digestive system Flashcards
describe the etiology and pathophysiology of hiatal hernias
stomach pushes up through opening in the diaphragm into the thoracic cavity, hernia can cut off blood supply to the stomach (strangulate)
describe the manifestations of hiatal hernias
dysphasia, GERD symptoms, could be asymptomatic, epigastric discomfort
describe the diagnosis, treatments, and complications of hiatal hernias
endoscopy and barium swallow
PPIs, H2 blockers, surgery, lifestyle changes
describe the etiology and pathophysiology of GERD
lower esophageal sphincter remains relaxed or weakened, regurgitation of stomach contents and acid into the esophagus and esophagus fails to push it back into the stomach. acidic gastric fluid causes mucosal damage, meta plasma of esophageal epithelial cells transform to stomach-like columnar cells
occurs more than twice a week for at least a few weeks, exacerbated by pregnancy, obesity, fatty foods, alcohol, coffee, smoking, gastroparesis, lying down
describe the manifestations of GERD
dysphasia, heartburn, epigastric pain, regurgitation, dyspepsia, laryngitis, trigger asthma attacks, coughing, aspiration
describe the diagnosis, treatment, and complications of GERD
dx: history, acid suppression trail, endoscopy
t: elevate head of bed 4-6 inches on blocks, lifestyle changes (eat sitting up, eat hours before bed, weight loss PPIs, antacids), laparoscopic anti reflux (fundoplication)
c: can lead to barrett’s esophagus and strictures
describe the etiology and pathophysiology of esophageal cancer
squamous: cancer invades lining of esophagus- more common with smoking and alcohol
adenocarcinoma: glandular tissue near stomach- more common with barrett’s esophagus
risks: >65, male, chronic alcohol use, smoking, barrett’s esophagus due to GERD
describe the manifestations of esophageal cancer
dysphasia, weight loss, change in eating patterns
describe the diagnosis, treatment, and complications of esophageal cancer
endoscopy and tissue biopsy
surgical resection, radiation, chemo
describe the etiology and pathophysiology of acute gastritis
acute and usually transient inflammation of the stomach lining
causes: medications (aspirin, NSAID), bacterial infection, alcohol abuse, corticosteroids, chemo, radiation to stomach, acute stress, infection, bile reflux
describe the manifestations of gastritis
epigastric pain, typically accompanied with nausea and vomiting
describe the diagnosis, treatments, and complications of gastritis
history and endoscopy
self-limiting, remove causative agents
describe the etiology and pathophysiology of chronic gastritis
causes atrophy of glandular stomach lining caused by autoimmune response with antibodies to gastric gland parietal cells
decreased intrinsic factor causes reduced iron absorption and anemia
describe the manifestations of chronic gastritis
few symptoms related to gastric changes if mild or moderate
describe the diagnosis, treatment, and complications of chronic gastritis
dx: endoscopy, biopsy, B12 tests
t: acid reducers, b12 and iron supple,ets for strophic gastritis
describe the etiology and pathophysiology of HP gastritis
HP colonize on mucus secreting epithelial cells of stomach lining (production of ammonia protects them from stomach acid)
HP enzymes/toxins irritate and erode stomach mucosa
HP are immunogenicity and cause inflammatory changes
describe the diagnosis and treatments of HP gastritis
endoscopy, breath and stool tests
antibiotics
describe the etiology and pathophysiology of PUD
inflammatory erosion of stomach or duodenum
hypersecretion of acid and pepsin, causing ineffective GI mucus production and poor cellular repair
caused by HP, NSAIDs, stress, alcohol, excessive caffeine, smoking, steroids, genetics
describe the manifestations of PUD
intense burning and gnawing pain occurring more frequently with an empty stomach that is relieved with antacids and eating
abdominal tenderness
chronic bleeding, hemorrhage, melena, hematemesis, and anemia
preforation of the stomach/intestine (peritonitis)
gastric outlet obstruction from scarring
describe the diagnosis, treatments, and complications of PUD
history (NSAID use important), serology and rapid urease test to detect HP, endoscopy
reduce acid levels, PPIs and H2 blockers, sucralfate to protect ulcers from acid, lifestyle changes, thermal coagulation therapy, hemp static clips, fibrin sealant
describe the etiology and pathophysiology of stomach cancer
risk factors include genetics, diets high in smoked/preserved foods (due to N-nitroso and benzopyrene), HP infection, autoimmune gastritis
describe the manifestations of stomach cancer
asymptomatic until cancer has metastasized
abdominal discomfort, appetite loss (meat), bleeding
describe the diagnosis, treatment, and complications of stomach cancer
endoscopy, CT, biopsy, ultrasound
surgery, radiation, chemo
describe the etiology and pathophysiology of irritable bowel syndrome
a functional GI disorder characterized by variable chronic and recurrent intestinal symptoms
no specific pathology- intestinal lining appears normal. could be a result of dysregulation of intestinal motor activity from the CNS, symptoms occur with mental/physical stress
describe the manifestations of irritable bowel syndrome
abdominal pain relieved by defecation and associated with a change in stool
chronic intermittent cramping lower abdominal pain lasting at least 12 weeks with diarrhea and constipation
abdominal dissension and bloating
describe the diagnosis, treatment, and complications of irritable bowel syndrome
