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Gastroenterology 3 Flashcards

1
Q

What is Rotor’s syndrome similar to?

A

Similar to Dubin-Johnson but milder (impaired liver excretion of conjugated bilirubin)

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2
Q

What differentiates Rotor’s syndrome from Dubin-Johnson?

A

No black liver

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3
Q

What are 2 mechanisms of neonatal jaundice?

A
  • ↑ bilirubin (more RBCs, shorter lifespan)
  • ↓ UDP-glucuronyl transferase activity (Takes 14 weeks for enzyme to reach adult level of function)
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4
Q

Neonatal jaundice results in increased [conjugated/unconjugated] bilirubin. This can lead to what condition?

A
  • Unconjugated
  • Kernicterus
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5
Q

Who is at the greatest risk for Neonatal jaundice?

A

Preterm infants

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6
Q

What is the treatment for Neonatal Jaundice?

A

Phototherapy - Converts bilirubin to lumirubin (more water soluble, allows excretion without conjugation)

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7
Q

What 2 substances do neck cells of the stomach secrete?

A

Mucous and bicarbonate

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8
Q

Where are parietal cells found?

A

In the gastric glands within the lamina propria of the mucosal layer of the stomach

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9
Q

Parietal cells are stained [color] in H&E staining

A

Pink (eosinophilic)

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10
Q

What are the 3 stimuli for Stomach acid secretion?

A
  • Gastrin (direct)
  • Gastrin (indirect)
  • Vagus nerve
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11
Q

What cells secrete gastrin? How does gastrin directly stimulate stomach acid secretion?

A
  • G cells in the antrum (distal) stomach
  • Binds to CCKb receptors on parietal cells
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12
Q

How does gastrin indirectly stimulate stomach acid secretion?

A

Gastrin binds to ECL cells → release histamine → stimulates parietal cells to release acid

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13
Q

How does the vagus nerve stimulate stomach acid secretion?

A

Releases ACh which activate M3 receptors on parietal cells

Acitvates G cells using gastrin releasing peptide (GRP) → gastrin secretion

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14
Q

What is a vagotomy? What was it previously used for?

A
  • Surgical disruption of vagus nerve to stomach
  • Old therapy for gastric ulcers
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15
Q

Why does atropine not work to suppress stomach acid secretion?

A

Blunts parietal stimulation by ACh but does not block stimulation by vagus nerve (GRP → gastrin secretion → HCL)

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16
Q

What cells secrete intrinsic factor?

A

Parietal cells

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17
Q

What 2 transporters are present on the luminal side of parietal cells?

A

H+/K+ ATPase, Cl- channel (separate secretion of H+ and Cl- for HCL)

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18
Q

Omeprazole, pantoprazole are classified under what drug class?

A

Proton pump inhibitor

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19
Q

H+ is formed by what enzyme in parietal cells?

A

Carbonic anhydrase (converts H2O and CO2 into HCO3- and H+)

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20
Q

What is the alkaline tide?

A

Increase of serum HCO3- after meals due to increase activity of carbonic anhydrase (to form HCL)

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21
Q

Vomiting can cause metabolic [acidosis/alkalosis]

A

Alkalosis

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22
Q

What are 2 mechanisms that explain how vomiting causes metabolic alkalosis?

A
  • Loss of HCL
  • Increased production of H
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23
Q

What are 2 mechanisms that explain how vomiting causes metabolic alkalosis?

A
  • Loss of HCl
  • Increased production of HCl leads to generation of HCO3-
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24
Q

Urinary [electrolyte] is useful in metabolic alkalosis with unknown cause.

A

Cl-

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25
Q

Unexplained metabolic alkalosis with low urinary Cl- suggests…

A

surreptitious vomiting

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26
Q

Unexplained metabolic alkalosis with high urinary Cl- suggests…

A

diuretic use (blocks NaCl resorption)

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27
Q

Parietal secretion is activated by what 3 gastrointestinal secretions?

A
  • Gastrin
  • ACh
  • Histamine
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28
Q

Parietal secretion is inhibited by what 2 gastrointestinal secretions?

A
  • Somatostatin
  • Prostaglandin

*inhibits proton pump

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29
Q

What is the second messenger for ACh?

A

Gq- IP3/Ca2+

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30
Q

What is the second messenger for histamine?

A

Gs- cAMP

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31
Q

What is the second messenger for somatostatin?

A

Gi- cAMP

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32
Q

What is the second messenger for gastrin?

