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UBC Medicine Preclinical GI Curriculum > GI Flashcards from Alia (Dropbox File) > Flashcards

GI Flashcards from Alia (Dropbox File)

1
Q

What are the derivatives of the foregut?

A

Anything from pharynx to major duodenal papilla, plus:

  • liver, pancreas
  • biliary apparatus
  • trachea, lungs which bud off the esophagus
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2
Q

What is the composition and innervation of the esophagus?

A
  • Top 2/3
    • somatic, striated
    • Vagus
  • Bottom 1/3
    • autonomic, smooth
    • Vagus nerve via celiac plexus
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3
Q

During the formation of the stomach, which way does it turn.
Where do the vagus nerves end up?

A
  • Clockwise 90 degrees
  • Lesser curvature on right
  • Greater curvature on left
  • Right vagus ends up behind stomach (posterior stomach)
  • Left vagus ends up in front of stomach (anterior stomach)
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4
Q

What are the mesenteries of the foregut?

A
  • Behind stomach: dorsal mesogastrium/mesentery
  • In front of stomach: ventral mesogastrium/mesentery → split by liver into lesser omentum (hepatoduodenal and hepatogastric ligaments) and falciform ligament
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5
Q

What is contained within the hepatoduodenal ligament?

A

Bile duct, hepatic artery, portal vein

(all incoming blood and outgoing bile)

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6
Q

What is one congenital malformation of the stomach?

S/Sx

A
  • Congenital hypertrophic pyloric stenosis: hypertrophy of the pylorus inhibiting passage of food into duodenum
  • Projectile vomiting due to outflow obstruction and vigorous peristalsis of stomach
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7
Q

What is the blood supply of the duodenum?

A

Both foregut/midgut

Celiac and superior mesenteric artery

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8
Q

What are congenital malformations of the duodenum?

S/Sx

A
  • Duodenal stenosis: incomplete recanalization of duodenum causing partial occlusion of lumen
  • Duodenal atresia: complete occlusion of the duodenum
  • S/Sx = vomiting (with bile) a few hours after birth
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9
Q

What forms the parenchyma of the liver?

A

The foregut liver bud grows upwards and meets the septum transversum

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10
Q

What forms the stroma of the liver?

A

The septum transversum (mesoderm) forms the stroma of the liver

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11
Q

What are the congenital malformations of the GB/liver?

A
  • Extrahepatic biliary atresia: failure of recanalization
  • Bifid gallbladder: duplication of gall bladder
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12
Q

How does the pancreas develop?

A
  • Ventral bud
    • Attached to the bile duct/liver
    • Rotates clockwise with the duodenum to join up with the dorsal bud of the pancreas
  • Dorsal bud
    • attached to posterior abdominal wall
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13
Q

Where does the main pancreatic duct develop?

Where does the dorsal pancreatic bud form?

A
  • Main pancreatic duct
    • forms as part of ventral pancreatic bud which is attached to the common bile duct
  • Acessory pancreatic duct
    • forms as a part of the dorsal pancreatic bud
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14
Q

What is an annular pancreas?

A

A malrotated pancreas which surrounds the duodenum and constricts it

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15
Q

What tissue is the spleen derived from?

Retro/secondary retro/intra?

A
  • Derived from mesogastrium mesenchymal cells
  • Intraperitoneal, develops between the 2 layers of the dorsal mesogastrium
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16
Q

Embryonic origin of esophagus lining?

Embryonic origin of muscular esophagus?

____peritoneal

A
  • Endoderm
  • Mesoderm
  • Intraperitoneal
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17
Q

Embryonic origin of stomach lining?

____peritoneal?

A
  • Lining- endoderm
  • Mesogastrium- mesoderm
  • intraperitoneal
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18
Q

Embryonic origin of liver parenchyma?

A

Foregut Endoderm

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19
Q

Embryonic origin of liver stroma?

A

Septum transversum mesoderm

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20
Q

Embryonic origin of GB?

A

Foregut endoderm

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21
Q

Embryonic origin of cystic and common bile duct?

