PATH - General Flashcards
Acute gastritis
Erosions can be caused by:
- NSAIDs
- Burns (Curling ulcer)
- Brain injury (Cushing ulcer)
“Burned by the Curling iron”
“Always Cushion the brain”
Especially common among alcoholics and patients taking daily NSAIDs (patients with rheumatoid arthritis).
Chronic gastritis
Mucosal inflammation, often leading to atrophy
(hypochlorhydria (DEC HCL)–>hypergastrinemia) and
intestinal metaplasia (INC risk of gastric cancers).
Due to:
*H pylori
-Most common
-INC risk of peptic ulcer disease, MALT lymphoma.
-Affects *antrum first and spreads to body of
stomach.
- Autoimmune
- Autoantibodies to *parietal cells and intrinsic factor
- INC risk of *pernicious anemia
- Affects *body/fundus of stomach
Ménétrier disease
Gastric hyperplasia of mucosa–>hypertrophied rugae (looks like brain gyri), excess mucus production with resultant protein loss and parietal cell atrophy with DEC acid production.
*Precancerous
Gastric ulcer
found in *PUD
DEC mucosal protection against gastric acid
Pain can be *Greater with meals
*weight loss
70% ass. w/ H. pylori
NSAIDs also cause
INC risk of carcinoma
Biopsy margins to rule out malignancy
often seen in older its
Duodenal ulcer
found in *PUD
DEC mucosal protection or INC gastric acid secretion
Hypertrophy of *Brunner glands
Pain *Decreases with meals
*weight gain
~ 90% ass. w/ H. pylori
found in *Zollinger-Ellison syndrome
Ulcer complications
Hemorrhage
Most common complication
Gastric, duodenal (*posterior> anterior)
Ruptured gastric ulcer on the *lesser curvature of stomach–>bleeding from *left gastric artery.
An ulcer on the *posterior wall of duodenum–>bleeding from *gastroduodenal artery.
Ulcer complications
Obstruction
Pyloric channel, duodenal
Ulcer complications
Perforation
Duodenal (anterior>posterior)
May see free air under diaphragm with *referred pain to the shoulder via phrenic nerve.
Crohn disease
Inflammatory bowel disease
thought to be caused by disorder response to intestinal bacteria
Affects Any portion of the GI tract, usually the *terminal
ileum and *colon.
*Skip lesions
*rectal sparing
*Transmural inflammation–>fistulas
Cobblestone mucosa, creeping fat, bowel wall
thickening (“string sign” on barium swallow), linear ulcers, fissures
*Noncaseating granulomas and lymphoid aggregates
Diarrhea that may or may not be bloody
Rash (pyoderma gangrenosum, erythema nodosum), eye inflammation (episcleritis, uveitis), oral
ulcerations (aphthous stomatitis), arthritis (peripheral, spondylitis).
Kidney stones (usually calcium oxalate), gallstones
COMPLICATIONS
Malabsorption/malnutrition, colorectal cancer, Fistulas, phlegmon/abscess, strictures, perianal disease
TX: Corticosteroids, azathioprine, antibiotics (eg,
ciprofloxacin, metronidazole), infliximab, adalimumab.
Ulcerative colitis
Inflammatory bowel disease
autoimmune
Colitis = colon inflammation.
- Continuous colonic lesions
- always with rectal involvement
- Mucosal and submucosal inflammation only
*Friable mucosal pseudo polyps with freely
hanging mesentery
*Loss of haustra “lead
pipe” appearance on imaging
Crypt abscesses and ulcers, bleeding
*no granulomas
*Bloody diarrhea
Rash (pyoderma gangrenosum, erythema nodosum), eye inflammation (episcleritis, uveitis), oral ulcerations (aphthous stomatitis), arthritis (peripheral, spondylitis).
1° sclerosing cholangitis. Associated with *p-ANCA
COMPLICATIONS
Malabsorption/malnutrition, colorectal cancer, Fulminant colitis, toxic megacolon, perforation
TX: 5-aminosalicylic preparations (eg, mesalamine),
6-mercaptopurine, infliximab, colectomy.