dx: patient symptoms, diagnostic tests to rule out other conditions
t: stress management, regulate bowel movements, dietary management (avoid trigger foods)
c: more common in women, associated with lactose intolerance
describe the etiology and pathophysiology of inflammatory bowel disease
chronic, incurable with unclear etiology. more prevalent in young adults
strongly associated with smoking
antibiotic use earlier in life
describe the manifestations of inflammatory bowel disease
diarrhea
fecal urgency
weight loss
abdominal pain
malabsorption and nutritional deficiencies common
anemia from loss of blood in the stool
dehydration
arthritis, uveitis, dermatology issues
describe the diagnosis, treatment, and complications of inflammatory bowel disease
endoscopy with biopsy, history, stool studies
describe the etiology and pathophysiology of chron’s disease
chronic, transmural inflammatory process
affects GI tract from mouth to anus
distal small intestines and ascending colon
skip lesions
granulomas form in intestine (cobblestoning)
can cause fistulas between GI tract and other sites
describe the manifestations of chron’s disease
abdominal cramping
diarrhea
fatigue
blood in stool
mouth sores
reduced appetite
weight loss
describe the diagnosis, treatment, and complications of chron’s disease
no cure- goal is remission
diet management and vitamin supplements
antidiarrheals
abdominal cramping inhibitors/antispasmodics
immunosuppressants
surgery (resection of bowel parts)
describe the etiology and pathophysiology of ulcerative colitis
involves large intestine starting in rectum moving upward through colon
mostly mucosal
lesions form in mucosal base layer, develop into crypt abscesses that can ulcerate
pseudopolyps
increases risk for colon cancer
describe the manifestations of ulcerative colitis
persistent diarrhea (10 bowl movements a day)
abdominal pain
distinction lasting days to months then remission and recurrence
describe the diagnosis, treatment, and complications of ulcerative colitis
can be cured with removal of all or part of rectum/colon
avoid trigger foods
fiber supplements
corticosteroids
anti-inflammatories
antidiarrheal
colon cancer screening
describe the etiology and pathophysiology of infectious enterocolitis
irritation in stomach, small or large intestine by pathogen or toxin
can be transmitted person to person (fecal oral), water, or food borne
damage of villi by pathogen or toxins
increased fluid shift into lumen of intestine, resulting in diarrhea (osmotic, inflammatory, secretory)
describe the pathogens in infectious enterocolitis
virus: affect superficial epithelium of small intestine (noro and rita virus)
bacteria: produce endotoxins that destroy mucosal epithelial cells
s. aureus, e. coli, salmonella
clostridium difficult colitis
describe the manifestations of infectious enterocolitis
nausea
vomiting
diarrhea
hyperactive bowels
electrolytes lost (potassium)
condition persists 2-10 days
describe the diagnosis, treatment, and complications of infectious enterocolitis
stool studies, history
IV fluid replacement
electorate replacement
bowel rest then BRAT diet
no dairy
probiotics
antibiotics and stool transplant for C. difficile
describe the etiology and pathophysiology of diverticular disease
colonic longitudinal uncles do not normally form a continuous layer, when bowel contracts bulging occurs between bands of muscle, when intraluminal pressure increases in haustra, walls herniate causing diverticula
low fiber diet major risk factor
describe the manifestations of diverticular disease
depend on severity of inflammation and location in bowels
abdominal pain, tenderness in lower left quadrant, nausea, vomiting, fever, altered bowel habits
describe the diagnosis, treatment, and complications of diverticular disease
abdominal x-ray, ultrasound, CT scan
dietary modification, adequate fluid and fiber intake, bowel training to ensure 1 per day, severe cases may require NPO, antibiotics/anti fungal, colectomy (partial or full)
diverticula
small outpouchings formed, can collect intestinal contents and form a colonic obstruction, most common in sigmoid and descending colon
diverticulosis
the condition of having diverticula
diverticulitis
inflammation of the diverticula
meckel diverticulum
an asymptomatic outpouching of all the layers of the small intestine wall
describe the etiology and pathophysiology of appendicitis
appendix becomes inflamed and gangrenous
can rupture or perforate releasing gut bacteria into abdomen, causing peritonitis
related to intraluminal obstructions from fecaliths (hard stool, gall stones, tumors, lymph nodes)
describe the manifestations of appendicitis
sudden onset of abdominal pain originating umbilical region and moves to RLQ (mcburney’s point)
abdominal distinction and rebound tenderness
nausea, vomiting, fever, diarrhea, constipation
describe the diagnosis, treatments, and complications of appendicitis
physical examination, abdominal x-ray or ultrasound, CT scan, elevated WBC levels
antibiotics, surgical removal
describe the etiology and pathophysiology of peritonitis
bacterial infection or leakage of intestinal content into peritoneal cavity
inflammation of peritoneum, it secretes a thick/sticky/fibrinous substance that seals off the damages of perforated area, motility area is also decreased. both limit spread of infection
gas and air build up in area of infection and low motility increases the pressure in the bowel
fluids shift into peritoneal cavity and bowel due to obstruction and pressure
what are the possible causes of peritonitis?
