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patho unit 3 > digestive system > Flashcards

digestive system Flashcards

1
Q

describe the etiology and pathophysiology of hiatal hernias

A

stomach pushes up through opening in the diaphragm into the thoracic cavity, hernia can cut off blood supply to the stomach (strangulate)

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2
Q

describe the manifestations of hiatal hernias

A

dysphasia, GERD symptoms, could be asymptomatic, epigastric discomfort

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3
Q

describe the diagnosis, treatments, and complications of hiatal hernias

A

endoscopy and barium swallow

PPIs, H2 blockers, surgery, lifestyle changes

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4
Q

describe the etiology and pathophysiology of GERD

A

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

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5
Q

describe the manifestations of GERD

A

dysphasia, heartburn, epigastric pain, regurgitation, dyspepsia, laryngitis, trigger asthma attacks, coughing, aspiration

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6
Q

describe the diagnosis, treatment, and complications of GERD

A

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

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7
Q

describe the etiology and pathophysiology of esophageal cancer

A

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

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8
Q

describe the manifestations of esophageal cancer

A

dysphasia, weight loss, change in eating patterns

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9
Q

describe the diagnosis, treatment, and complications of esophageal cancer

A

endoscopy and tissue biopsy

surgical resection, radiation, chemo

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10
Q

describe the etiology and pathophysiology of acute gastritis

A

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

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11
Q

describe the manifestations of gastritis

A

epigastric pain, typically accompanied with nausea and vomiting

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12
Q

describe the diagnosis, treatments, and complications of gastritis

A

history and endoscopy

self-limiting, remove causative agents

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13
Q

describe the etiology and pathophysiology of chronic gastritis

A

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

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14
Q

describe the manifestations of chronic gastritis

A

few symptoms related to gastric changes if mild or moderate

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15
Q

describe the diagnosis, treatment, and complications of chronic gastritis

A

dx: endoscopy, biopsy, B12 tests

t: acid reducers, b12 and iron supple,ets for strophic gastritis

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16
Q

describe the etiology and pathophysiology of HP gastritis

A

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

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17
Q

describe the diagnosis and treatments of HP gastritis

A

endoscopy, breath and stool tests

antibiotics

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18
Q

describe the etiology and pathophysiology of PUD

A

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

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19
Q

describe the manifestations of PUD

A

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

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20
Q

describe the diagnosis, treatments, and complications of PUD

A

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

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21
Q

describe the etiology and pathophysiology of stomach cancer

A

risk factors include genetics, diets high in smoked/preserved foods (due to N-nitroso and benzopyrene), HP infection, autoimmune gastritis

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22
Q

describe the manifestations of stomach cancer

A

asymptomatic until cancer has metastasized

abdominal discomfort, appetite loss (meat), bleeding

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23
Q

describe the diagnosis, treatment, and complications of stomach cancer

A

endoscopy, CT, biopsy, ultrasound

surgery, radiation, chemo

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24
Q

describe the etiology and pathophysiology of irritable bowel syndrome

A

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

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25
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
26
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
27
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
28
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
29
describe the diagnosis, treatment, and complications of inflammatory bowel disease
endoscopy with biopsy, history, stool studies
30
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
31
describe the manifestations of chron’s disease
abdominal cramping diarrhea fatigue blood in stool mouth sores reduced appetite weight loss
32
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)
33
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
34
describe the manifestations of ulcerative colitis
persistent diarrhea (10 bowl movements a day) abdominal pain distinction lasting days to months then remission and recurrence
35
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
36
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)
37
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
38
describe the manifestations of infectious enterocolitis
nausea vomiting diarrhea hyperactive bowels electrolytes lost (potassium) condition persists 2-10 days
39
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
40
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
41
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
42
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)
43
diverticula
small outpouchings formed, can collect intestinal contents and form a colonic obstruction, most common in sigmoid and descending colon
44
diverticulosis
the condition of having diverticula
45
diverticulitis
inflammation of the diverticula
46
meckel diverticulum
an asymptomatic outpouching of all the layers of the small intestine wall
47
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)
48
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
49
describe the diagnosis, treatments, and complications of appendicitis
physical examination, abdominal x-ray or ultrasound, CT scan, elevated WBC levels antibiotics, surgical removal
50
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
51
what are the possible causes of peritonitis?
appendicitis, diverticulitis, ulcers, trauma, etc
52
describe the manifestations of peritonitis
classic triad (pain, rigidity, tenderness) blood and fluid shift into peritoneum fever, nausea, vomiting septic shock electrolyte imbalances
53
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
54
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
55
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
56
describe the diagnosis, treatments, and complications of celiac disease
serology (positive antibody tiger of IgA TTG) intestinal biopsy remove all gluten from diet
57
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
58
describe the manifestations of adenomatous polyps
usually none bowel changes stool changes blood in stool abdominal pain
59
describe the diagnosis, treatment, and complications of adenomatous polyps
endoscopy surgical removal
60
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
61
describe the manifestations of colorectal cancer
usually none for a long time bleeding change in bowel habits and/or stool characteristics
62
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
63
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
64
describe the manifestations of alcohol induced liver disease
RUQ pain and tenderness nausea malaise jaundice fever darkened urine hepatomegaly ————- 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
65
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
66
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
67
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)
68
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 ————————— weight loss and exercise, bariatric surgery, medication
69
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
70
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
71
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
72
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
73
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
74
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
75
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
76
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
77
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
78
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
79
describe the manifestations of pancreatitis
LUQ pain/tenderness, nausea/vomiting/diarrhea, fever, tachycardia, dehydration, malnutrition, jaundice
80
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)

patho unit 3 (6 decks)

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