Chapter 13: The GI Tract Flashcards by Kelly Patel

Disordered esophageal motility (uncoordinated peristalsis) with inability to relax the lower esophageal sphincter (LES)
S/S: Dysphagia for solids & liquids, putrid breath, High LES pressure on esophageal manometry, “bird-beak” sign on barium swallow study
Results in hypertrophy/dilation of esophagus
What is damaged?
How can the damage occur?
What is there an increased risk of?

Achalasia

1) Loss or damaged ganglion cells in the myenteric plexus
2) idiopathic or secondary to known insult (viral, autoimmune, genetic) In Latin America, complication of Chagas Disease
3) Esophageal Squamous cell carcinoma

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Thin protrusion of esophageal mucosa membranes, most often into the lumen of upper esophagus
Presents with dysphagia for poorly chewed food, esophageal substernal pain, and aspiration or regurgitation of foods and liquids
Increased risk for esophageal sqamous cell carcinoma

Esophageal Web

Rings are thicker and contain smooth muscle

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Cervical esophageal web (cause dysphagia)
Mucosal lesions of the mouth and pharynx
Iron-deficiency anemia
What is a potential complication?

Plummer-Vinson Syndrome
Carcinoma of oropharynx and upper esophagus
Remember: Plummers DIG (dysphagia, iron def, glossitis)

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Autoimmune disease characterized by activation of fibroblasts and deposition of collagen (fibrosis)
Esophageal smooth muscle atrophy, decreased LES pressure, dysmotility, then acid reflux and dysphagia, then stricture > Barrett esophagus, and aspiration
Which antibodies would you look for?
What is CREST Syndrome (throwback thursday)?
Why do we care about this in the GI Unit?

Scleroderma
Anti-Scl70 and anti-Centromere antibodies (for CREST)
CREST (systemic sclerosis, limited type): Calcinosis/anti-Centromere antibodies, Raynaud Phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasias of the skin

Disease affects the lower esophageal sphincter primarily, lack of peristalsis, dysphagia

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Outpouching of pharyngeal mucosa through an acquired defect in the muscular wall (false diverticulum)
Arises above the upper esophageal sphincter at the junction of the esophagus and pharynx
Cause: disordered fxn of cricopharyngeal musculature
Presents with dysphagia, obstruction, and halitosis
Regurgitation of food eaten previously in absence of dysphagia

Zenker Diverticulum

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Herniation of the stomach through an enlarged diaphragmatic opening
S/S: heartburn, regurgitation due to incompetence of LES
2 types:
1) cap of gastric mucosa move upward, above diaphragm due to enlargement of hiatus and laxity of circumferential CT, resolves on its own
2) portion of gastric fundus herniates through a defect in the diaphragmatic CT and lies beside the esophagus, extreme case = stomach herniates into thorax, these hernias need surgery

Hiatal Hernia

1) Sliding hernia
2) Paraesophageal hernia

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Name it!
Transmural, usually distal esophageal rupture due to violent retching; surgical emergency
Leads to air in mediastinum, subcutaneous emphysema

Boerhaave syndrome

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Name it!
Infiltration of esosinophils in the esophagus in atopic pts.
Food allergens lead to dysphagia, heartburn, strictures.
Sensation of food “sticking” upon swallowing
ID’d after found Unresponsive to GERD therapy

Eosinophilic esophagitis

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1) associated with lye ingestion and acid reflux
2) Painless bleeding of dilated submucosal veins in lower 1/3 of esophagus 2ndary to portal HTN & cirrhosis, these veins are prone to rupture and hemorrhage

1) Esophageal strictures

2) Esophageal varices

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Associated with reflux, infection in immunocompromised
Dysphagia, severe pain on swallowing
Can have Candida (white pseudomembrane), herpes (punched-out ulcers), CMV (linear ulcers) or be due to chemical ingestion

(Infective) esophagitis

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Commonly presents as heartburn and regurgitation upon lying down. May also present with nocturnal cough and dyspnea, adult-onset asthma. Decrease in LES tone.