A

Gq- IP3/Ca2+

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33
Q

What is the second messenger for prostaglandin?

A

Gi- cAMP

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34
Q

Cimetidine, ranitidine, famotidine, and nizatidine are classified under what drug class? What effect will this have?

A

Histamine (H2) blocker, blunts acid secretion

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35
Q

Misoprostol is a [drug class]. What effect will this have on the GI system?

A

PGE1 analog, blunts acid secretion

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36
Q

_____ cells are found in the upper layers of the gastric glands and _____ cells are found in the deeper layers.

A

Parietal, Chief

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37
Q

Chief cells stain [color] on H&E staining.

A

dark colored (basophilic)

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38
Q

What do chief cells secrete?

A

Pepsinogen (converted to pepsin by H+)

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39
Q

What stimulates the release for pepsinogen?

A

vagus nerve (i.e. about to eat, thinking about eating)

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40
Q

What does pepsin do?

A

digest protein

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41
Q

What are 3 effects of gastrin?

A
  • Stimulates H+ secretion by parietal cells (directly and indirectly)
  • Stimulates growth of gastric mucosa
  • Increases gastric motility
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42
Q

What is the most important parietal cell receptor?

A

histamine

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43
Q

Gastrin is released in response to [4]

A
  • Stomach distention
  • Alkalinization
  • Amino acids (especially phenylalanine and tryptophan)
  • Vagal stimulation (mediated by GRP)
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44
Q

Gastrin release is inhibited by [2]

A
  • Low pH
  • Somatostatin
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45
Q

What is Zollinger-Ellison Syndrome?

A
  • Gastrin secretin tumor that occurs in the duodenum or pancreas
  • Leads to excessive acid secretion and hypertrophy of mucosa
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46
Q

What are 4 common symptoms seen in Zollinger-Ellison Syndrome?

A
  • Abdominal pain: improves with food
  • Chronic diarrhea: low pH in intestine inactivates pancreatic enzymes + inhibits sodium/water absorption → poor digestion, steatorrhea
  • Ulcers: most in distal duodenum
  • Heartburn
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47
Q

What are 2 ways to diagnose a Gastrinoma?

A
  • Fasting serum gastrin levels
  • Secretin test
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48
Q

What are 2 ways to diagnose a Gastrinoma?

A
  1. Fasting serum gastrin levels
  2. Secretin test
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49
Q

What is a secretin test? What does it test for?

A

A secretin test measures the gastrin level in response to secretin administration. Normal G cells are inhibited by secretin, but Gastrinomas are stimulated by it.

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50
Q

What happens to gastrin levels after secretin administration?

A

Gastrin levels will rise after secretin administration.

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51
Q

What does the secretin test help differentiate?

A

It helps differentiate gastrinomas from other causes of increased gastrin.

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52
Q

What are 3 possible treatments for Gastrinomas?

A
  1. High dose proton pump inhibitor
  2. Octreotide (somatostatin analog)
  3. Surgical excision
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53
Q

What is pernicious anemia?

A

Pernicious anemia is an autoimmune gastritis that leads to the loss of parietal cells and intrinsic factor, resulting in the inability to absorb Vitamin B12.

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54
Q

What is a typical lab finding in pernicious anemia?

A

High gastrin levels leading to G-cell hyperplasia.

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55
Q

What cells release Cholecystokinin?

A

I cells in the small intestine.

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56
Q

What are 4 effects of Cholecystokinin?

A
  1. Stimulate gall bladder contraction
  2. Relaxation of sphincter of Oddi
  3. Stimulate pancreatic enzyme secretion
  4. Inhibits gastric emptying
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57
Q

How does Cholecystokinin stimulate pancreatic enzyme secretion?

A

It binds to CCK receptors in the vagus nerve, leading to ACh release which stimulates the pancreas.

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58
Q

What are 2 stimuli for Cholecystokinin release?

A
  1. Fatty acids and monoglycerides (not triglycerides)
  2. Amino acids
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59
Q

When is a HIDA scan performed?

A

To evaluate RUQ pain, usually when Ultrasound is non-diagnostic.

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60
Q

How is a HIDA scan performed? What information can be obtained?

A

Administer 99mTc-hepatic iminodiacetic acid, which should concentrate in the bladder and pass to the intestines. Radioactivity can be followed, and failure to fill the gallbladder suggests obstruction.

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61
Q

What GI hormone can sometimes be administered with a HIDA scan? What can this tell us?

A

Cholecystokinin can be administered to measure gall bladder ejection fraction before and after.

