DIT review - GI 1 Flashcards

1
Q

What are the neres that innervate each of the branchial arches

A

1st arch - CN V

2nd arch - CN VII

3rd arch - CN IX

4th-6th arches - CN X

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2
Q

Describe the branchial origin, as well as nerves responsible for taste, sensation, and motor of anterior 2/3 of tongue

A
  • Anterior 2/3:
    • Origin - 1st and 2nd branchial arch
    • Taste - CN VII
    • Sensation - CN V3
    • Motor - CN XII
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3
Q

Describe the branchial origin, as well as nerves responsible for taste, sensation, and motor of posterior 1/3 of tongue

A
  • Posterior 1/3:
    • Origin - 3rd and 4th branchial arch
    • Taste - CN IX, CN X (very posterior)
    • Sensation - CN IX, CN X (very posterior)
    • Motor - CN XII
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4
Q

Most common location of salivary gland tumors

A

Parotid gland

Usually benign; if they are located in a smaller gland, more likely to be malignant

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5
Q

Compare and contrast gastrischisis to omphalocele

A
  • Gastroschisis
    • Defect in abd wall
    • Extruding viscera not covered by sac
    • Other anomalies less common
  • Omphalocele
    • Defect in abd wall
    • Extruding viscera covered by sac (composed of peritoneum and amnion)
    • Liver often found protruding
    • Other anomalies common
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6
Q

Describe the defect and presentation of tracheoesophageal fistula

A
  • Most common type is esophageal atresia with distal tracheoesophageal fistula
    • Aka blind upper esophagus with lower esophagus joined to trachea
  • Presentation:
    • Polyhydramnios in utero
    • Air in stomach (visible on X-ray) – due to fistula
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7
Q

What are the components of CREST syndrome

A

Seen in limited type scleroderma

· Calcinosis / anti-centromere antibody

· Raynoud

· Esophageal dysmotility

· Sclerodactyly (tightening of skin with loss of wrinkles)

· Telangiectasias

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8
Q

What is the metaplastic change associated with Barret esophagus

A

Nonkeratinized stratified squamous –> columnar

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9
Q

What is Boerhaave syndrome

A
  • Transmural, usually distal esophageal rupture
  • Due to violent retching
  • Surgical emergency
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10
Q

Causes of esophagitis

A
  • GERD
  • Candida (white pseudomembrane)
  • CMV (linear ulcers)
  • HSV (punched-out ulcers)
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11
Q

Triad of Plummer-Vinson Syndrome

A
  • Dysphagia (due to Esophageal web)
  • Iron deficiency anemia
  • Glossitis
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12
Q

What is the most common esophageal cancer in America and what are its associations?

A
  • Adenocarcinoma
    • Occurs in distal 1/3 of esophagus
    • Associated with chronic GERD, Barrett esophagus, obesity, achalasia
    • More common in America
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13
Q

What is the most common esophageal cancer worldwide and what are its associations?

A
  • Squamous cell carcinoma
    • Occurs in the proximal 2/3 of esophagus
    • Associated with alcohol, smoking, and hot liquids
    • More common worldwide
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14
Q

Describe the branches of the celiac trunk

A
  • Celiac trunk - Pharynx, esophagus, proximal duodenum, liver, gallbladder, pancreas, spleen
    • Common hepatic artery
      • Gastroduodenal artery
        • R gastroepiploic - greater curvature of stomach (anastomoses with L gastroepiploic)
        • Anterior superior pancreaticoduodenal à head of pancreas, proximal duodenum
      • Right gastric artery - lesser curvature of stomach (anastomoses with L gastric a.)
      • Proper hepatic artery
    • Splenic artery - spleen
      • Left gastroepiploic artery - greater curvature of stomach
    • Left gastric artery - lesser curvature of stomach
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15
Q

What is the purpose of gastrin, and how does it accomplish this?

A
  • G-cells
    • Located in the antrum of the stomach (lower stomach)
    • Produce gastrin in response to decreased HCl
      • Gastrin can directly stimulate parietal cells to make gastric acid, but . . .
      • Gastrin’s main mechanism of action is to increase acid secretion mostly via effect on ECL cells –> histamine release –> histamine activation of parietal cells
    • Gastrin release stimulation by:
      • Phenylalanine
      • Tryptophan
      • Calcium
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16
Q

What is Zollinger-Ellison syndrome

A
  • Gastrin-secreting tumor (gastrinoma) of pancreas or duodenum
    • Too much gastrin à too much gastric acid à recurrent duodenal ulcers
  • Diagnosis:
    • Positive secretin stimulation test
      • Gastrin levels remain elevated even after administration of secretin, which normally inhibits gastrin release
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17
Q

Common causes of acute gastritis

A
  • NSAIDs - decreased PGE2 - decreased gastric mucosa protection
  • Burns (Curling ulcer) - hypovolemia - mucosal ischemia
  • Brain injury (Cushing ulcer) - increased vagal stimulation - increased ACh - increased H+ production
18
Q

Causes of chronic gastritis

A
  • H. Pylori
  • Autoimmune – antibodies against parietal cells
19
Q

Compare and contrast gastric vs. duodenal peptic ulcer disease (effect of eating, association with H. Pylori, other causes, risk for carcinoma)

A
  • Gastric ulcer:
    • Pain worse with meals
    • 70% due to H. Pylori
    • Other causes include NSAIDs
    • Increased risk of carcinoma
  • Duodenal ulcer:
    • Pain decreases with meals
    • 90% due to H. Pylori
    • Other causes include Zollinger-Ellison syndrome
    • Generally benign
20
Q

What is triple therapy for H. Pylori

A
  • Triple therapy = PPI + clarithromycin (or metronidazole) + amoxicillin
21
Q

What is menetrier disease?

