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GI/Nutrition > Review Flashcards > Flashcards

Review Flashcards

1
Q

The majority of epithelial components of the GI tract and accessory organs are derived from __________.

A

Endoderm

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2
Q

Folding in the __________ plane yields the primitive gut tube?

A

Transverse

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3
Q

Folding in the __________ plane yields the 3 subdivisions of the primitive gut tube.

A

Sagittal

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4
Q

What do the ventral and dorsal mesenteries do?

A

Attach the stomach to the body wall

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5
Q

Which way does the stomach rotate?

A

90˚ clockwise — LARP

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6
Q

How does the midgut loop rotate?

A

Rotates 90˚ counterclockwise around SMA
Midgut retracts and rotates another180˚ counterclockwise
cranial first (left) then caudal (right) (10 weeks)

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7
Q

The cloaca is partitioned by the ______________.

A

Urorectal septum - mesenchyme

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8
Q

What do the liver and biliary system develop from?

A

Ventral foregut endoderm

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9
Q

What does the pancreas develop from?

A

2 buds - dorsal and ventral foregut endoderm

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10
Q

Which bud forms the majority of the mature pancreas?

A

Dorsal pancreatic bud - FGF2 (notocord) inhibits Sonic -> Pancreatic development

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11
Q

Duodenal atresia/stenosis

A

Failure of duodenum to recanalize
Vomiting of stomach contents and bile
Leads to polyhydramnios

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12
Q

Extrahepatic biliary atresia

A

Jaundice, clay colored stools - death w/o surgical correction

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13
Q

Gastroschisis

A

Abdominal viscera extrude thru abdominal wall
Lateral to umbilicus on R
Eviceration

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14
Q

Omphalocele

A

Herniation of abdominal contents into proximal umbilicus
Failure to retract
Assoc. w/ cardiac and urogenital abnormalities

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15
Q

Non-rotation/malrotation

A

Abnormal intestine placement – volvulus

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16
Q

Mekel diverticulum

A

Out-pocketing of ileum

May become inflamed, mimic appendicitis

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17
Q

Hirschsprung disease

A

Aganglionosis of colon

Megacolon, dilated region = normal

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18
Q

What are the 4 main layers of upper GI tract?

A
  1. Mucosa
  2. Submucosa
  3. Muscularis Externa
  4. Adventitia/Serosa
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19
Q

What does the Submucosal (Meissner’s Plexus) control?

A

The muscularis mucosae - thin layer of smooth muscle

Movement, blood flow, gland secretion

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20
Q

What does the Myenteric (Auerbach’s plexus) control?

A

The muscularis externa - inner circular and outer longitudinal

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21
Q

Serosa

A

Simple squamous epithelium + CT in peritoneal cavity

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22
Q

What kind of epithelium does the esophagus have?

A

Stratified squamous

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23
Q

In what layers of the esophagus are glands located and what do they secrete?

A
  1. Mucosa: Cardiac glands - mucus

2. Submucosa: Mucus cells - basal nucleus & serous cells - central nucleus

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24
Q

What type of epithelium does the stomach have?

A

Simple columnar

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25
Q

What are the 5 types of enteroendocrine cells and what do they secrete?

A 
G Cells: Gastrin
EC cells: Serotonin
D cells: SST
A cells: Enteroglucagon
ECL cells: Histamine
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26
Q

What do parietal (oxyntic) cells secrete?

A

HCl and gastric intrinsic factor

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27
Q

What do chief sell secrete?

A

Digestive enzymes - stimulated by vagus nerve and secretin

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28
Q

What are the 3 phases of meal response?

A
  1. Cephalic phase
  2. Gastric phase
  3. Intestinal phase
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29
Q

What happens in the cephalic phase?

A

Think about food - Vagus - G cells + Parietal cells - HCl (30%)

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30
Q

What happens in the Gastric phase?

A

Food enters stomach - distention - G cells - HCl(60%)

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31
Q

What happens in the intestinal phase?

A

Chyme released into duodenum, gastric emptying slows
Enterogastric reflex
CCK and secretin suppress gastric activity (10% HCl)

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32
Q

Enterogastric reflex

A

Intestinal distention sends gastric inhibitory impulses thru the ENS

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33
Q

The sequence of peristalsis is determined by the ______________.

A

Nucleus ambiguus - “central pattern generator”

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34
Q

The cricopharyngeus muscle makes up what?

A

UES

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35
Q

True or false: Vagal efferents synapse on both inhibitory and excitatory myenteric neurons?

A

True
Excitatory: 2nd mess, Substance P
Inhibitory: cGMP, block Ca, hyperpol

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36
Q

What are 3 common mechanical causes of dysphagia?

A

Peptic stricture, esophageal ring, cancer

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37
Q

What are 3 common neuromuscular causes of dysphagia?

A

Achalasia, esophageal spasm, dysmotility

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38
Q

Chronic heartburn can lead to _______________.

A

Peptic stricutre

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39
Q

Progressive dysphagia + heartburn and regurgitation to both solids and liquids is indicative of what?