Gastroesophageal Reflux Disease

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Mucosal lacerations at the gastroesophageal junction due to severe vomiting. Leads to painful hematemesis. Usually found in alcoholics and bulimics.

Mallory-Weiss Syndrome

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Glandular metaplasia: replacement of nonkeratinized stratified squamous epithelium with intestinal epithelium (nonciliated columnar w/goblet cells) in the distal esophagus.
Due to chronic acid reflux (GERD)
Associated with esophagitis, esophageal ulcers, and increased risk of esophageal adenocarcinoma correlated with length of esophagus involved and the degree of dysplasia

Barrett Esophagus

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Patient presentation: progressive dysphagia (first solids, then liquids) and weight loss, poor prognosis
2 Types of cancer? Usual locations for each?
Risk factors? AABCDEFFGH

Esophageal cancer
1) Squamous cell carcinoma = worldwide, upper 2/3 of esophagus, (achalasia, alcohol, cigs, diverticula (Zenker), esophageal web, hot liquids)

2) Adenocarcinoma = US, lower 1/3, (Barrett esophagus, cigs, Fat (obesity), GERD)

Others: familial

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Hypertrophy of the pylorus causes obstruction.
Palpable “olive” mass in epigastric region
Nonbilious projectile vomiting in first month of life
Could lead to hypochloremic alkalosis (loss of HCl)
Most common indication for abdominal surgery in the 1st 6 months of life (treat: surgical incision)
More often in firstborn males

Congenital pyloric stenosis

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Mucosal barrier breakdown/necrosis, may extend to deeper tissues forming ulcer = inflammation b/c permit acid-induced injury (hypersecretion of gastric acid usually)
Widespread petechial hemorrhages
Could be benign abdominal discomfort or full on hemorrhage
Causes:
Stress
NSAIDs (decreased PGE2 leads to decreased gastric mucosa protection)
alcohol
uremia
burns (decreased plasma volume leads to sloughing of gastric mucosa) SPECIAL NAME?
brain injury (Increased vagal tone => increased ACh => increased H+ production) SPECIAL NAME?

Acute gastritis (erosive)

Remember:
BURNED by the CURLING iron.
Always CUSHion the BRAIN.

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Chronic, diffuse inflammatory disease of the body and fundus of stomach
Autoimmune disorder characterized by:
destruction of parietal cells, Autoantibodies to parietal cells & intrinsic factor, pernicious Anemia, and Achlorhydria
Associated with other autoimmune disorders: grave’s, addison, vitiligio, T1DM etc.
What’s pernicious anemia? No, really I don’t remember Unit 1. GAHHHHH.
Increased risk for what?

Autoimmune atrophic gastritis (chronic gastritis) Remember: type A (Autoimmune), type B (H. pylori Bacteria)
Pernicious anemia = megaloblastic anemia caused by malabsorption of Vit B12 owing to a deficiency of intrinsic factor.
Increased risk for gastric adenocarcinoma (intestinal type)

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Break time. I dare you to stand up and dance to this for 30 seconds.

https://www.youtube.com/watch?v=VzSdPxlGGZc

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Chronic inflammatory disease of antrum of stomach
PMNs, plasma cells
What is the most common cause of this disease?
What is there an increased risk for ?

Chronic gastritis
H. pylori found on epithelial surface of stomach (no invasion)
Increased risk of ulcercation, MALT lymphoma, and gastric adenocarcinoma

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Gastric hypertrophy with protein loss (albumin), parietal cell atrophy, and increase mucous cells.
Hyperplastic hypersecretory gastropathy
Precancerous, need regular endoscopy
Rugae of stomach are so hypertrophied they look like brain gyri. ENLARGED RUGAE = enlarged stomach.
S/S: postprandial pain, relieved by antacids, weight loss, peripheral edema, maybe ascites

Menetrier disease

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Normal flat mucosal surface of stomach replaced by villiform projections with fibromuscular proliferation in the lamina propria
Inflammation is minimal unlike H. pylori gastritis
Causes?