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62
Q

What cells release secretin?

A

S cells of the duodenum.

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63
Q

What stimulates secretin secretion?

A
  1. H+ in duodenum
  2. Fatty acids in duodenum
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64
Q

What are 4 effects of Secretin?

A
  1. Increases HCO3- secretion by pancreatic duct cells (raises pH in small intestine)
  2. Inhibits gastric H+ secretion
  3. Increases bile secretions
  4. Promotes pancreatic flow: water secreted with bicarb
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65
Q

What does somatostatin do to GI hormones?

A

Somatostatin inhibits most GI hormones.

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66
Q

Where is somatostatin found?

A
  1. Originally discovered in the hypothalamus
  2. Released by D cells throughout the GI tract
  3. Found in nerves throughout the body
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67
Q

What are the 2 stimuli for somatostatin secretion in the GI tract?

A
  1. Low pH (no food in stomach)
  2. Decreased vagus nerve stimulation
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68
Q

How does somatostatin regulate digestion/acid secretion?

A

When pH rises with food in the stomach, somatostatin release is inhibited, allowing other GI hormones to function. Acid in the stomach without food causes somatostatin release, shutting down other hormones.

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69
Q

What are 6 effects of somatostatin in the GI tract?

A
  1. Inhibit gastric H+ secretion
  2. Inhibits pepsinogen secretion
  3. Inhibit gall bladder contraction
  4. Inhibit intestinal fluid secretion
  5. Inhibit pancreatic fluid secretion
  6. Inhibit insulin and glucagon release
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70
Q

What drug class is Octreotide? What are 4 indications for this drug?

A

Octreotide is a somatostatin analog.

Indications include:
1. Acromegaly
2. GI bleed/bleeding varices
3. Carcinoid syndrome: can improve flushing and diarrhea
4. Gastrinoma/Glucagonoma

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71
Q

What is Acromegaly?

A

A hormonal disorder that results from excess growth hormone.

Not included in the provided text.

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72
Q

What are GI bleed/bleeding varices?

A

Conditions related to bleeding in the gastrointestinal tract, often due to varices.

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73
Q

What is Carcinoid syndrome?

A

A condition that can improve flushing and diarrhea.

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74
Q

What are Gastrinoma and Glucagonoma?

A

Types of neuroendocrine tumors that secrete gastrin and glucagon, respectively.

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75
Q

Why is Ocretotide used in GI bleeding?

A

Reduces splanchnic blood flow in bleeding varices.

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76
Q

What 2 effects does Glucose-dependent insulinotropic peptide (GIP) have?

A
  • Stimulates insulin release
  • Blunts H+ secretion
77
Q

GIP is released by what cells?

A

K cells of the duodenum/jejunum.

78
Q

What stimulates GIP release?

A

Glucose, fatty acids, amino acids.

79
Q

Is oral glucose metabolized slower or faster than IV glucose?

80
Q

Does IV glucose stimulate GIP release?

81
Q

Vasoactive Intestinal Peptide (VIP) is synthesized in what type of cells?

82
Q

What triggers the release of Vasoactive Intestinal Peptide (VIP)?

A

Action potential on target cells.

83
Q

What are 3 effects of Vasoactive Intestinal Peptide (VIP)?

A
  • Causes relaxation of smooth muscle: Important for LES
  • Raises pH: stimulates pancreatic HCO3- secretion, bicarb draw water and increases pancreatic flow
  • Inhibits gastric H+ secretion
84
Q

What is a VIPoma?

A

Rare VIP secreting tumors in pancreas (islet cells).

85
Q

What are 3 classic findings in a patient with VIPoma?

A
  • Watery diarrhea (secretory diarrhea): Tea-colored, odorless, resembles cholera
  • Hypokalemia (from high volume diarrhea)
  • Achlorhydria (high pH in stomach)
86
Q

VIPoma is sometimes referred to as the?

A

WDHA syndrome.

87
Q

VIPoma normally occurs in children or adults?

88
Q

What are 3 possible treatments for VIPoma?

A
  • Octreotide
  • Fluid/electrolyte replacement
  • Surgical resection (may not be possible due to metastasis)
89
Q

What is the prognosis for VIPoma?

90
Q

What is the function of motilin?

A

Promotes motility in the fasting state.

91
Q

When are Motilin levels the highest?

A

Between meals.

92
Q

[Drug] binds motilin receptors and is used to treat gastroparesis.

A

Erythromycin.

