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
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
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)
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
5
Q
What is contained within the hepatoduodenal ligament?
A
Bile duct, hepatic artery, portal vein
(all incoming blood and outgoing bile)
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
7
Q
What is the blood supply of the duodenum?
A
Both foregut/midgut
Celiac and superior mesenteric artery
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
9
Q
What forms the parenchyma of the liver?
A
The foregut liver bud grows upwards and meets the septum transversum
10
Q
What forms the stroma of the liver?
A
The septum transversum (mesoderm) forms the stroma of the liver
11
Q
What are the congenital malformations of the GB/liver?
A
- Extrahepatic biliary atresia: failure of recanalization
- Bifid gallbladder: duplication of gall bladder
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
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
14
Q
What is an annular pancreas?
A
A malrotated pancreas which surrounds the duodenum and constricts it
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
16
Q
Embryonic origin of esophagus lining?
Embryonic origin of muscular esophagus?
____peritoneal
A
- Endoderm
- Mesoderm
- Intraperitoneal
17
Q
Embryonic origin of stomach lining?
____peritoneal?
A
- Lining- endoderm
- Mesogastrium- mesoderm
- intraperitoneal
18
Q
Embryonic origin of liver parenchyma?
A
Foregut Endoderm
19
Q
Embryonic origin of liver stroma?
A
Septum transversum mesoderm
20
Q
Embryonic origin of GB?
A
Foregut endoderm
21
Q
Embryonic origin of cystic and common bile duct?
A
Foregut endoderm
22
Q
Embryonic origin of pancreas
_______ peritoneal
A
- Foregut endoderm
- Starts as intraperitoneal → secondary retroperitoneal
23
Q
Embryonic origin of spleen
A
Mesoderm
24
Q
Parasympathetic and Sympathetic innervation of the esophagus
A
- Parasympathetic
- upper 1/3: striated
- Vagus
- Lower 2/3: smooth
- vagus via celiac plexus
- upper 1/3: striated
- Sympathetic
- T1-T10
25
**Stomach**
## Footnote
* Arterial supply
* Venous supply
* Nervous supply
* **Arterial supply**
* Celiac artery
* **Venous supply**
* Portal vein → IVC
* **Nervous supply**
* Parasympathetic
* Hepatic (L) vagus (anterior)
* celiac (R) vagus (posterior)
* Sympathetic
* T6-T10
26
The ENS includes the _____ plexus located _____ and the _____ plexus in the \_\_\_\_\_.
## Footnote
* **Myenteric plexus**, outer muscle layers
* **Submucosal plexus**, submucosa
27
The myenteric plexus is involved in the motility of the Gi via \_\_\_\_\_\_\_
* Tonic \>\< of sphincters
* Rhythmic segmentation
* Oscillatory movements
* Peristalsis
28
The submucosal plexus mainly innervates \_\_\_\_\_\_
* Villi for movement
* Endocrine cells
* Secretory cells
* Blood vessels
29
What are the roles of hormones in gut motility?
Secondary role in motility via modification of ENS inputs of movement
## Footnote
* modulate responses to ICCs, impact intracellular Ca concentration
* influence resting contractility of muscle in upper GI
30
What is the main control of motility in the gut?
Mainly controlled by **ENS** → specifically **myenteric plexus**
31
What is the main control of secretion in the GI?
Both neural and hormonal → more closely related
32
Describe the effects of gastrin release
* Gastrin is released from **G cells** when **stimulated by release of GRP** from neurons
* Gastrin stimulates **ECL** → **histamine**
* Gastrin → **Parietal cell** → **HCL**
33
Describe the effects of Ach release from neurons
* Ach released from neurons with **PNS stimulation**
* Ach → **ECL** → **histamine**
* Ach → **parietal cell** → **HCl**
34
Describe the effects of histamine release from ECL cells
Histamine causes release of HCl from parietal cell
35
Describe the effects of intrinsic interneurons in the ENS
* Direct to parietal cells → HCl
* Through GRP/G cells → gastrin
36
How does the PNS affect the ENS?
## Footnote
* input?
* effects?
Vagal nuclei + Sacral spinal cord preganglionic fibers synapse in the ENS → postganglionic fibers
## Footnote
* to the Muscularis externa, muscularis mucosae, secretory cells, endocrine cells, blood vessels
37
How does the SNS affect the ENS?
## Footnote
* input?
* effects?