Reactive (Chemical) gastropathy

Chronic NSAID use

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Focal destruction of gastric mucosa
Pain can be greater with meals = weight loss
H. pylori in 70%
Mechanism is decreased mucosal protection (due to H. pylori chronic gastritis causing epithelial injury) against gastric acid
These pts secrete waay less acid than normal ppl (gastric hyposecretion)
Other causes are NSAIDS
Increased risk of carcinoma
Often occurs in older patients

Peptic Ulcer Disease

Specifically Gastric Ulcer

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Focal destruction of duodenal mucosa
Pain decreases with meals = weight gain
H. pylori infection in 100% (=> cytokines => increased gastrin release/decreased somatostatin => increased gastric acid secretion)
Mechanism is decreased mucosal protection or increased gastric acid secretion
Other causes are Zollinger-Ellison syndrome
Generally benign
Hypertrophy of Brunner glands
Seen in ppl with cirrhosis 10x than normal ppl

Peptic Ulcer Disease

Duodenal Ulcers

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Tend to be nonagressive tumors in the stomach
Aggressive in small & large intestines
Overexpression of c-kit (gain of function mutation)
Derived from pacemaker cells of Cajal
Usually submucosal, covered by intact mucosa, spindle shaped cells in whorls and interlacing bundles w/cytoplasmic vacuoles embedded in a collagenous stroma

Gastrointestinal Stromal Tumors (GISTs)

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What is the most important causative agent for stomach cancer and is implicated in about 2/3rds of cases?

H. pylori

H. pylori Smoking Nitrosamines A diet high in starch, smoked, or cured fish and meat, pickled vegetables

Possible factors in carcinoma of stomach

Stomach cancer is almost always adenocarcinoma. Early aggressive local spread and node/liver metastasis. Often presents with acanthosis nigricans. Two types? 1) associated with H. pylori, dietary nitrosamines (smoked foods), tobacco smoking, achlorhydria, chronic gastritis. Commonly located on lesser curvature; looks like ulcer with raised margins, originate from areas of intestinal metaplasia 2) not associated with H. pylori, signet ring cells, stomach wall grossly thickened and leathery (linitis plastica)

1) Intestinal | 2) Diffuse *linitis plastica = entire stomach involved

Difference in appearance of a benign peptic ulcer and an ulcerating adenocarcinoma?

Benign ulcer = punchout margins and a smooth base | Cancer = firm, raised and nodular, lateral margins are irregular and its base is ragged

Involvement of left supraclavicular node by metastasis from stomach

Virchow node

Bilateral metastases to ovaries, abundant mucus, signet ring cells

Krukenberg Tumor

Subcutaneous periumbilical metastasis

Sister mary joseph nodule

Endocrince cells in gastric mucosa may give rise to neoplasms not usually hormonally active Sometimes secrete 5-HT Hypergastrinemia associated with autoimmune gastritis

Gastric neuroendocrine tumors (low grade malignancies) | Metastasis can cause carcinoid syndrome

Metastatic spread if level of esophagus carcinoma involved: 1) Upper 1/3 2) Middle 1/3 3) Lower 1/3

Lymph node spread 1) Cervical, internal jugular, supraclavicular 2) paratracheal, hilar, aortic, cardiac, paraesophageal (aka. mediastinal or tracheobronchial) 3) celiac, retroperitoneal and gastric nodes

True diverticulum Persistence of the vitelline duct, outpouching of the gut on the antimesenteric ileal border May contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue Most common congenital anomaly of the GI tract Can cause Melena, RLQ pain, intussuception, volvulus, or obstruction near the terminal ileum What are the five 2's to remember?

Meckel Diverticulum 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)

