Exam 6: GI Disorders Flashcards

1
Q

gastric parietal cells

A

secrete hydrochloric acid and intrinsic factor -> necessary for the absorption of vitamin B12 in the small intestine

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2
Q

gastric goblet cells

A

secrete mucus and prostaglandin E2 (PGE2), a lipid-rich molecule, which exerts a strong protective effect. PGE2 stimulates gastric mucus production and bicarbonate secretion, which reduce the effects of HCL

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3
Q

GERD

A

Epi: most common GI disorder

Patho: Decreased closure of the LES, which allows acidic gastric contents to reflux up into the esophagus. Acid of the stomach damages the esophageal epithelium.

Two types: erosive or non-erosive (difference in damage to esophageal mucosa)

CM: Frequent heartburn = pyrosis, reflux (regurgitation) with bitter taste gastric contents into mouth, dysphagia, chest pain, chronic cough, hoarseness, wheezing

Complication: metaplasia of cells at the gastroesophageal junction = Barrett’s esophagus = can lead to esophageal cancer

Diagnosis: S/S, endoscopy, pH testing, biopsy

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4
Q

Hiatal hernia

A

Protrusion or herniation of the stomach through the esophageal hiatus of the diaphragm

Sliding hiatal hernia is common, non-significant in asymptomatic people

With GERD and large hiatal hernia can cause further irritation/pain requiring intervention

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5
Q

Peptic ulcer disease (PUD)

A

Inflammatory erosion in the stomach or duodenal lining. Ulceration occurs four times more often in the duodenum than in the stomach.

Etiology: H. Pylori & NSAIDS. Advanced age, prior PUD

Patho: exact process not clearly known. H. Pylori induce inflammation release cytokines to continue to mucosal damage. NSAIDS like aspirin thought to inhibit prostaglandin synthesis.

CM: epigastric pain, burning/gnawing, b/t meals, comes and goes

Diagnosis: endoscopy, biopsy for H. Pylori

Complications: Can lead to perforation (peritonitis), hemorrhage (acute abdominal pain), penetration

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6
Q

Upper GI bleed

A

bleeding in the esophagus, stomach, or duodenum (from lesion, erosion, ulceration, varicosed vein)

CM: Hematemesis, coffee ground emesis, melena
Slow chronic bleed -> iron deficiency anemia, fatigue, lethargy
Acute large GI bleed -> anxiety, dizziness, weakness, shortness of breath, tachycardia, tachypnea, pallor

Diagnostic: CBC, Endoscopy, positive FOBT

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7
Q

Pyloric stenosis

A

Constriction of the pyloric sphincter that impairs the movement of gastric contents into the small intestines

Etiology: build up of thick muscularis layer or fibrous tissue from PUD

CM: Delayed emptying of the gastric contents causes distension, can develop into pyloric obstruction

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8
Q

Bowel obstruction

A

Etiology: mechanical physical obstruction (adhesions, hernia, neoplasms) or nonmechanical which is reduced or absent peristalsis. (Paralytic ileus, Crohn’s, gallstones, intussusception, volvulus)

CM: vary depending on severity -> Abdominal pain, distention distal to site, N/V, hyperactive bowel sounds. Pain occurs in waves with peristalsis. partial = liquid diarrhea.

Diagnosis: Abdominal X-Ray -> excessive gas proximal to obstruction, CT & US

Complications: ischemic bowel, perforation, shock, infection, death. Can have fluid and electrolyte imbalances *small bowel absorbs a lot of water

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9
Q

Small bowel obstruction

A

post-surgery adhesions (bond sections of intestine together) -> typically requires surg intervention

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10
Q

Large bowel obstruction

A

colon cancer, diverticular disease, volvulus

generally in the stigmoid colon

high mortality if not caught early

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11
Q

Celiac disease

A

autoimmune disease w/ genetic component triggered from environmental (gluten)

patho: destroys intestinal villi from inflammation, flattens intestinal wall and reduces absorption

CM: excessive gas, muscle wasting, steatorrhea, weight loss, concern for anemias from lack of absorption of protein

diagnosis: serology celiac panel (immune) -> positive antibody titer of IgA, upper endoscopy

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12
Q

Irritable bowel syndrome (IBS)

A

Altered bowel activity and S/S w/ no pathological change

Experience periods of frequent abdominal pain, bloating, constipation/diarrhea, mucus in stools

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13
Q

Inflammatory bowel disease (IBD)

A

Pathological changes to the GI track
Failure of immune regulation
Ulcerative colitis
Crohn’s disease

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14
Q

Crohn’s disease

A

unclear etiology (genetics, autoimmune, environment)

entire bowel wall and all layers affected - any area of GI tract, chronic inflammation -> large immune response,