A

Foregut endoderm

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22
Q

Embryonic origin of pancreas

_______ peritoneal

A
  • Foregut endoderm
  • Starts as intraperitoneal → secondary retroperitoneal
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23
Q

Embryonic origin of spleen

A

Mesoderm

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24
Q

Parasympathetic and Sympathetic innervation of the esophagus

A
  • Parasympathetic
    • upper 1/3: striated
      • Vagus
    • Lower 2/3: smooth
      • vagus via celiac plexus
  • Sympathetic
    • T1-T10
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25
Q

Stomach

  • Arterial supply
  • Venous supply
  • Nervous supply
A
  • Arterial supply
    • Celiac artery
  • Venous supply
    • Portal vein → IVC
  • Nervous supply
    • Parasympathetic
      • Hepatic (L) vagus (anterior)
      • celiac (R) vagus (posterior)
    • Sympathetic
      • T6-T10
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26
Q

The ENS includes the _____ plexus located _____ and the _____ plexus in the _____.

A
  • Myenteric plexus, outer muscle layers
  • Submucosal plexus, submucosa
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27
Q

The myenteric plexus is involved in the motility of the Gi via _______

A
  • Tonic >< of sphincters
  • Rhythmic segmentation
  • Oscillatory movements
  • Peristalsis
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28
Q

The submucosal plexus mainly innervates ______

A
  • Villi for movement
  • Endocrine cells
  • Secretory cells
  • Blood vessels
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29
Q

What are the roles of hormones in gut motility?

A

Secondary role in motility via modification of ENS inputs of movement

  • modulate responses to ICCs, impact intracellular Ca concentration
  • influence resting contractility of muscle in upper GI
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30
Q

What is the main control of motility in the gut?

A

Mainly controlled by ENS → specifically myenteric plexus

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31
Q

What is the main control of secretion in the GI?

A

Both neural and hormonal → more closely related

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32
Q

Describe the effects of gastrin release

A
  • Gastrin is released from G cells when stimulated by release of GRP from neurons
  • Gastrin stimulates ECL → histamine
  • Gastrin → Parietal cell → HCL
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33
Q

Describe the effects of Ach release from neurons

A
  • Ach released from neurons with PNS stimulation
  • Ach → ECL → histamine
  • Ach → parietal cell → HCl
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34
Q

Describe the effects of histamine release from ECL cells

A

Histamine causes release of HCl from parietal cell

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35
Q

Describe the effects of intrinsic interneurons in the ENS

A
  • Direct to parietal cells → HCl
  • Through GRP/G cells → gastrin
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36
Q

How does the PNS affect the ENS?

  • input?
  • effects?
A

Vagal nuclei + Sacral spinal cord preganglionic fibers synapse in the ENS → postganglionic fibers

  • to the Muscularis externa, muscularis mucosae, secretory cells, endocrine cells, blood vessels
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37
Q

How does the SNS affect the ENS?

  • input?
  • effects?
A

Input: preganglionic fibers → sympathetic ganglia → postganglionic fibers

  • directly to the blood vessels
  • to the ENS → muscularis externa, muscularis mucosa, secretory cells, endocrine cells
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38
Q

Where is auerbach’s plexus?

  • Main results…

Where is Meissner’s plexus?

  • Main results…
A
  • Auerbach = external myenteric → secretory, smooth muscle
  • Meissner = submucosal → mostly secretory
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39
Q

What are the main inhibitory NTs in the myenteric plexus?

What is the result of these NTs?

A

NO, VIP, ATP

  • Decrease contraction, increase secretomotor
  • Overall slow food passage and increase digestion
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40
Q

What are the main excitatory NTs in the myenteric plexus?

A
  • Ach
  • Substance P
  • Serotonin
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41
Q

What are the (2) functions of the submucosal plexus?

A
  • Movement of villi
  • Secretion of endocrine and exocrine
42
Q

What are the major stimulatory hormones of the submucosal plexus?