How can you remember the malabsorption syndromes? | These Will Cause Devestating Absorption Problems

``` Tropical Sprue Whipple disease Celiac Sprue Disaccharide deficiency Abetalipoproteinemia Pancreatic Insufficiency ```

Why do you need to worry about CF patients with GI problems in neonatal period?

Highly viscous mucous may block the pancreatic duct and thicken intestinal contents Tenacious meconium may accumulate and obstruct the small intestine

Infarcted bowel, becomes edematous and diffusely purple Hemorrhage is prominent Mucosal surface w/irregular white sloughs Dysfxn of smooth muscle = interfere peristalsis => adynamic ileus (bowel proximal to the lesion is dilated and filled with fluid) S/S: abrupt abdominal pain, bloody diarrhea, hematemesis, and shock (MODS)

Superior Mesenteric Artery Occlusion causes Acute Intestinal Ischemia

Atherosclerotic narrowing of major splanchnic arteries intermittent abdominal pain Pain starts w/i 1/2 hour of eating and lasts for a few hours Eventually: fibrosis and stricture formation, obstruction, malabsorption due to stasis, bacterial overgrowth

Chronic Intestinal Ischemia aka intestinal angina

Autoimmune-mediated intolerance of gliadin (wheat) leading to malabsorption and steatorrhea. Associated with HLA-DQ2 & 8 Anti-endomysial, anti-tissue transglutaminase, and anti-gliadin antibodies Blunting of villi, crypt hyperplasia, lymphocytes in lamina propria Decreased mucosal absorption that primarily affects distal duodenum and/or proximal jejunum Dx: tissue transglutaminase antibodies Association with dermatitis herpetiformis What is there an increased risk of developing?

Celiac sprue | Increased risk of malignancy (T-cell lymphoma and small bowel carcinoma) if refractory to good dietary control.

Systemic tissue damages w/ Infection with Tropheryma whipplei (Gram +) PAS + Foamy macrophages containing partially destroyed organisms in intestinal lamina propria, mesenteric nodes causing compression of lacteals => fat malabsorption and steatorrhea Cardiac valves, Arthralgias, and Neurologic symptoms, lymph nodes Occurs in Older men

Whipple Disease | Remember: Foamy whipped cream in a CAN

``` Most common is lactase deficiency => milk intolerance Normal appearing villi Osmotic diarrhea (due to lactose) Also self-limited lactase deficiency occurs following injury (viral, diarrhea) Lactose tolerance test is + for deficiency if: giving lactose produces symptoms and glucose rises ```

Disaccharidase deficiency

Autosomal Recessive deficiency of apolipoprotein B-48 (defective chylomicron formation) and B-100 (absent plasma VLDL and LDL) Fat accumulation in enterocytes Child: failure to thrive, steatorrhea, acanthocytosis, ataxia, night blindness

Abetalipoproteinemia

Due to cystic fibrosis, obstructing cancer and chronic pancreatitis. Causes malabsorption of fat and fat soluble vitamins (ADEK) Increased neutral fat in stool Use D-xylose absorption test: 1) normal urinary excretion in pancreatic insufficiency 2) Decreased excretion w/intestinal mucosa defects or bacterial overgrowth

Pancreatic insufficiency

Malignant proliferation of neuroendocrine cells + for chromogranin Small bowel most common site Submucosal polyp-like nodule Secretes 5-HT (metabolized by liver MAO to 5-HIAA then excreted in urine) If this tumor metastasizes: 5-HT bypasses liver metabolism so result is _____ syndrome. Characterized by: bronchospasm, diarrhea, flushing of skin, triggered by EtOH/stress

``` Carcinoid Tumor (now being called neuroendocrine tumor more often) Carcinoid syndrome ```

What is carcinoid heart disease?

R-sided valvular fibrosis (increased collagen) leading to tricuspid regurgitation and pulmonary valve stenosis. L-sided valvular lesion not seen b/c lung MAO metabolizes the 5-HT. Result of metastasis of carcinoid tumor

Etiology: Disordered response to intenstinal bacteria maybe What: full thickness inflammation w/knife-like fissures Location: any portion of GI tract, usually terminal ileum, SKIP lesions, RECTAL SPARING Symptoms: RLQ pain with nonb-or-bloody diarrhea Grossly: COBBLESTONE mucosa, creeping FAT, bowel wall thickening, string sign on barium swallow due to strictures, transmural inflammation => fistulas Histology: Lymphoid aggregates with noncaseating GRANulomas (Th1 mediated) Complications: strictures => obstruction, perianal disease, fistulas, malabsorption w/nutritional def, calcium oxalate nephrolithiasis, colorectal cancer, gallstones

Crohn Disease Remember: think of a FAT GRANny and an old CRONE SKIPping down a COBBLESTONE road away from the WRECK (rectal sparing)

Migratory polyarthritis, erythema nodosum, ankylosing spondylitis, pyoderma grangrenosum, apthous ulcers, uveitis, kidney stones Associations of what? Association unique to this?