appendicitis, diverticulitis, ulcers, trauma, etc
describe the manifestations of peritonitis
classic triad (pain, rigidity, tenderness)
blood and fluid shift into peritoneum
fever, nausea, vomiting
septic shock
electrolyte imbalances
describe the diagnosis, treatment, and complications of peritonitis
abdominal x-ray- free air under diaphragm if organ perforation
paracentesis- sample of peritoneal fluid
confirm with CT scan or laparotomy
peritoneal lavage, IV fluids, IV antibiotics, insertion of a nasogastric tube (decompress GI tract), surgery to remove source of infection
complication: decreased motility of intestine, undirected content isn’t moved further
describe the etiology and pathophysiology of celiac disease
hypersensitivity reaction to gluten, genetic and autoimmune disease
inappropriate T cell mediated disorder against alpha gliadin
inflamed gut loses absorptive villi (can’t absorb nutrients)
risk factors: turner syndrome, autoimmune diseases, diabetes 1
describe the manifestations of celiac disease
gluten ingestion triggers symptoms
steatorrhea (loss of fat in stools) may develop
malnutrition is a concern (weight loss, hair and nail changes, impaired growth and development in infants and children)
cramps, bloating, gas, diarrhea, constipation
describe the diagnosis, treatments, and complications of celiac disease
serology (positive antibody tiger of IgA TTG)
intestinal biopsy
remove all gluten from diet
describe the etiology and pathophysiology of adenomatous polyps
most common intestinal neoplasm; a mass that protrudes into the lumen of the gut. can be sessile (raised) or pedunculated (on a stalk), benign, or malignant
altered replication of the crypt epithelial cells causes benign mucosal neoplasms from cells that have proliferated beyond what was needed to replace cells that are normally shed and die through apoptosis, common in rectal and sigmoid colon
can be tubular, villous, tubulovillous
precancerous
RF: aging, genetics, IBD, smoking, alcohol use, obesity
describe the manifestations of adenomatous polyps
usually none
bowel changes
stool changes
blood in stool
abdominal pain
describe the diagnosis, treatment, and complications of adenomatous polyps
endoscopy
surgical removal
describe the etiology and pathophysiology of colorectal cancer
cause is unknown
RF: colon polyps, aging (40s), family history, IBD, high fat/sugar low fiber diet, decreased vitamin intake, aspirin use decreases risk
describe the manifestations of colorectal cancer
usually none for a long time
bleeding
change in bowel habits and/or stool characteristics
describe the diagnosis, treatment, and complications of colorectal cancer
colonoscopy, fecal occult blood test, barium enema, rectal examination
surgical removal- only known recognized primary treatment
chemotherapy and radiation for adjunctive therapy
describe the etiology and pathophysiology of alcohol induced liver disease
acute disorder that is reversible with transient symptoms. will resolve with cessation of alcohol ingestion, long-term effects can remain. liver becomes modular and misshapen, nodules compress hepatic veins, impairing the outflow of blood causing portal hypotension
alcohol is a potent toxin to hepatomata’s, which are metabolized in the liver by ADH and MEOS. H+ and free radicals are produced.