A

Achalasia or Scleroderma

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40
Q

What 3 diagnostic tests allow to to visualize the upper GI tract?

A
  1. Upper GI endoscopy - structure
  2. Esophageal manometry - function - gold stnadard for motor disorders
  3. Rad. Esophagram - structure and function
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41
Q

Achalasia

A

Impaired LES relaxation and loss of peristalsis - loss of inhibitory NO activity

42
Q

How do you treat achalasia?

A

NO donors &/or anticholinergics, BOTOX, operative

43
Q

What is the most important barrier to protect the esophagus from acid erosion?

A

Constant LES tone

44
Q

What is the #1 and #2 treatment for GERD?

A
  1. Lifestyle modification - weight loss, elevation of bed, avoid late/trigger meals
  2. PPI
45
Q

Eosinophilic Esophagitis

A

Epithelial infiltration by large #s of eosinophils superficially (15-20%)
T cell med hypersensitivity - Allergic rxn to inhaled/ingested allergens - MBP, IL5, IL13

46
Q

How does eosinophilic esophagitis present differently in adults vs. children?

A
  1. Adults: Dysphagia

2. Kids: Nausea, burning and food intolerance

47
Q

What 3 things may clue you in to eosinophilic esophagitis?

A
  1. Failure of acid suppressive meds
  2. Hx/FHx of atopia - atopic dermatitis, rhinitis, or asthma
  3. Corrugated esophagus, longitudinal furrows
48
Q

How do you treat Eosinophilic Esophagitis?

A
  1. Elimination diet

2. Steroids - topical

49
Q

What are causes of chemical esophagitis?

A

Acid, alkali (lye), alcohol, excessively hot fluids, smoking

Pills may lodge and dissolve - NSAIDs, Doxycycline

50
Q

What are common causes of viral esophagitis?

A

HSV - punched out ulcers, nuclear inclusions

CMV - shallow ulceration, cytoplasmic and nuclear inclusions

51
Q

What are other causes of infectious esophagitis?

A

Candida, bacterial - can invade LP and cause necrosis

52
Q

What are causes of iatrogenic esophagitis? (3)

A

Chemo, GVHD, radiation

53
Q

What skin disorders also have esophagitis? (4)

A

Bullous pemphigoid and epidermolysis bullosa, lichen planus, and Crohn’s disease

54
Q

Barretts Esophagus

A

Normal squamous epithelium is replaced by metastatic columnar mucosa

55
Q

What defines intestinal metaplasia in Barrett’s Esophagus?

A

Goblet cells - distinct mucus vacuoles

56
Q

What gene is likely involved in Barrett’s?

A

Cdx

57
Q

Who typically gets adenocarcinoma of the esophagus?

A

White, middle-aged male, western countries

58
Q

What are characteristics of esophageal adenocarcinoma?

A

Distal 1/3 of esophagus

Chromosomal changes and p53 mutations early

59
Q

Who gets squamous cell carcinoma of the esophagus?

A

African American males, >45yo, Iran, China, Hong Kong, Brazil

60
Q

What are risks for developing esophageal SCC?

A

EtOH, tobacco, poverty, Achalasia, Plummer-Vinson Syndrome, hot beverages

61
Q

What are characteristics of esophageal SCC?

A

Middle 1/3
Small grey/white plaque like thickenings - may invade
Travels to LN

62
Q

What are 6 ways saliva provides defense against bacteria?

A
  1. Lysozyme: Kills Gram +
  2. Peroxidase: Makes reactive Bromide and Iodine - kills bacteria
  3. Lactoferrin: Bind Fe
  4. IgA
  5. Defensins: pore complexes
  6. Mucins: modulate adhesion of bacteria
63
Q

Baseline slow wave activity of the stomach is mediated by which cells?

A

Interstitial cells of Cajal

64
Q

What is the goal for the small intestine to see calories?

A

1-4 kcal/min delivery

65
Q

What is fasting motor activity?

A

Max strength, frequency, and coordination to clear large solids (enteric coated meds)

66
Q

Contraction failure

A

Impaired triturition, retention of gastric contents, distention, pain and early satiety

67
Q

Accommodation failure

A

Food, mostly liquid moves too rapidly thru small bowel
Fluid enters lumen - weight loss
Unabsorbed food to colon - bacterial fermentation
Hypoglycemia
Duodenal Ulcer

68
Q

MMC failure

A

Failure to clear undigestible material

Bezoar, poor drug delivery, sm. intestine bacterial overgrowth

69
Q

Gastroparesis

A

Delayed emptying w/o mechanical obstruction
Early satiety, postprandial fullness, NV, bloating, pain
Must exclude other causes

70
Q

What two things do you get with Vagal injury?

A

Poor accommodation - liquids empty fast

Poor antral grinding - solids empty slow

71
Q

What is the mechanism of disfunction in diabetics?

A
  1. Extrinsic vagal dysfunction
  2. Loss of enteric neurons
  3. Loss of interstitial cells of Cajal
  4. Hyperglycemia effects motor fx
  5. Rapid or slow emptying
72
Q

Causes of elevated H+ secretion

A

INC gastrin, vagal tone, histamine, parietal cell mass, paraneoplastic or
DEC acid to antrum (retained antrum)

73
Q

By what mechanism does Zollinger Ellison Syndrome cause severe ulcer disease and where are they located?