``` Crohn disease kidney stones (calcium oxalate) ```

Treatment for Crohn disease?

Corticosteroids, azathioprine, methotrexate, infliximab, adalimumab

Etiology: Autoimmune What: colon inflammation, always rectal involvement Location: Begins in rectum, can extend up to the cecum, remainder of GI unaffected Symptoms: LLQ pain (rectum) with bloody diarrhea Grossly: mucosal and submucosal ulcers, friable mucosal pseudopolyps w/freely hanging mesentary, lead pipe sign on imaging b/c loss of haustra Histology: crypt abscesses with neutrophils and ulcers, bleeding, no granulomas (Th2 mediated) Complications: Malnutrition, toxic megacolon, colorectal carcinoma (worse w/right sided colitis or pancolitis, concern with >10 yrs, risk based on extent&duration)

Ulcerative Colitis ``` Remember: ULCCCERS Ulcers Large Intestine Continuous Colorectal carcinoma Crypt abscess Extends proximally Red diarrhea Sclerosing cholangitis ```

Primary sclerosing cholangitis, p-ANCA, ankylosing spondylitis, sacroilitis, migratory polyarthritis, apthous ulcers, uveitis, erythema nodosum, pyoderma gangrenosum Associations of what? Association unique to this?

Ulcerative colitis | Primary sclerosing cholangitis

Treatment for Ulcerative colitis?

ASA preparations (sulfasalazine) 6-mercaptopurine infliximab and colectomy

Acute inflammation of the appendix Due to: 1) In child? 2) In adult? S/S: initial diffuse periumbilical pain migrates to McBurney point (1/3 distance from the anterior superior iliac spine to umbilicus), fever, nausea. Rupture of appendix will result in what? The signs?

Appendicitis 1) Lymphoid hyperplasia (can follow GI infections) 2) Fecalith Rupture: peritonitis, may see psoas, obturator, and Rovsing signs, guarding, rebound tenderness periappendiceal abscess is a common complication

Defective relaxation and peristalsis of rectum and distal sigmoid colon (rectum permanently contracted) Associated with Down Syndrome Results from congenital failure of ganglion cells (neural crest derived) to descend into the wall (missing Myenteric plexus and Auerbach plexus) What do these nerve plexuses do? RET gene mutation (congenital) Chaga's disease (destroy's ganglion cells = megacolon) S/S: bilious emesis, abdominal distention and failure to pass meconium 1st 24 hrs of life, empty rectal vault on DRE, Congenital megacolon proximal to obstruction could rupture

Hirschsprung Disease Myenteric = regulates motility Auerbach = regulates blood flow, secretions, and absorption

Outpouchings of mucosa and submucosa through the muscularis propria Related to wall stress, constipation, straining, and low-fiber diet, risk increases with age Arise where vasa recta traverse the muscularis propria

Colonic diverticula

Acquired malformation of mucosal and submucosal capillary beds Usually in cecum and ascending colon due to high wall tension Rupture presents as hematochezia

Angiodysplasia

ischemic damage to colon Watershed infarct at the splenic flexure atherosclerosis of SMA a common cause Postprandial pain and weight loss, infarction results in pain and bloody diarrhea

ischemic colitis | “angina"

Relapsing abdominal pain with bloating, flatulence, and change in bowel habits (diarrhea or constipation) that improves with defecation Classically in middle-age females Disturbed intestinal motility, no identifiable pathological changes Increase dietary fiber to improve symptoms