93
Q

What are the phases of digestion and what is occurring?

A

Cephalic: Think about eating, sight/smell of food, dominated by Vagus nerve (H+ and gastrin secretion).

Gastric phase: Consume food → gastric distension, increase gastric pH, amino acids.

Intestinal phase: Food reaches intestines, CCK, Secretin, GIP release.

94
Q

What are the types of exocrine cells in the pancreas?

A
  • Acinar cells
  • Ductal cells
95
Q

Salivary duct cells are permeable or impermeable to water?

A

Impermeable.

96
Q

Pancreatic ductal cells are permeable or impermeable to water?

A

Permeable.

97
Q

What does pancreatic fluid consist of?

A

Bicarb, water and electrolytes (Na+, Cl-, K+).

98
Q

What do acinar cells in the pancreas secrete?

A

Enzymes and some fluid (mostly Na, Cl).

99
Q

What do ductal cells in the pancreas secrete?

A

Bicarb, water.

100
Q

What 2 electrolytes remain constant despite changes in flow rate?

A

Na+, K+ (always isotonic).

101
Q

When there is a low pancreatic fluid flow, there is a high or low Cl- and high or low bicarb concentration?

A

High Cl-, Low bicarb.

102
Q

What is the Cl- and bicarb concentration when there is low pancreatic fluid flow?

A

High Cl-, Low bicarb

103
Q

What is the Cl- and bicarb concentration when there is high pancreatic fluid flow?

A

Low Cl-, High bicarb

104
Q

Why is bicarb high in pancreatic fluid when the flow rate is high?

A
  • Bicarb secreted in small ducts and reabsorbed in large ducts
  • Reabsorption ineffective at high flow rates
105
Q

What is the main stimulus for HCO3- secretion in pancreatic fluid?

106
Q

What is the main stimulus for pancreatic enzyme release in pancreatic fluid?

A
  • Main stimulus is Cholecystokinin
  • Also ACh via vagovagal reflexes
107
Q

Name 6 pancreatic enzymes.

A
  • α-amylase
  • Lipase
  • Phospholipase A
  • Colipase
  • Proteases
  • Trypsinogen
108
Q

α-amylase digests _____ which is normally found in _____

A

Starch, plants

109
Q

Starch contains what 2 molecules?

A
  • Amylin: linked D-glucose chain
  • Amylopectin: branched chain polymer of D-glucose units
110
Q

α-amylase hydrolyzes what bond?

A

Breaks α1-4 linkages

111
Q

What are the 2 types of α-amylase? Where do they function?

A
  • Salivary amylase: optimal pH >6, inactivated in stomach
  • Pancreatic amylase: functional in small intestine
112
Q

What 3 pancreatic enzymes are elevated in acute pancreatitis?

A
  • Pancreatic amylase
  • Pancreatic lipase
113
Q

α-amylase breaks down amylose and amylopectin into what 3 molecules?

A
  • Maltose (2 glucose)
  • Maltotriose (3 chain glucose)
  • Limit Dextrins: short polysaccharides that have a branch
114
Q

What is the rate limiting step of carbohydrate digestion?

A

Digestion of carbs at intestinal brush border

115
Q

Carbohydrates are absorbed in what form?

A

Monosaccharides

116
Q

After digestion via α-amylase, further digestion is needed at the [location]. This is done via what enzymes?

A
  • Intestinal brush border
  • “Oligosaccharide hydrolases”: Maltase, Sucrase, Lactase
117
Q

What are the 3 monosaccharides absorbed by the small intestine?

A

Glucose, fructose, galactose

118
Q

Pancreatic lipase hydrolyzes what bonds? What is the result?

A
  • Hydrolyzes 1- and 3- bonds of triglycerides
  • Result: fatty acids plus monoglycerides
119
Q

What does Phospholipase A2 hydrolyze?

A

Phospholipids

120
Q

Phospholipase A2 is secreted as a proenzyme and activated by…

121
Q

What are 4 pancreatic enzymes that digest protein?

A
  • Trypsin
  • Chymotrypsin
  • Elastase
  • Carboxypeptidases
122
Q

All protein digestion enzymes are secreted as?

A

Proenzymes (zymogens)

123
Q

How are protein digestion enzymes activated?

A

Pancreas secretes trypsinogen → activated to trypsin via

124
Q

What are protein digestion enzymes secreted as?

A

Proenzymes (zymogens)

125
Q

How are protein digestion enzymes activated?