A
  • Gastric hyperplasia of mucosa cells of the stomach
    • Leads to hypertrophied rugae which look like brain gyri
  • Atrophy of parietal cells - decreased gastric acid production
  • Increased risk of gastric carcinoma
22
Q

Presentation of gastric carcinoma

A
  • Weight loss, early satiety, acanthosis nigracans, Leser-Trelat sign
23
Q

What is Sister Mary Joseph nodule

A

Gastric carcinoma metastasis to subcutaneour periumbilical

24
Q

What is an acute gastric ulcer associated with elevated ICP or head trauma

A

Cushing ulcer

  • Brain injury (Cushing ulcer) - increased vagal stimulation -increased ACh - increased H+ production
25
Q

What is acute gastric ulcer associated with severe burns

A

Curling ulcer

26
Q

What is duodenal atresia and how does it present?

A
  • Failure of the duodenum to recanalize, so it is basically a blind pouch
  • Presents as bilious vomiting and abdominal distension
  • X-ray will should “double bubble”
    • Buildup of air distal to the pyloric sphincter (within the blind pouch)
    • Buildup of air proximal to the pyloric sphincter within the stomach
27
Q

Where is secretin produced and what is its function?

A
  • Produced by S cells of the duodenum
  • Increase pancreatic HCO3- secretion in order to neutralize gastric acid
  • Decreases gastric acid secretion
28
Q

Where is CCK produced and what is its function?

A
  • Produced by I cells of the duodenum
  • Stimulated in response to fatty acids
  • Increases pancreatic secretions
  • Increased gallbladder contractility
  • Relaxes the Sphincter of Oddi
  • Decreases gastric emptying
29
Q

Where is somatostatin produced and what is its function

A
  • Produce by D cells of pancreas and GI mucosa
  • Shuts down everything:
    • Gastrin, CCK, Secretin, GIP, VIP, Insulin, Glucagon
30
Q

Where is VIP produced and what is its function?

A
  • Produced by smooth muscle cells in gut and parasympathetic ganglia
  • Relaxes smooth muscle and sphincters throughout the GI tract
    • Causes copious diarrhea
31
Q

Symptoms of a VIPoma

A
  • VIPoma - WDHA (watery diarrhea, hypokalemia, achlorhydria)
32
Q

Name all of the retroperitoneal structures

A

SAD PUCKER:

S - suprarenal (adrenal) glands

A - Aorta and IVC

D - 2-4th part of duodenum

P - Pancreas (except tail)

U - ureters

C - Colone (ascending and descending)

K - Kidneys

E - thoracic esophagus

R - rectum

33
Q

Describe abetalipoproteinemia

A
  • Autosomal recessive
  • Lack of apoprotein B
    • B48 needed for chylomicron secretion from the intestinal cells
      • Enterocytes fill with chylomicrons that cannot pass into circulation
      • Fat malabsorption, steatorrhea, failure to thrive
    • B100 needed for LDL reuptake in the liver
34
Q

What is the characteristic histology of abetalipoproteinemia

A

Acanthocytes (“spur cells”)

35
Q

Pathogenesis and histology of celiac disease

A
  • Autoimmune tolerance to gliadin (gluten protein found in wheat)
  • Wheat protein cross-reacts with small bowel tissue leading to:
    • Inflammation
    • Antibodies against gliadin and tissue transglutaminase
  • Histology:
    • Blunting of villi
    • Crypt hyperplasia
    • Intraepithelial lymphocytosis
36
Q

Why can you get temporary lactose intolerance from enteritis?

A
  • Lactase is located at tips of villi
    • Temporary lactase deficiency can occur with enteritis when there is injury to the tips of villi
37
Q

Presentation of Tropical sprue

A
  • Unknown cause – probably infectious
  • Looks like celiac but:
    • Affects the entire small bowel
    • Responds to antibiotics
38
Q

What are the antibodies associated with celiac?

A

Anti-gliadin

Anti-transglutaminase

39
Q

What disease is associated with weight loss, diarrhea, arthritis, fever, adenopathy, and hyperpigmentation?

A

Whipple disease

40
Q

Describe Whipple disease (cause, presentation, histology)

A
  • Infection with Tropheryma whipplei
  • Symptoms:
    • Weight loss, lymphadenopathy, hyperpigmentation, cardiac symptoms, arthralgias, neurologic symptoms
  • Histology:
    • PAS (+) foamy macrophages in intestinal lamina propria
41
Q

What is the characteristic histology of abetalipoproteinemia

A
  • Will see abnormal star-shaped RBCs called acanthocytes (spur cells) - irregular spikes (vs. Echinocytes/burr cells)
  • Lack of apoprotein B
    • B48 needed for chylomicron secretion from the intestinal cells
      • Enterocytes fill with chylomicrons that cannot pass into circulation
      • Fat malabsorption, steatorrhea, failure to thrive
    • B100 needed for LDL reuptake in the liver