**skip lesions (patchy through small & large). risk for fistulas or abscesses

CM: abdominal pain, diarrhea, fatigue, weight loss

Diagnosis: colonscopy/endoscopy, biopsy, anemia labs

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15
Q

Ulcerative colitis

A

unclear etiology

episodes of inflammation in colon and rectum (inc in T, B, plasma IgG & IgE)

**continuous inflammation large bowel only

risk for colorectal cancer

CM: diarrhea, abd pain, melena

Diagnosis: scopy (psuedopolyps seen)

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16
Q

Appendicitis

A

Children/YA more common; can be caused by trauma

Patho: narrowing of the lumen from obstruction (build up of bacteria/inflammation) leads to ischemia

CM: starts vague abd pain -> RLQ, radiates from umblicus to RLQ (Psoas, Rovsing’s, & Obturator’s signs)

Needs surgical treatment or could rupture

HCG to r/o ectopic, UA to r/o stone or pylo

17
Q

Diverticulitis

A

Patho: weakened bowel wall muscles -> protrusion of diverticula which can fill with intestinal content and become inflammed -> can lead to a mass/obstruction

CM: LLQ abd pain, N/V, fever, constipation/diarrhea

Diagnosis: ^ CRP (>50), ^ WBCs, abd imaging

18
Q

Peritonitis

A

inflammation of peritoneum

can happen after perforation (trauma, ulcer, appendix, diverticula) surgery, or ectopic preg

CM: rebound tenderness, distention/rigid abd, fever

19
Q

Bilirubin metabolism

A

bilirubin from RBC breakdown (unconjugated)

Liver converts to water soluble form (conjugated)

conjugated excreted in bile -> feces

20
Q

Protein metabolism

A

Liver synthesizes and breaks down protein -> creates ammonia to be able to break down

ammonia (NH3) is integrated into urea and excreted through kidneys

21
Q

Stages of hepatitis

A

Prodromal (preicterus period)

Icterus period
7-14 days

Recovery period
1-4 months

Carrier state: infection with HBV and HCV no symptoms but can transmit
*no carrier state for HAV

22
Q

Hep A

A

fecal-oral route

Diagnosis: elevated IgM and antibodies to A (IgG anti HAV)

self-limiting
no carrier state

23
Q

Hep B

A

blood/sexual contact

most don’t recover entirely -> can lead to cirrhosis or failure or cancer

Diagnosis: HBsAg antigen and antibodies, best indicator is HBV DNA in serum (HBcAg)

24
Q

Hep C

A

blood (IV use)

lots of carriers and asymptomatic

AST, ALT, HCV antibody testing

25
Q

alcoholic liver disease

A

pts w/ 30 or more grams of ETOH

broken into 3 stages
Fatty liver: accumulation of fat in hepatocytes (steatosis) liver yellow and enlarged
Alcoholic hepatitis: increase in alcohol intake leads to inflammation and necrosis of liver cells. Hepatic tenderness, pain, anorexia, nausea, fever, jaundice, ascites or liver failure can be fatal
Alcoholic cirrhosis: continued drinking leads to fibrotic liver and end stage liver diseases

26
Q

Non-alcoholic fatty liver disease

A

liver has fat tissue in the cells in many cases from type II diabetes, metabolic syndrome or hyperlipidemia

asymptomatic, need biopsy.

NASH or nonalcoholic steatohepatitis same idea.

27
Q

Cirrhosis

A

Functional liver w/ fibrous tissue and nodules -> vascular disruption and blockages

CM: RUQ tender, jaundice (hyperbilirubinemia), spider angioma, caput medusa, steatorrhea, dark urine, hepatic encephalopathy, **portal HTN, ascites, esophageal varices

Diagnosis: ^ AST and ALT, hypertriglyceridemia, hypercholesterolemia, hyperbilirubinemia, hypoalbuminemia, coag disturbances
US & biopsy

28
Q

Portal hypertension

A

Fibrotic liver pushing on the hepatic portal vein.

build up of fluid and this fluid has to go somewhere so it builds up in other veins and out into the peritoneal cavity -> ascites

Collateral veins also develop to take off pressure, but these vessels are weak and easily rupture. -> esophageal varices which are prone to rupture and cause an upper GI bleed

29
Q

Pancreatitis

A

Etiology: gallstones (blockage) or ETOH abuse

Digestive enzymes perform autodigestion and damage pancreatic cells -> edema, vascular insufficiency, ischemia

CM: epigastric pain, N/V, Cullen or Grey Turner signs (bleeding)

Diagnosis: ^ amylase & lipase & BGL, leukocytosis, hypocalcemia, abd US, CT

30
Q

Cholelithiasis

A

Gallstones

F’s: forty, female, fat, fair, and fertile

lodge in cystic duct and cause backup/pain -> can cause necrosis