A

Pancreas secretes trypsinogen → activated to trypsin via enterokinase at brush border → trypsin activates all other protein enzymes

126
Q

What is the underlying pathophysiology of acute pancreatitis?

A

Blocked secretion of enzymes while synthesis ongoing → Large amounts of trypsin activated → Trypsin activates more trypsin → activates other protein digestion enzymes → ‘Auto-digestion’

127
Q

Which pancreatic enzyme is more specific for pancreatic damage?

128
Q

What are 3 possible indications for Pancreatic Enzyme Replacement?

A
  • Cystic fibrosis
  • Chronic pancreatitis
  • Post pancreatectomy
129
Q

What are 3 histological findings in Reflux esophagitis?

A
  • Basal zone (epithelium) hyperplasia
  • Lamina propria papilla elongate
  • Eosinophils and neutrophils (eosinophils normally not present in mucosal layer of esophagus)
130
Q

What may pediatric GERD develop due to?

A

Immature lower esophageal sphincter

131
Q

What are 6 risk factors for GERD?

A
  • Alcohol
  • Smoking
  • Obesity
  • Fatty foods
  • Caffeine
  • Hiatal Hernia
132
Q

What are 4 GERD symptoms?

A
  • Heartburn
  • Damage to enamel of teeth
  • Dysphagia
  • Respiratory symptoms: cough, dyspnea, asthma (adult-onset)
133
Q

What is a treatment for refractory GERD?

A

Nissen fundoplication, reserved for patients that do not respond to medical therapy

134
Q

What are 2 classes of drugs used to treat GERD?

A
  • Proton pump inhibitors
  • Histamine (H2) blockers
135
Q

Name a Histamine (H2) blocker.

A

Famotidine, Ranitidine, Nizatidine, Cimetidine

136
Q

What are 3 potential consequences of GERD?

A

Ulcers, Fibrosis, Strictures

137
Q

What is Lye? Where is it commonly found?

A

Alkali substances found in household cleaners, causes liquefactive necrosis of the mucosal layer of esophagus

138
Q

Who usually ingests Lye accidentally, and what can it lead to in the esophagus?

A

Children, Strictures

139
Q

What can long-standing GERD result in?

A

Barrett’s esophagus

140
Q

What is Barrett’s esophagus?

A

Metaplasia of esophagus (Squamous epithelium → intestinal epithelium)

141
Q

What are 2 histological findings seen in Barrett’s esophagus?

A
  • Intestinal mucosa: non-ciliated columnar epithelium
  • Goblet cells
142
Q

How is Barrett’s esophagus diagnosed? What is the next step if Barrett’s is seen?

A
  • Endoscopy
  • If Barrett’s seen → regular surveillance endoscopy + Biopsies to look for carcinoma
143
Q

What is an important risk factor for esophageal cancer?

144
Q

What is the classic presentation of esophageal cancer?

A
  • ‘Progressive dysphagia’: starts with solids, progresses to liquids
  • Weight loss, hematemesis
145
Q

What are the 2 types of esophageal cancer? What form is most common in the US/worldwide?

A
  • Squamous Cell carcinoma (most common worldwide)
  • Adenocarcinoma (most common in US)
146
Q

What are the 2 types of esophageal cancer?

A
  1. Squamous Cell Carcinoma (most common worldwide)
  2. Adenocarcinoma (most common in US)
147
Q

What disease is Esophageal Adenocarcinoma associated with?

A

Esophageal Adenocarcinoma is associated with GERD.

148
Q

What are two risk factors for Esophageal Adenocarcinoma?

A
  1. GERD (GERD → Barrett’s → Glandular epithelium)
  2. Obesity
149
Q

In what part of the esophagus does Squamous Cell Carcinoma develop?

A

SCC develops in the mid or upper esophagus.

150
Q

In what part of the esophagus does Adenocarcinoma develop?

A

Adenocarcinoma develops in the lower 1/3 of the esophagus.

151
Q

What are 5 risk factors for esophageal squamous cell carcinoma?

A
  1. Food (alcohol, hot tea)
  2. Achalasia (backup of food)
  3. Esophageal webs (backup of food)
  4. Zenker’s
  5. Lye ingestion
152
Q

What are 2 symptoms unique to esophageal squamous cell carcinoma?

A
  1. Hoarse voice
  2. Cough
153
Q

What lymph node(s) drain the upper esophagus?

A

Cervical nodes

154
Q

What lymph node(s) drain the middle esophagus?

A
  1. Mediastinal nodes
  2. Tracheobronchial nodes
155
Q

What lymph node(s) drain the lower esophagus?

