancer early manifestions
weight loss and jaundice
Pancreatic cancer mortality rate
metastases occur early
- mortality 95%
celiac disease
Malabsorption syndrome; genetics
celiac disease defect is where
intestinal enzyme (gliadin)
- prevents the breakdown of gluten
- atrophy of villi in intestine
celiac disease: first signs
usually as children when cereals are first introduced into the diet
celiac disease manifestations
Steatorrhea, muscle wasting, failure to gain weight
Irritability and malaise common
celiac disease diagnosis
blood tests
celiac disease treatment
gluten free diet, intestinal mucosa returns to normal after a few weeks without gluten
Chron disease: where?
May affect anywhere in digestive tract, SI most affects
Chron disease: describe the inflammatoin
inflammation occurs in characterist distribution
-“skip” lesions - affected areas are separated by areas of normal tissue
Chron disease: what causes obstructed areas?
Progressive inflammation and fibrosis
- damaged walls impair processing and absorption of food
- inflammation stimulates intestinal motililty
Chron disease interferes with digestion and absoption, leading to what?
Hypoproteinemia, avitaminosis, malnutrition, possibly steatorrhea
complications of Chrons disease
Adhesions between loops may form and fistulas may develop.
Chrons disease in children: complications
delayed growth and sexual maturation
Chrons disease treatment
Glucocorticoids
Ulcerative colitis
inflammation starts in rectum and progresses through colon. mucosa and submucosa are inflammed.
Ulcerative colitis: tissue destruction inferes with what
absorption of fluid and electrolytes in colon
Ulcerative colitis: when might megacolon develop
severe acute episodes
Ulcerative colitis s/s
diarrhea, up to 12 a day
- contains blood and mucus
- cramps
IBS manifestions
Lower abdominal pain
Diarrhea
Constipation, alternating with diarrhea
Bloating, nausea
IBS diagnosis
signs and symptoms
- Testing for food allergies
- Testing for bacterial or parasitic infections
- No single cure for IBS
IBS treatment
Team approach Anti-inflammatory meds Antimotility agents Nutritrional supplements Antimicrobials Immunotherapeutic agents Surgical resection
Appendicitis
Obstruction of lumen; fluid builds inside
- purulent exudate, swollen
Appendicitis treatment
surgical removal and antimicrobial drugs
treatment of diverticulitis
antimicrobial drugs
dietary modifications to prevent stasis
Diverticulitis stasis
material trapped in pouch leads to inflammation and infection
colorectal cancer: most malignancies develop from what
adenomatous polyps
- early diagnosis essential
colorectal cancer: risk factors
genetics
Long-term ulcerative colitis
environmental factors (low fiber)
colorectal cancer. treatment
surgical removal with radiation and or chemo
intestinal obstruction: what
lack of movement of intestinal content through intestine - most common in SI
intestinal obstruction: mechanical obstruction
Result from tumors, adhesions, hernias, other tangible obstructions
intestinal obstruction: functional or adynamic obstructions
result from impairment of peristalsis
- spinal cord injry
Peritonitis
inflammtion of peritoneal membranes
Chemical peritonitis may result from
Enzymes released with pancreatitis
Urine leaking form a ruptured bladder
Chyme spilled from a perforated ulcer
Bile escaping from the ruptured gallbladder
Blood
Any other foreign material in the cavity
Bacterial peritonitis caused by
Direct trauma affecting the intestine
Ruptured appendix
Intestinal obstruction and gangrene
pelvin inflammatory disease in women
when (peritonitis) infection reaches the cavity through fallopian tubes