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411 > W11 Upper GI > Flashcards

W11 Upper GI Flashcards

1
Q

What are the 4 basic GI processes ?

A

Motility
Secretion
Digestion
Absorption

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2
Q

What actions are mixing movements involved with ?

A

Redistributing luminal contents locally
Enhancing the exposure to digestive secretions
Exposing luminal contents to GI tract absorbing surfaces

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3
Q

What is the purpose of propulsive movements in the GI tract ?

A

Move luminal contents forward

Rate of propulsion varies with specific function of region

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4
Q

What actions do the inner circular layer and outer longitudinal layer of the muscularis externa have ?

A

Inner: contraction—> constriction of lumen
Outer: contraction —> shortening of the GI tract

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5
Q

Where does the myenteric plexus lie and what is its purpose?

A

Between 2 layers of muscularis externa

Coordinates muscularis externa contractions

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6
Q

What initiates contraction of smooth muscle ?

A

Increased cytoplasmic calcium

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7
Q

Where does the sarcoplasmic reticulum associate with the plasma membrane ?

A

At indentations known as cavaeoli

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8
Q

How are contractile acto-myosin filaments arranged ?

A

Obliquely

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9
Q

Where are cytoskeleton filaments anchored ?

A

Dense body junctions

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10
Q

Where are smooth muscle cells physically and electrically coupled?

A

Gap junctions

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11
Q

What activates myosin light chain kinase (MLCK)

A

Calcium binding to calmodulin when there is increased intracellular calcium concentration

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12
Q

What occurs when MLCK phosphorylates myosin light Chain

A

Myosin can bind to actin and begin the shortening process

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13
Q

What terminates the contraction of smooth muscle

A

Myosin light chain phosphatase

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14
Q

How does a voltage change in smooth muscle lead to a release of Ca2+ ?

A

Depolarization of SM membrane —> activate voltage gated calcium channel
—> Ca2+ influx —> SR calcium channel release —> calcium induced calcium release in SM cell

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15
Q

Outline pharmacy-mechanical coupling for the release of Ca2+

A

Compound triggers production of IP3 at sarcolemma —> diffuse through cytosol —> activate IP3 receptor to open —> Ca2+ diffuses out of SR into cytosol —> initiate contraction

no change in membrane potential

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16
Q

What 4 factors regulate GI motility ?

A

Intrinsic electrical properties of smooth muscle cells
Enteric nervous system
Autonomic nervous system
Other systems (eg. Brain, immune, hormones)

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17
Q

What are the pacemaker cells in smooth muscle ?

A

Interstitial cells of Cajal (ICC)

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18
Q

What are slow waves ?

A

Depolarising potentials

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19
Q

Where do slow waves propagate ?

A

From pacemaker cells into adjacent SM cells through gap junctions —> electrical signals flow between cells

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20
Q

What helps modulate the duration and amplitude of slow waves ?

A

Neurotransmitters/agonists that are released by enteric motor neurons

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21
Q

If slow wave depolarizations reach AP threshold what is the result ?

A

A burst of action potentials

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22
Q

What is the number of APs stimulated by a slow wave proportional to ?

A

The duration the slow wave remains above the AP threshold

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23
Q

How does the speed at which [Ca2+] increases in myoplasm of SM when it is depolarizer compared to skeletal and cardiac muscle ?
How do the kinetics of the contraction compare?

A

Very slow

Equally slow

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24
Q

What comprises the enteric nervous system ?

A

The submucosal and myenteric plexuses

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25
Q

Why is the enteric nervous system considered reflexive ?

A

It can operate entirely within the GI wall w/o external input

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26
Q

What are the 3 main components of the enteric nervous system?

A

Sensory neurons (mechanoreceptors, osmoreceptors, chemoreceptors)
Interneurons (excitatory and inhibitory)
Secretomotor cells

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27
Q

What do secretomotor cells influence ?