A
  1. Celiac nodes
  2. Gastric nodes
156
Q

What are 3 infectious causes of esophagitis?

A
  1. Candida: White membranes
  2. HSV-1: Can involve esophagus, ‘Punched out’ ulcers
  3. CMV: AIDS (CD4<50), form Linear ulcers
157
Q

What is Eosinophilic Esophagitis?

A

An immune mediated allergic reaction (unknown antigen).

158
Q

What are 3 findings in a classic scenario of Eosinophilic Esophagitis?

A
  1. Dysphagia
  2. Poor response to GERD treatment
  3. Eosinophils on biopsy
159
Q

What is Achalasia?

A

Inability to relax lower esophageal sphincter.

160
Q

What causes Achalasia?

A

Due to loss of ganglion cells in Auerbach’s plexus.

161
Q

What are 2 causes of Achalasia?

A
  1. Often idiopathic
  2. Chronic Chagas Disease (Protozoa: Trypanosoma cruzi)
162
Q

What are 2 symptoms of Achalasia?

A
  1. Dysphagia to solids and liquids
  2. Bad breath (food accumulation in esophagus)
163
Q

What are 2 diagnostic tests used for achalasia?

A
  1. Barium swallow: ‘bird’s beak’
  2. Esophageal manometry: Shows ↑ LES tone in achalasia
164
Q

What are esophageal varices?

A

Dilated submucosal vein, usually in lower 1/3 esophagus.

165
Q

What are esophageal varices usually caused by?

A

Usually due to portal hypertension (cirrhosis).

166
Q

Esophageal varices can lead to what?

A

Esophageal varices can lead to upper GI bleeding.

167
Q

What is the treatment for esophageal variceal bleed?

A

Emergent endoscopy for banding/ligation.

168
Q

What is Malloy-Weiss Syndrome?

A

Damage to esophageal mucosa at GE junction.

169
Q

What causes Malloy-Weiss Syndrome?

A

Caused by severe chronic vomiting i.e. Alcoholism, bulimia.

170
Q

How does Malloy-Weiss Syndrome present?

A

Painful hematemesis (Epigastric pain or pain in the back).

171
Q

What is BoerHaave Syndrome?

A

Transmural rupture of esophagus.

172
Q

What causes BoerHaave Syndrome?

A

Result of severe, chronic vomiting or retching.

173
Q

What is a radiology and clinical finding seen in BoerHaave Syndrome?

A

Air in mediastinum on chest x-ray (pneumomediastinum).

174
Q

What is a radiology and clinical finding seen in BoerHaave Syndrome?

A

Air in mediastinum on chest x-ray (pneumomediastinum)

175
Q

What is a physical exam finding in BoerHaave Syndrome?

A

Subcutaneous emphysema: crackling sound when you press on the neck due to air under the skin

176
Q

What are Esophageal Webs and Rings?

A

Extension of mucosa into lumen of esophagus which obstructs movement of food → dysphagia

177
Q

Where are Esophageal Webs located?

A

Webs: upper esophagus

178
Q

Where are Esophageal Rings located?

A

Rings: lower esophagus

179
Q

What is the risk associated with Esophageal Webs and Rings?

A

Increased risk for squamous cell carcinoma

180
Q

What is a Schatzki Ring?

A

Type of esophageal ring at the squamocolumnar junction

181
Q

What type of mucosa is found in a Schatzki Ring?

A

Squamous mucosa proximally, columnar distally

182
Q

What is the clinical triad seen in Plummer-Vinson Syndrome?

A

Iron deficiency anemia, beefy red tongue: damage to tongue mucosal layer, esophageal web

183
Q

What demographic is commonly affected by Plummer-Vinson Syndrome?

A

Middle-age, white women

184
Q

Zenker’s diverticulum is a [true/false] diverticulum?

185
Q

What layers of the GI tract are involved in Zenker’s diverticulum?

A

Breakdown of muscular layer in esophagus that allows mucosa/submucosa to protrude

186
Q

Where does Zenker’s diverticulum occur?

A

At the junction of the esophagus and pharynx

187
Q

How is a Zenker’s diverticulum usually formed?

A

Cricopharyngeal muscle fails to relax → Chronic high pressure in pharynx to force food down → diverticulum

188
Q

What is the classic location of a Zenker’s diverticulum?

A

At the junction of the esophagus and pharynx, formed by the cricopharyngeal muscle

First Aid (18 decks)

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