Irritable bowel syndrome
Recurrent abdominal pain associated with ≥ 2 of the following:
-Pain improves with defecation
-Change in stool frequency
-Change in appearance of stool
Chronic symptoms may be
diarrhea-predominant, constipation-predominant, or mixed
Diverticulum
Blind pouch protruding from the alimentary tract that communicates with the lumen of the gut
Most often in *sigmoid colon.
*“True” diverticulum—all *3 gut wall layers outpouch (eg, Meckel).
*“False” diverticulum or pseudodiverticulum—
only *mucosa and submucosa outpouch.
Occur especially where *vasa recta perforate muscularis externa.
Diverticulosis
- Many false diverticula of the colon, commonly
- sigmoid
Caused by INC intraluminal pressure and focal weakness in colonic wall.
Associated with low-fiber diets.
Complications include diverticular bleeding
(painless hematochezia), diverticulitis
Diverticulitis
Diverticulosis with inflamed microperforations classically causing LLQ pain, fever, leukocytosis.
Complications: abscess, fistula (colovesical fistula–>pneumaturia), obstruction (inflammatory stenosis), perforation (–>peritonitis).
Treat with percutaneous drainage or surgery.
Treat with antibiotics
Zenker diverticulum
Pharyngoesophageal *false diverticulum
*Esophageal dysmotility causes herniation of mucosal tissue at *Killian triangle between the thyropharyngeal and cricopharyngeal parts of
the *inferior pharyngeal constrictor
dysphagia, obstruction, gurgling, aspiration, foul breath, neck mass.
Most common in elderly males.
Meckel diverticulum
*True diverticulum
Persistence of the *vitelline
duct.
May contain ectopic acid–secreting gastric mucosa and/or pancreatic tissue.
Most common congenital anomaly of GI tract.
melena, *RLQ pain, intussusception, volvulus, or obstruction near terminal ileum.
The six 2’s:
- 2 times as likely in males.
- 2 inches long.
- 2 feet from the ileocecal valve.
- 2% of population.
- Commonly presents in first 2 years of life.
- May have 2 types of epithelia (gastric/pancreatic).
Hirschsprung disease
Congenital *megacolon characterized by lack
of *ganglion cells/enteric nervous plexuses
(Auerbach and Meissner plexuses) in *distal
segment of colon
Due to failure of neural crest
cell migration
mutations in *RET
bilious emesis, abdominal
distention, and failure to pass meconium within 48 hours–>chronic constipation
Risk INC with Down syndrome
Volvulus
Twisting of portion of bowel around its mesentery
can lead to obstruction and
infarction
Can occur throughout the
GI tract
*Midgut volvulus more common in *infants and children.
*Sigmoid volvulus more
common in *elderly
Intussusception
Telescoping of proximal bowel segment into
distal segment, commonly at *ileocecal junction
intermittent abdominal pain often with *“currant jelly” stools.
Majority of cases occur in children
Abdominal emergency
in early childhood
*bull’s-eye appearance
on ultrasound.
Acute mesenteric ischemia
Critical blockage of intestinal blood flow (often embolic occlusion of *SMA)–>small bowel necrosis–>abdominal pain out of proportion to physical findings
May see red *“currant jelly” stools.
Chronic mesenteric ischemia
“Intestinal angina”
atherosclerosis of *celiac artery, SMA, or IMA–>intestinal hypoperfusion–>postprandial epigastric pain–>food aversion and weight loss.
Colonic ischemia
Reduction in intestinal blood flow causes ischemia.
Crampy abdominal pain followed by hematochezia.
Commonly occurs at *watershed areas (splenic flexure, distal colon).
Typically affects elderly
Angiodysplasia
Tortuous dilation of vessels–>hematochezia.
Most often found in *cecum, terminal ileum, ascending colon.
More common in older patients.
Adhesion
Fibrous band of scar tissue
commonly forms after surgery
most common cause of small bowel obstruction
Can have well-demarcated necrotic zones
Ileus
Intestinal hypomotility without obstruction–>constipation and DEC flatus
Associated with abdominal surgeries, opiates, hypokalemia, sepsis.
Meconium ileus
In *cystic fibrosis, meconium plug obstructs intestine, preventing stool passage at birth.