A
  • Ach,
  • VIP
43
Q

Define: co-localization

A

A neuron that contains more than one NT

44
Q

D: secretomotor neuron

A

A neuron that induces a gland

45
Q

D: slow wave

A
  • Spontaneous rhythmic fluctuations in the resting membrane potential intrinsic to the GIT
  • Frequency is region specific
  • Slow wave because 5 seconds long
46
Q

D: tonic contraction

D: sphincter

A
  • Tonic contraction
    • sites of circular muscle contraction that separate different areas of GIT
  • Sphincter
    • areas of prolonged tonic contraction to help ensure unidirectional movement
47
Q

What are the ICCs?

A
  • Pacemaker cells of the GI → myenteric plexus and muscle layers
  • Generate and propagate slow waves
48
Q
  • Explain the AP of a slow wave
    • Channels
    • Ions
A
  • Rising phase
    • Calcium in through voltage gated Ca channels
  • Plateau phase
    • K out through Ca dependent K channels open = Ca
  • Repolarization phase
    • K out through Ca dependent K channels
49
Q

What is the relationship between slow wave and spike potentials, what is the result?

A
  • Slow waves reach threshold, trigger spikes
  • Each spike potential releases more Ca via voltage gated Ca channels
  • This results in a greater contraction force
50
Q

Name 5 ways calcium is INCREASED in a GI cell

A
  1. Voltage gated Ca channels
  2. Receptor activated Ca channels → respond to ligand
  3. Stretch activated Ca channels
  4. Neurotransmitter/hormone receptor → PLC → IP3 → Ca released from ER
  5. Store operated Ca channels → respond to decreased intracellular Ca (as it’s being used up)
51
Q

Name 3 ways calcium is DECREASED in GI cell

A
  1. Ca is extruded from cells via Ca-ATPase pump
  2. Ca is extruded via Na/Ca exchangers
  3. Ca is taken up into intracellular stores
52
Q

How does NE/E effect the GI cell?

A
  • Cause K efflux from cells, leads to hyperpolarization → relaxation
  • Inhibits contraction
53
Q

Pharyngeal peristalsis is triggered by ____ and mediated by pharyngeal muscles

A

Bolus of food triggering tactile receptors in pharynx

54
Q
  • Where is primary peristalsis controlled?
  • What are the outflow neural tracts to esophagus?
  • Primary peristalsis does not ___________
A
  • In the Swallowing center
    • Nucleus ambiguous → striated muscle, sequential activation
    • DMNV → smooth muscle, intrinsic regulation via myenteric plexus
    • Vagal innervation of smooth muscle = sequential activation
  • Primary peristalsis does not require sensory info from esophagus
55
Q
  • What triggers secondary peristalsis?
  • What is the nuclear outflow tract that results?
A

Bolus → sensory neurons → DMVN → vagal innervation of smooth muscle via myenteric plexus

56
Q

What is reflex relaxation?

A

Neurally mediated relaxation of sphincter in response to bolus in the pharynx (UES) or esophagus (LES)

57
Q

What are the 4 steps in Parietal cell HCl excretion?

A
  1. H/K exchanger pumps H+ into lumen
  2. OH- formed by making H+ from water → HCO3-
  3. HCO3- exchanged for Cl- at basolateral side
  4. Cl- is pumped out of the apical side via channel
58
Q

What is the tubulovesicular system of the parietal cell?

A

When stimulated, tubulovesicles can fuse with canaliculus system to increase SA of the parietal cell for pumping out acid

59
Q

How is pepsin activated?

A
  • Pepsinogen → (HCl) → pepsin
  • Pepsin can also autocatalysis and convert more pepsinogen
60
Q

What are the characteristics of H. pylori that enable it to colonize the stomach?

A
  • High mutation rate
  • Motility
  • Attach to epithelial cells
  • Urease
61
Q

What are 3 types of antacids?