A 
Gastrin secreting NE tumor
Isolated gastrinoma (75%)
Multiple Endocrine Neoplasia 1 (25%)
Distal duodenum and jejunum
74
Q

You suspect your patient has ZE, so you decide to do a secretin stimulation test. What must the Gastrin level be, to confirm the diagnosis?

A

Inc in Gastrin > 120

75
Q

What are other causes of gastrin-mediated inc. H+ secretion (5)

A 
H. pylori (dec. SST)
Antral G cell hyperplasia
Retained antrum
Gastric outlet obstruction
Renal failure
76
Q

What things cause decreased acid secretion

A
  1. Meds
  2. Inflammatory destruction of parietal cells
  3. Acute H. pyloric infection
  4. Vagal injury
  5. VIP producing tumors
77
Q

What 4 main symptoms will you see in a person with dec. acid secretion?

A
  1. Impaired protein digestion
  2. Impaired Fe, Ca, B12 absorption
  3. GI bacterial overgrowth
  4. Impaired delivery of drugs
78
Q

Decreased secretion of _________ and ________ is also affected by conditions that inhibit acid secretion.

A
  1. Pepsin

2. Lipase

79
Q

In the early stage of H. pylori infection, where is the infection commonly seen and what are the 3 main characteristics?

A

Antrum
Blocked D cell SST secretion
Inc. Gastrin/Acid
Duodenal ulcers

80
Q

In the late stage of H. pylori infection, where is the infection commonly seen and what are the 3 main characteristics?

A

Corpus/fundus
Destruction of parietal cells: inc gastrin & dec acid
Gastric ulceration

81
Q

Which 3 gastric neoplasias are associated with H. pylori infection?

A

Adenocarcinoma
MALToma
Carcinoid

82
Q

When is H. pylori typically acquired, and where is it common?

A

Childhood

Developing countries

83
Q

Autoimmune gastritis

A

Lymphocytic inflammation - destruction of parietal cells (Associated w/ CD, T1DM, Thyroid)
Inherited - parietal cells and IF
Women x3

84
Q

What is Atrophic Metastatic Gastritis and what can it lead to?

A
  1. Destruction of normal mucosa and replacement by metastatic elements (Goblet cells)
  2. Gastric cancer, gastric carcinoid
85
Q

What are the direct effects of NSAIDs on gastric toxicity?

A
  1. Trapped in epi cells
  2. Uncoupling of ox phos
  3. Dec. energy production
  4. Inc. cell permeability and rapid cell death
86
Q

What are the systemic effects of NSAIDs on gastric toxicity?

A

Blocks COX1:
Dec. mucosal BF and O2 delivery
Dec. mucin, bicarb and phospholipid
Epi proliferation and migration

87
Q

What is the difference between and ulcer and an erosion?

A

Ulcer - thru muscularis mucosa

Erosion - superficial to muscularis mucosa

88
Q

What two risk factors increase the chance of developing peptic ulcer disease?

A

Increased age and smoking

89
Q

90% of peptic ulcer disease is due to NSAIDs, __________, and unknown NSAID use.

A

H. pylori

90
Q

What are the symptoms of peptic ulcer disease?

A
  1. Chronic dyspeptic epigastric pain (2-3hrs - DU)
  2. Nausea, anorexia, weight loss
  3. Diarrhea = fistula
  4. May be asymptomatic
91
Q

In the setting of peptic ulcer disease, what does hematemesis indicate?

A

Loss of 25% of BV

92
Q

In the setting of peptic ulcer disease, what does melana indicate?

A

Loss of 33% of BV

93
Q

Who gets gastric adenocarcinoma?

A

Asian, hispanic, black, older men in developing countries

smoking, salt, nitrates

94
Q

What is the most common type of gastric adenoCA and what is it’s main risk factor?

A 
Intestinal type (50-70%)
H. pylori
95
Q

What is diffuse type gastric adenoCA associated with, what does it look like, and who gets it?

A
  1. Blood group A
  2. Signet ring cell histology
  3. Younger men or women
    * More aggressive
96
Q

What is the mutation associated w/ hereditary diffuse gastric adenocarcinoma and how is it inherited?

A

E-cadherin gene
AD
38 yo, inc. risk of breast cancer

97
Q

Is diffuse type EBV associated gastric adenocarcinoma considered more or less aggressive on average?

A

Less

98
Q

Who gets gastric lymphoma/MALToma and what is it associated with?

A

50-60 yo men

H pylori, if no t(11;18) and doesn’t extend below submucosa

99
Q

What are gastric carcinoid tumors are caused by and who gets them?

A

ECL sells that prolif and transform in response to inc. gastrin - Achlorhydria, ectopic gastrin
Women 60s/70s

100
Q

What is the typical course for gastric carcinoid?

A 
< 10%
Sporadic type (20%) from normal circ. Gastrin - 65% present w/ hepatic/local mets

GI/Nutrition (6 decks)

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