ADH: H+ forms nicotinamide adenine dinucleotide, causes liver cell damage and disrupts metabolic process
MEOS: acetaldehyde and free radicals are produced. this damages hepatic yes, increases fat synthesis in the liver, and increases collagen and fibrogenesis. can progress to hepatitis and cirrhosis
describe the manifestations of alcohol induced liver disease
RUQ pain and tenderness
nausea
malaise
jaundice
fever
darkened urine
hepatomegaly
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hepatic encephalopathy
confusion
disorientation
stupor
coagulation dysfunction
spontaneous bruising and bleeding
hyperbilirubinemia
jaundice
hematemesis
hepatomegaly
splenomegaly
portal hypertension with esophageal varicose
ascites
spider angioma
proximal muscle wasting
gynecomastia in males
restlessness
mood disturbance
delirium tremens
seizures
describe the diagnosis, treatments, and complications of alcohol induced liver disease
AST and ALT elevation
hypertriglyceridemia
hypercholesterolemia
hyperbilirubinemia
hypoalbuminemia
coagulation disturbances
liver biopsy
cessation of alcohol, improve nutrition, high protein diet, improvement of liver function if there is six months of abstinence from alcohol
describe the etiology and pathophysiology of nonalcoholic fatty liver disease
associated with metabolic syndrome, insulin resistance, and obesity due to the lipids accumulating in hepatocytes and formation of free radicals. hepatocytes accumulate triglycerides and free fatty acids, which induce free radical formation. these free radicals damage hepatocytes. cells can rupture causing inflammatory response which is damaging to liver
describe the manifestations of nonalcoholic fatty liver disease
abnormal liver enzyme levels may be present
NASH: edema, jaundice, fatigue, obvious signs of liver impairment
can lead to hepatocellular carcinoma (HCC)
describe the diagnosis, treatment, and complications of nonalcoholic fatty liver disease
no specific bio markers or blood tests
liver biopsy is key test
false negative if sample is not taken from high fat content area
patient who is obese, metabolic syndrome with elevated liver enzymes should be evaluated for NAFLD
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weight loss and exercise, bariatric surgery, medication
describe the etiology and pathophysiology of cirrhosis
silent and gradual. liver is irreversibly damaged with collagen and fibrous tissue infiltration
cause: HCV, alcoholic liver disease, NAFLD
describe the manifestations of cirrhosis
decreased bile synthesis
decreased fat digestion and steatorrhea
decreased coagulation factors- bruising and bleeding
decreased albumin synthesis- edema and ascites
lack of thrombopoietin- low platelets and bleeding
decreased conjugation of bilirubin- jaundice
loss of detoxification process- high levels of drugs and hormones
loss of destination process- high nitrogen in blood, lyses RBCs and platelets
anemia and thrombocytopenia
hypocalcemia
hepatic encephalopathy
hepatorenal syndrome
describe the diagnosis, treatment, and complications of cirrhosis
blood test
CBC, metabolic panel, liver panel
abstinence from alcohol, good nutrition, management of complications, liver transplant
describe the etiology and pathophysiology of liver cancer
primary cancer starts in liver, secondary is metastatic tumors from other cancers
rf: chronic hepatitis and cirrhosis leads to repeated cell damage, death, and regeneration. there’s an increased risk of cellular mutations that become cancerous cells
describe the manifestations of liver cancer
symptoms occur late and are same as those for hepatitis and liver failure
paraneoplastic syndromes: due to ectopic hormones and growth factors
describe the diagnosis, treatment, and complications of liver cancer
routine screening for people with chronic hepatitis or carriers
ultrasound, CT, MRI
liver biopsy
surgical resection, ablation, chemo, radiation
describe the etiology and pathophysiology of cholecystitis
acute or chronic inflammation of the gallbladder.
gallstones: most common cause, concentrated bile salts damage gallbladder mucosal cells
acalculous cholecystitis: inflammation without stones due to trauma, burns, sludge, can result in gangrene and perforation
describe the manifestations of cholecystitis
RUQ episodic colicky pain after eating especially fatty meals
anorexia and feeling of fullness
mild fever
mild elevation in AST, ALT, WBC, bilirubin, alkaline phosphatase
describe the diagnosis, treatment, and complications of cholecystitis
WBC, ESR, C-RP elevation
liver enzymes
bilirubin levels
abdominal ultrasound
cholecystogram
CT and ERCP
HIDA scan
cholecystectomy
lithotripsy
pain medications
oral medications can be used to reduce gallstones (ursodiol)
low fat diet
describe the etiology and pathophysiology of pancreatitis
autodigestion by pancreas’s own digestive enzymes due to trypsin activation results in inflammatory response which further damages tissues. this causes pancreatic insufficiency and malabsorption. acute forms are caused by alcohol and gallstones. risks: hyperlipidemia, hypercalcemia, surgical trauma, medications
describe the manifestations of pancreatitis
LUQ pain/tenderness, nausea/vomiting/diarrhea, fever, tachycardia, dehydration, malnutrition, jaundice
describe the diagnosis, treatment, and complications of pancreatitis
dx: ranson’s criteria, elevated WBC/ESR/C-RP, liver function tests, serum amylase and lipase elevate with pancreatic inflammation, abdominal ultrasound, endoscopic retrograde cholangiopancreatography
t: supportive management, IV fluids, nasogastric suction, pain management, ursodial used to dissolve biliary stones, nasogastric feedings may be needed, surgery for acute abdomen, no alcohol
c: infected pancreatic necrosis, pancreatic pseudocysts, hypotension, renal failure, liver failure, respiratory failure (ARDS)