  • Their uses?
  • Side effects?
A

CaCO3, Mg(OH)2, Al(OH)3

  • Bind with H+ in the stomach to neutralize
  • Ca/Al → constipation
  • Mg → osmotic diarrhea
62
Q

H2 antagonists

  • nomenclature
  • metabolism
  • How they work
A
  • Cimetidine, ranitidine (new version)
  • Rapidly absorbed, renal elimination
  • Reversibly bind to H2 receptors on basal side of parietal cell
    • Make histamine harder to bind to H2 receptors
63
Q

PPI

  • nomenclature
  • Metabolism
  • MOA
A
  • Omeprazole, pantoprazole
  • Absorbed, excreted via liver
  • Irreversible inhibition of proton pump on parietal cells
64
Q

Coating agents

  • nomenclature
  • MOA
A
  • Sucralfate
  • Complex aluminum and sucrose → paste in stomach → induce PG synthesis, mucous and bicarbonate (Bismuth)
65
Q

PG analogue

  • nomenclature
  • MOA
A
  • Misoprostol
  • PG analogue binds EP3 receptor to increase bicarbonate, mucous and decrease acid production
66
Q

D2 blockers (prokinetic)

  • nomenclature
  • Metabolism
  • MOA
A
  • Metoclopramide, domperidone
  • Increase LES tone and stimulates upper GI contraction
67
Q

H pylori serology

  • pros
  • cons
A
  • Pro
    • very specific, very sensitive, non invasive
  • Con
    • antibody titers can remain high even after a year after elimination
    • Not useful to test for eradication
68
Q

Urea breath test

  • method
  • uses
A
  • Method
    • give radioactively labeled urea
    • if HP is present, it will metabolize urea to bicarb (labeled) + ammonia
    • Measure bicarb in breath
  • Use
    • document eradication
69
Q

Esophagogastroduodenoscopy

  • uses
A

Useful to diagnose peptic ulcer diseases → can obtain biopsy specimens

70
Q

Barium X ray

  • pros
  • cons
A
  • Pros
    • Good for visualizing strictures, obstructions
  • Cons
    • radiation, endoscopy better for H pylori infection/malignancy
71
Q

Ambulatory 24H esophageal pH monitoring

  • uses
A

GERD

72
Q

GERD

  1. Define
  2. 2 major causes
  3. resulting pathology
A
  1. reflux occurring from transient relaxation of LES due to reduced LES pressure or increased abdominal pressure
  2. 2 major causes
    1. impaired resting LES
    2. Transient inappropriate relaxation of LES
  3. Major cause of Barrett’s Esophagus
73
Q

How does GERD cause Barrett’s esophagus?

A

Acid reflux → esophageal inflammation, ulceration and bleeding → muscle spasm/stricture→ increased risk of Barrett’s esophagus → increased risk of adenocarcinoma

74
Q

Gastritis

  • Definition
  • (7) causes
A

Epithelial damage of stomach + inflammation

  1. stress-critically ill patients even with normal gastric acid secretion
  2. NSAIDs
    • no prostaglandins
    • Large, bleeding diffuse ulcers
  3. Alcohol
    • no proof but PPI and H2 antagonists empirically prescribed
  4. H.pylori
    • inflammation+lymphocytes
  5. pernicious anemia
    • autoimmune, destroying fundic glands/parietal cells
    • Achlorhydria + pernicious anemia
  6. sarcoidosis, Crohn’s (gum to bum)
  7. infection
75
Q

Peptic ulcer disease

  • Definition
  • (3) Major causes
A
  • Disruption of mucosal integrity of stomach, duodenum or both, caused by local inflammation
  1. Zollinger-ellison syndrome
    • (hypersecretory)
  2. NSAID
  3. H pylori

Usually normal mechanisms are superimposed by H Pylori and concurrent NSAID use

76
Q

How does H pylori cause infection?

A

H pylori urease converts urea into ammonia to neutralize pH → cag A and Vac A confer ability to bind to stomach lining → immune reaction → cytokines → increased acid secretion, lower somatostatin production

77
Q

What are the two types of gastric cancer, and their macroscopic characteristics?

Which has a worse prognosis?

A
  • Diffuse form
    • poorly differentiated, lacks glandular structure, worse prognosis
  • Intestinal form
    • glandular structure, lower stomach areas, dietary and environmental risk factors
78
Q

How does intestinal type cancer develop?

A
  • Initiation and progression from inflammation caused by H pylori infection or poor dietary choices
  • Cigarette smoking and NSAIDS and genetics also play a role
79
Q

What are Sister Mary Joseph nodes?