**Input**: preganglionic fibers → sympathetic ganglia → postganglionic fibers
## Footnote
* directly to the blood vessels
* to the ENS → muscularis externa, muscularis mucosa, secretory cells, endocrine cells
38
Where is auerbach’s plexus?
## Footnote
* Main results…
Where is Meissner’s plexus?
* Main results…
* **Auerbach** = external myenteric → secretory, smooth muscle
* **Meissner** = submucosal → mostly secretory
39
What are the main inhibitory NTs in the myenteric plexus?
What is the result of these NTs?
**NO, VIP, ATP**
## Footnote
* Decrease contraction, increase secretomotor
* Overall slow food passage and increase digestion
40
What are the main excitatory NTs in the myenteric plexus?
* Ach
* Substance P
* Serotonin
41
What are the (2) functions of the submucosal plexus?
* Movement of villi
* Secretion of endocrine and exocrine
42
What are the major stimulatory hormones of the submucosal plexus?
## Footnote
* Ach,
* VIP
43
Define: co-localization
A neuron that contains more than one NT
44
D: secretomotor neuron
A neuron that induces a gland
45
D: slow wave
* Spontaneous rhythmic fluctuations in the resting membrane potential intrinsic to the GIT
* Frequency is region specific
* Slow wave because 5 seconds long
46
D: tonic contraction
D: sphincter
* **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
What are the ICCs?
## Footnote
* Pacemaker cells of the GI → myenteric plexus and muscle layers
* Generate and propagate slow waves
48
* Explain the AP of a slow wave
* Channels
* Ions
* **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
What is the relationship between slow wave and spike potentials, what is the result?
* 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
Name 5 ways calcium is INCREASED in a GI cell
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
Name 3 ways calcium is DECREASED in GI cell
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
How does NE/E effect the GI cell?
* Cause K efflux from cells, leads to hyperpolarization → relaxation
* Inhibits contraction
53
Pharyngeal peristalsis is triggered by ____ and mediated by pharyngeal muscles
Bolus of food triggering tactile receptors in pharynx
54
* Where is primary peristalsis controlled?
* What are the outflow neural tracts to esophagus?
* Primary peristalsis does not \_\_\_\_\_\_\_\_\_\_\_
* 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
* What triggers secondary peristalsis?
* What is the nuclear outflow tract that results?
Bolus → sensory neurons → DMVN → vagal innervation of smooth muscle via myenteric plexus
56
What is reflex relaxation?
Neurally mediated relaxation of sphincter in response to bolus in the pharynx (UES) or esophagus (LES)
57
What are the 4 steps in Parietal cell HCl excretion?
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
What is the tubulovesicular system of the parietal cell?
When stimulated, tubulovesicles can fuse with canaliculus system to increase SA of the parietal cell for pumping out acid
59
How is pepsin activated?
* Pepsinogen → (HCl) → pepsin
* Pepsin can also autocatalysis and convert more pepsinogen
60
What are the characteristics of H. pylori that enable it to colonize the stomach?
* High mutation rate
* Motility
* Attach to epithelial cells
* Urease
61
What are 3 types of antacids?
## Footnote
* Their uses?
* Side effects?
**CaCO3, Mg(OH)2, Al(OH)3**
## Footnote
* Bind with H+ in the stomach to neutralize
* **Ca/Al** → constipation
* **Mg** → osmotic diarrhea
62
**H2 antagonists**
## Footnote
* nomenclature
* metabolism
* How they work
* 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
**PPI**
## Footnote
* nomenclature
* Metabolism
* MOA
* Omeprazole, pantoprazole
* Absorbed, excreted via liver
* Irreversible inhibition of proton pump on parietal cells
64
**Coating agents**
## Footnote
* nomenclature
* MOA
* Sucralfate
* Complex aluminum and sucrose → paste in stomach → induce PG synthesis, mucous and bicarbonate (Bismuth)
65
**PG analogue**
## Footnote
* nomenclature
* MOA
* Misoprostol
* PG analogue binds EP3 receptor to increase bicarbonate, mucous and decrease acid production
66
**D2 blockers (prokinetic)**
## Footnote
* nomenclature
* Metabolism
* MOA
* Metoclopramide, domperidone
* Increase LES tone and stimulates upper GI contraction
67
**H pylori serology**
## Footnote
* pros
* cons
* **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
**Urea breath test**
## Footnote
* method
* uses
* **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
**Esophagogastroduodenoscopy**
## Footnote
* uses
Useful to diagnose peptic ulcer diseases → can obtain biopsy specimens
70
**Barium X ray**
## Footnote
* pros
* cons
* **Pros**
* Good for visualizing strictures, obstructions
* **Cons**
* radiation, endoscopy better for H pylori infection/malignancy
71
**Ambulatory 24H esophageal pH monitoring**
## Footnote
* uses
GERD
72
**GERD**
## Footnote
1. Define
2. 2 major causes
3. resulting pathology
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
How does GERD cause Barrett’s esophagus?