A

Smooth muscle
Epithelial cells that secrete or absorb fluid/electrolytes
Enteric endocrine cells

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28
Q

What can the intrinsic reflex arc for motility respond to and what actions does it have ?

A

Mucosa can sense mechanical, chemical or thermal change —> activate reflex arc which can inhibit or contract SM cells

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29
Q

How does the ANS influence GI motility ?

A

Influences ongoing ENS activity
Directly affects SM and glands
Alters GI hormone levels

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30
Q

How does parasympathetic input affect GI tract in general ?

A

Increases motility and GI secretions

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31
Q

How does sympathetic drive affect the GI system ?

A

Decreased motility and decreased volume of secretions

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32
Q

How is swallowing coordinated ?

A

Initiation is voluntary —> reflexive and is coordinated by swallowing center of medulla oblongata

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33
Q

Describe the oral phase of swallowing

A

Push food bolus toward back of oral cavity and up against palate by using the tongue —> activate sensory receptors in the back of the throat

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34
Q

Describe the pharyngeal phase of swallowing ?

A

Touch and pressure receptors in the pharyngeal palate are activated by food bolus —> info sent to medulla via trigeminal nerve (CN V) —>
Initiate reflexive component of swallowing —> contraction of pharyngeal wall behind bolus pushes food toward esophagus
- tongue prevents food from travelling back to mouth
- uvula elevates to seal nasal passages
- epiglottis closes over trachea

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35
Q

Describe the esophageal phase of swallowing

A

Swallowing centre relaxes pharyngoesophageal sphincter
Swallowing center initiates primary peristaltic waves by enteracting with the ENS
Gastroesophageal sphincter opens when food bolus is against this region
(Reflexive relaxation mediated by vagus nerve)

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36
Q

Describe primary peristalsis

A

Inner circular muscle contacts —> pinching ring
Outer longitudinal muscle contracts in front of pinched ring —> decrease length of tube
Sequence propagates along length of esophagus
Takes 5-9 seconds

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37
Q

Describe secondary peristalsis

A

Reflexive
Activated when luminal contents become lodged
- distension of GI walls —> stretch receptors —> stimulate ENS —> coordinate strong peristaltic wave to dislodge contents

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38
Q

What are the 2 dominant motility paradigms in the small intestine

A

Segmentation
- ensures thorough mixing
Migrating mobility complex
- moves luminal contents along

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39
Q

Describe small intestine segmentation

A

During meal

Alternating contractions and relaxations of adjacent sections of small intestine

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40
Q

What initiates segmentation in small intestine ?

A

Distension of lumen
Presence of enterogastrone gastrin
Parasympathetic input

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41
Q

Describe the action of migrating mobility complex in small intestine

A
  • following absorption of meal
  • begins at duodenal-gastric junction
  • weak parastaltic contractions
  • second wave begins slightly more distally —> travel slightly further
    ~2 hours from stomach to large intestine
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42
Q

Acid neutralizing/lower drugs

A

Antacids
Histamine H2 receptor antagonists
Proton pump inhibitors

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43
Q

Antacids and their mechanism of action

A

Hydroxide and/or carbonate salts
Direct neutralization of stomach acid
—> increase gastric pH

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44
Q

How might antacids affect the absorption of other drugs ?

A

Counter ions are poorly absorbed and may chelate other drugs and effect their absorption
Increased pH may also affect absorption of other drugs

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45
Q

Indications for antacids

A

Heartburn/ mild GERD

Dyspepsia

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46
Q

Side effects of antacids

A

Carbonate based salts —> belching
Ca2+ containing: hypercalcemia
Al3+ containing: constipation, hypophosphatemia —> impaired absorption
Mg 2+ containing : diarrhea

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47
Q

Suffix of H2 receptor agonists

A

Tidine

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48
Q

Mechanism of action of H2 receptor antagonists

A

Competitive, selective block of histamine H2 receptors —> reduced (60-70%) acid secretion
Most effective in nocturnal acid secretion