Irritable Bowel Syndrome

``` colonic polyps (>50% rectosigmoid colon) serrated appearance on microscopy (increased risk for adenocarcinoma) but otherwise benign most common type usually arise in L colon benign, no malignant potential ```

hyperplastic colonic polyps

neoplastic proliferation of glands 2nd most common type of colonic polyp benign, but PREMALIGNANT (precursor to colorectal carcinoma) Risk increases with size, villious histology, epithelial dysplasia S/S: aymptomatic, lower GI bleed, partial obstruction, secretory diarrhea

Adenomatous colonic polyps Progress to adenocarcinoma via adenoma-carcinoma sequence Remember: villious = villanous

What are the 4 steps of the adenoma-carcinoma squence?

1) APC mutation (sporadic or germline), increased risk of polyp formation 2) K-ras mutation leads to formation of polyp 3) DCC knocked out (late adenoma) 4) p53 mutation and increased expression of COX = carcinoma

What impedes the progression from adenoma to carcinoma in the adenoma-carcinoma sequence?

Aspirin! taken to inhibit the COX

AD disorder with 100s-1000s of adenomatous colonic polyps, pancolonic, rectum Inherited APC mutation (chr 5) increases likelihood of the “2nd hit” mutation to develop polyps Carcinoma develops by age 40 100% progress to CRC unless colon resected

Familial Adenomatous Polyposis (FAP)

FAP with fibromatosis (non-neoplastic proliferation of fibroblasts) and osteomas (usually arise in skull, benign tumor of bone)

Gardner syndrome

FAP with CNS tumors (medulloblastoma and glial tumors)

Turcot syndrome | Remember: Turcot = Turban (head/CNS)

Hamartomatous (disorganized normal tissue, benign) polyps in children

Juvenile polyp/polyposis

Hamartomatous polyps throughout GI Mucocutaneous hyperpigmentation (freckle-like spots) on lips, oral mucosa, genital skin AD disorder Increased risk of colorectal, breast, and gynecologic cancer

Peutz-Jeghers Syndrome

What are the two pathways that colorectal carcinoma may arise?

Adenoma-carcinoma sequence | Microsatellite instability

AD disorder Inherited mutations in DNA mismatch repair enzymes causes microsatellite instability Colorectal carcinoma arises de novo (not from adenomatous polyps) at relatively early age, usually right sided, proximal colon involved 80% progress to CRC

HNPCC (hereditary nonpolyposis colorectal carcinoma) aka Lynch Syndrome Increased risk for colorectal, ovarian, and endometrial carcinoma

Napkin ring lesion Decreased stool caliber (change in bowel habits) LLQ pain, blood streaked stool Usually due to adenoma-carcinoma sequence

Left sided colorectal carcinoma remember: Right side bleeds, left side obstructs

``` Grows as a raised lesion Iron deficiency anemia (occult bleeding) Fatigue, weakness Vague pain Usually due to microsatellite instability ```

Right sided colorectal carcinoma remember: Right side bleeds, left side obstructs

Colorectal carcinoma is associated with what microbe?

Streptococcus bovis which causes subacute endocarditis, bacteremia

Fibrous band of scar tissue Forms after surgery Most common cause of small bowel obstruction Can have well-demarcated necrotic zones

Adhesion

Early bilious vomiting w/proximal stomach distention (double bubble on X-ray) b/c of failure of small bowel recanalization Associated with Down syndrome

Duodenal atresia

Reduction in intestinal blood flow causes ischemia Pain after eating => weight loss Commonly occurs at splenic flexure and distal colon Affects elderly typically

Ischemic colitis

In cystic fibrosis, meconium plug obstructs intestine, preventing stool passage at birth

Meconium ileus

Necrosis of intestinal mucosa and possible perforation Colon is usually involved, but can involve entire GI tract. In neonates, more coomon in preemies (decreased immunity)

Necrotizing enterocolitis

What are you suspicious of? Fe deficiency anemia in males (>50) and in Postmenopausal females Apple core lesion on barium enema

Colorectal cancer

Gastrin secreting tumor of pancreas or duodenum Acid hypersecretion (due to HIGH gastrin) causes recurrent ulcers in distal duodenum and jejunum PResents with abdominal pain (peptic ulcer disease, distal ulcers) diarrhea (malabsorption) May be associated with MEN1

Zollinger-Ellison Syndrome

Chapter 13: The GI Tract Flashcards

(78 cards)