Necrotizing enterocolitis
Seen in *premature, *formula-fed infants with *immature immune system
Necrosis of intestinal
mucosa (primarily *colonic) with possible perforation, which can lead to *pneumatosis intestinalis,
free air in abdomen, portal venous gas.
Cirrhosis
diffuse bridging fibrosis (via stellate cells) and regenerative nodules
disrupt normal architecture of liver; INV risk for hepatocellular carcinoma (HCC)
Etiologies include alcohol (60–70% of cases in the US), nonalcoholic steatohepatitis, chronic viral hepatitis, autoimmune hepatitis, biliary disease, genetic/metabolic
disorders.
Portal hypertension
INC pressure in portal venous system
Etiologies include cirrhosis (most common cause in Western countries), vascular obstruction (portal vein thrombosis, Budd-Chiari syndrome), schistosomiasis.
Reye syndrome
Rare, often fatal childhood hepatic encephalopathy
mitochondrial abnormalities, fatty liver (microvesicular fatty change), hypoglycemia, vomiting, hepatomegaly, coma
Associated with viral infection (especially VZV and influenza B) that has been *treated with aspirin
*Avoid aspirin in children, except in those with *Kawasaki disease.
Budd-Chiari syndrome
Thrombosis or compression of hepatic veins with *centrilobular congestion and necrosis–>congestive liver disease
Associated with hypercoagulable states, polycythemia vera, postpartum state, HCC
May cause *nutmeg liver (mottled appearance).
a1-antitrypsin
deficiency
Misfolded gene product protein aggregates in
hepatocellular ER–>cirrhosis with PAS⊕ globules in liver
Codominant trait
In lungs, DEC α1-antitrypsin–>uninhibited elastase
in alveoli–>DEC elastic tissue–>panacinar emphysema.
Jaundice
Abnormal yellowing of the *skin and/or *sclera due to *bilirubin deposition.
Hyperbilirubinemia 2°
to INC production or DEC disposition (impaired hepatic uptake, conjugation, excretion)
Unconjugated (indirect)
hyperbilirubinemia
Hemolytic
physiologic (newborns)
Crigler-Najjar
Gilbert syndrome
Conjugated (direct)
hyperbilirubinemia
*Biliary tract obstruction: gallstones, cholangiocarcinoma, pancreatic or liver cancer, liver fluke
Biliary tract disease:
- 1° sclerosing cholangitis
- 1° biliary cirrhosis
Excretion defect:
- Dubin-Johnson syndrome
- Rotor syndrome
Mixed (direct and indirect)
hyperbilirubinemia
Hepatitis
cirrhosis
Physiologic neonatal jaundice
At birth, immature *UDP-glucuronosyltransferase–>unconjugated hyperbilirubinemia–>jaundice/
kernicterus (bilirubin deposition in brain, particularly basal ganglia)
Occurs after first 24 hours of life and usually resolves without treatment in 1–2 weeks
TX: phototherapy (non-UV)
Wilson disease (hepatolenticular degeneration)
Recessive mutations in hepatocyte copper-transporting ATPase (ATP7B gene; chromosome 13)–>inadequate copper excretion into bile and blood (*DEC serum ceruloplasmin, INC urine copper).
Copper accumulates, especially in liver, brain, cornea, kidneys, joints.
Presents before age 40 with liver disease, neurologic
disease (dysarthria, dystonia, tremor, parkinsonism), psychiatric disease, **Kayser-Fleischer rings
(deposits in Descemet membrane of cornea), hemolytic anemia, renal disease (eg, Fanconi
syndrome).
TX: chelation with penicillamine or trientine, oral zinc.
Hemochromatosis
Recessive mutations in *HFE gene (C282Y>H63D, chromosome 6)–>abnormal iron sensing and INC intestinal absorption (INC ferritin, INC iron, DEC TIBC–>INC transferrin saturation)
*Iron accumulates, especially in liver, pancreas, skin, heart, pituitary, joints.