Acid reflux → esophageal inflammation, ulceration and bleeding → muscle spasm/stricture→ increased risk of Barrett’s esophagus → increased risk of adenocarcinoma
74
**Gastritis**
## Footnote
* Definition
* (7) causes
**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
**Peptic ulcer disease**
## Footnote
* Definition
* (3) Major causes
* 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
How does H pylori cause infection?
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
What are the two types of gastric cancer, and their macroscopic characteristics?
Which has a worse prognosis?
* **Diffuse form**
* poorly differentiated, lacks glandular structure, worse prognosis
* **Intestinal form**
* glandular structure, lower stomach areas, dietary and environmental risk factors
78
How does intestinal type cancer develop?
* 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
What are Sister Mary Joseph nodes?
Where are they?
Periumbilical lymphadenopathy
80
Which gastric cancer has a younger age of onset?
Intestinal
81
Which gastric cancer is endemic?
## Footnote
Intestinal (diet + environmental factors are common in certain areas)
82
Which gastric cancer is associated with H pylori?
Intestinal
83
Which gastric cancer is associated with hereditary factors?
## Footnote
Gastric
84
Which gastric cancer is more common in women?
## Footnote
Gastric
85
**GIST** (gastrointestinal stromal tumor)
## Footnote
* What type of cell/tissue is involved?
* Symptomatic?
* Where?
* Most common gastric stromal/mesenchymal tumor
* Small tumors are symptomatic
* In the distal stomach and small intestine
86
**Barrett’s esophagus**
## Footnote
* Cause
* Result
* Classification
* diagnosis
* **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
**Esophageal cancer**
## Footnote
* (2 types)
* prognosis
* risk factors
* **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
How do you differentiate a peptic ulcer from a duodenal ulcer based on symptoms?
* **Duodenal**
* improved by food, antacids
* **Gastric**
* made worse by food
89
What are symptoms of a duodenal ulcer?
* Epigastric pain
* nausea and vomiting
* pain relieved by eating
* dyspepsia
90
**True or false**
## Footnote
* most people with H pylori develop ulcer disease
**FALSE**
## Footnote
* 60% of the world infected, only 10% get ulcers
91
**True or false**
## Footnote
* most people with a DU/peptic ulcer disease have H Pylori
True
92
NSAIDs + H. pylori increases incidence of \_\_\_\_\_\_\_\_
Peptic ulcer disease
93
H. pylori is eradicated when found because…
* Associated with higher risk of PUD
* Associated with gastric cancer
94
What is standard first triple therapy for H. pylori?
* PPI (prazole, irreversible binding to proton pump)
* 2 Abx: Clarithrymycin, Amoxicillin (or metronidazole)
95
What is standard second course triple therapy for H. pylori?
* PPI
* Bismuth subsalicylate
* 2 Abx: Metronidazole, tetracycline
96
What are some causes of oropharyngeal dysphagia?
* **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
What are some causes of esophageal dysphagia?
* **Mechanical obstruction**
* stricture
* esophageal cancer
* **Motility**
* achalasia (failure to relax)
* scleroderma
* diffuse esophageal spasm
98
Pathology in foregut refers to __________ via innervation by \_\_\_\_\_\_\_
* Epigastric region
* T5-T9
99
How can you differentiate heartburn from angina?
* Heartburn not worsened by exercise
* Experienced post prandially, while lying down, bent over
100
What is dyspepsia more commonly known as?
* Dyspepsia = indigestion
* Heartburn and regurgitation
* Bloating, pain
101
What is Sjorgen’s disease
What are the implications for GI problems?
* Autoimmune disease where exocrine glands (tears and saliva) are destroyed
* Cannot make proper bolus
UBC Medicine Preclinical GI Curriculum
flashcards
Decks in class (2)
# Cards