Where are they?

A

Periumbilical lymphadenopathy

80
Q

Which gastric cancer has a younger age of onset?

A

Intestinal

81
Q

Which gastric cancer is endemic?

A

Intestinal (diet + environmental factors are common in certain areas)

82
Q

Which gastric cancer is associated with H pylori?

A

Intestinal

83
Q

Which gastric cancer is associated with hereditary factors?

A

Gastric

84
Q

Which gastric cancer is more common in women?

A

Gastric

85
Q

GIST (gastrointestinal stromal tumor)

  • What type of cell/tissue is involved?
  • Symptomatic?
  • Where?
A
  • Most common gastric stromal/mesenchymal tumor
  • Small tumors are symptomatic
  • In the distal stomach and small intestine
86
Q

Barrett’s esophagus

  • Cause
  • Result
  • Classification
  • diagnosis
A
  • Cause
    • Distal squamous mucosa replaced by metaplasia columnar epith + goblet cells due to GERD
  • Result
    • major risk factor for esophageal adenocarcinoma
  • Classification
    • short <3cm from GE junction
    • long >3cm from GE junction
  • Diagnosis
    • endoscopy
87
Q

Esophageal cancer

  • (2 types)
  • prognosis
  • risk factors
A
  • 2 types
    • (1) squamous cell (smoking or alcohol irritates squamous lining)
    • (2) adenocarcinoma from GERD
  • Poor prognosis
  • Risk factors
    • tobacco, breast cancer, GERD, obesity, hot beverages
88
Q

How do you differentiate a peptic ulcer from a duodenal ulcer based on symptoms?

A
  • Duodenal
    • improved by food, antacids
  • Gastric
    • made worse by food
89
Q

What are symptoms of a duodenal ulcer?

A
  • Epigastric pain
  • nausea and vomiting
  • pain relieved by eating
  • dyspepsia
90
Q

True or false

  • most people with H pylori develop ulcer disease
A

FALSE

  • 60% of the world infected, only 10% get ulcers
91
Q

True or false

  • most people with a DU/peptic ulcer disease have H Pylori
A

True

92
Q

NSAIDs + H. pylori increases incidence of ________

A

Peptic ulcer disease

93
Q

H. pylori is eradicated when found because…

A
  • Associated with higher risk of PUD
  • Associated with gastric cancer
94
Q

What is standard first triple therapy for H. pylori?

A
  • PPI (prazole, irreversible binding to proton pump)
  • 2 Abx: Clarithrymycin, Amoxicillin (or metronidazole)
95
Q

What is standard second course triple therapy for H. pylori?

A
  • PPI
  • Bismuth subsalicylate
  • 2 Abx: Metronidazole, tetracycline
96
Q

What are some causes of oropharyngeal dysphagia?

A
  • Neurological
    • Parkinson’s
    • Huntington’s
    • MS
    • Brainstem lesion
  • Muscular/rheumatologic
  • Metabolic
    • Cushing’s Disease
    • Wilson’s Disease
  • Infectious
    • Polio
    • Diptheria
    • Lyme disease
    • Botulism
    • Syphilis
97
Q

What are some causes of esophageal dysphagia?

A
  • Mechanical obstruction
    • stricture
    • esophageal cancer
  • Motility
    • achalasia (failure to relax)
    • scleroderma
    • diffuse esophageal spasm
98
Q

Pathology in foregut refers to __________ via innervation by _______

A
  • Epigastric region
  • T5-T9
99
Q

How can you differentiate heartburn from angina?

A
  • Heartburn not worsened by exercise
  • Experienced post prandially, while lying down, bent over
100
Q

What is dyspepsia more commonly known as?

A
  • Dyspepsia = indigestion
  • Heartburn and regurgitation
  • Bloating, pain
101
Q

What is Sjorgen’s disease

What are the implications for GI problems?

A
  • Autoimmune disease where exocrine glands (tears and saliva) are destroyed
  • Cannot make proper bolus

UBC Medicine Preclinical GI Curriculum (2 decks)

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