*Hemosiderin (iron) can be identified on liver MRI or
biopsy with Prussian blue stain
Classic triad of cirrhosis, diabetes mellitus, skin pigmentation (“bronze diabetes”)
Also causes dilated cardiomyopathy (reversible), hypogonadism, arthropathy (calcium pyrophosphate
deposition)
*HCC is common cause of death.
TX: repeated phlebotomy, chelation with deferasirox, deferoxamine, oral deferiprone
Biliary tract disease
May present with pruritus, jaundice, dark urine, light-colored stool, hepatosplenomegaly
Typically with cholestatic pattern of LFTs (INC conjugated bilirubin, INC cholesterol, INC ALP).
Primary sclerosing cholangitis
Biliary tract disease
Unknown cause of concentric *“onion skin” bile duct fibrosis–>alternating
strictures and dilation with
*“beading” of intra- and
extrahepatic bile ducts
Classically in *middle-aged men with IBD
Associated with *ulcerative
colitis.
p-ANCA ⊕
INC IgM
Can lead to 2° biliary cirrhosis. INC risk of cholangiocarcinoma and
gallbladder cancer
Primary biliary cirrhosis
Biliary tract disease
Autoimmune reaction–>lymphocytic infiltrate+granulomas–>destruction of *intralobular bile ducts.
Classically in *middle-aged
women.
Anti-mitochondrial antibody⊕
INC IgM
Associated with other autoimmune conditions (eg, Sjögren syndrome, Hashimoto thyroiditis, CREST, rheumatoid arthritis, celiac disease).
Secondary biliary cirrhosis
Biliary tract disease
Extrahepatic biliary obstruction–>INC pressure in intrahepatic ducts–>injury/fibrosis and
bile stasis.
Patients with known obstructive lesions (gallstones, biliary strictures, pancreatic carcinoma).
May be complicated by
ascending cholangitis.
Gallstones (cholelithiasis)
INC cholesterol and/or bilirubin, DEC bile salts, and
gallbladder stasis all cause stones
2 types of stones:
*Cholesterol stones (radiolucent with 10–20%
opaque due to calcifications)
-80% of stones
-Associated with obesity, Crohn disease, advanced age, estrogen therapy, multiparity, rapid weight loss, Native American origin.
*Pigment stones (black=radiopaque, Ca2+ bilirubinate, hemolysis; brown=radiolucent,
infection)
-seen in patients with Crohn
disease, chronic hemolysis, alcoholic cirrhosis, advanced age, biliary infections,
total parenteral nutrition (TPN).
Risk factors (4 F’s):
- Female
- Fat
- Fertile (pregnant)
- Forty
Most common complication is *cholecystitis; also acute pancreatitis, ascending cholangitis.
Charcot triad of *cholangitis:
-Jaundice
-Fever
-RUQ pain
Cholecystitis
Acute or chronic inflammation of gallbladder usually from cholelithiasis (stone at neck of
gallbladder with gallbladder wall thickening)
Gallstones most commonly blocking the cystic duct–>2° infection
rarely acalculous due to ischemia and stasis,
or 1° infection (CMV)
Murphy sign⊕
INC ALP if bile duct becomes involved (ascending cholangitis)
Porcelain gallbladder
Calcified gallbladder due to chronic cholecystitis
usually found incidentally on imaging
TX: *prophylactic cholecystectomy due to high rates of gallbladder cancer (mostly adenocarcinoma).
Acute pancreatitis
Autodigestion of pancreas by pancreatic enzymes
Diagnosis by 2 of 3 criteria:
-acute epigastric pain often radiating to the back
-*INC serum amylase or
lipase (more specific) to 3× upper limit of normal
-characteristic imaging findings
Complications: pseudocyst (lined by granulation tissue, not epithelium), necrosis, hemorrhage, infection, organ failure (ARDS, shock, renal failure), hypocalcemia (precipitation of Ca2+ soaps).
Chronic pancreatitis
Chronic inflammation, atrophy, calcification of the pancreas
Mutations in CFTR (cystic fibrosis) can cause chronic pancreatic insufficiency
Major causes are alcohol abuse and idiopathic
Can lead to pancreatic insufficiency–>Steatorrhea, fat-soluble vitamin deficiency, diabetes mellitus