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49
Q

Pharmacokinetics of H2 receptor antagonists

A

Oral, IM and IV formulations

Oral: bioavailability ~50%, peak absorption in 1-3 hours, twice daily administration

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50
Q

Indications for H2 receptor antagonists

A

GERD
Peptic ulcer disease
Dyspepsia
Prevention of bleeding from stress related gastritis

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51
Q

Common Side effects of H2 receptor antagonists

A

Diarrhea or constipation
Headache
Drowsiness/fatigue
Muscle pain

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52
Q

Rare side effects of H2 receptor antagonists

A 
Confusion/agitation 
Delirium/hallucinations 
Slurred speech 
Gynecomastia 
Blood dyscrasias
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53
Q

Suffix of PPIs

A

Prazole

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54
Q

Mechanism of action of PPIs

A

Irreversible inactivation of Proton pump common to all triggers of gastric acid secretion

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55
Q

Indications for proton pump inhibitors

A

Gastric and duodenal ulcers
GERD
Prevention of bleeding from stress related gastritis
Gastric hypersecretory conditions

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56
Q

Common side effects of PPIs

A

Nausea
Diarrhea (or constipation)
Abdominal pain
Flatulence

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57
Q

What are up to 80% of peptic ulcers correlated with ?

A

Presence of H.pylori in GI tract

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58
Q

What is the standard triple therapy for peptic ulcer disease with H. Pylori infection ?

A
  • PPI + two antibiotics for 2 weeks
    - clarithromycin and amoxicillin or metronidazole
  • PPI alone for 6 weeks
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59
Q

What is misoprostol

A

Prostaglandin E1 analogue

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60
Q

Mechanism of action of misoprostol

A

Direct parietal cell inhibition and mucus cell stimulation

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61
Q

Pharmacokinetics of misoprostol

A

Short half life —> frequent dosing

No impact on cytochrome P450 enzymes

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62
Q

Indications for misoprostol

A

NSAID- induced ulcers

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63
Q

Contraindications for misoprostol

A

Pregnancy

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64
Q

Side effects of misoprostol

A

Diarrhea
Abdominal cramping
Uterine contraction

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65
Q

Composition of sucralfate

A

Al(OH)3-sucrose surface complex

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66
Q

Mechanism of action of sucralfate

A

Acid interaction —> anionic surfaced sucrose —> bind to charged ulcer proteins —> viscous, sticky, protective barrier
- indirect stimulation of PGE2 production

67
Q

Pharmacokinetics of sucralfate

A

Localized action
Short affect ~6 hours
Take on empty stomach

68
Q

Indications for sucralfate

A

Gastric and duodenal ulcers

69
Q

Side effects of sucralfate

A

Al3+ induced constipation

May reduce absorption of some other drugs

70
Q

Bismuth subsalicylate (pesto-bismo) mechanism of action

A

Coat ulcers —> protective barrier
Increased PGE2, HCO3- and mucus production
Antimicrobial against H. Pylori
Reduces stool frequency

71
Q

Pharmacokinetics of Bismuth subsalicylate

A

Dissociates in stomach —> acts locallly

Only salicylate substantially absorbed

72
Q

Indications for bismuth subsalicylate

A

Adjuvant to triple therapy for H.pylori- induced ulcers

Acute diarrhea

73
Q

Contraindications for bismuth subsalicylate

A

Children with viral infections —> Reye’s syndrome

Allergies to ASA

74
Q

Side effects of bismuth subsalicylate

A

Black stool
Blackening of tongue
Constipation

75
Q

Examples of pro kinetic drugs

A

Metoclopramide and domperidone

76
Q

Mechanism of action of pro kinetic drugs

A

Dopamine D2 receptor antagonists
Metoclopromide has activity as agonist of serotonin (5-HT) receptors
Relieve basal dopamine inhibition of upper GI tract, stimulating peristalsis and facilitating gastric emptying

77
Q

Pharmacokinetics of pro kinetic drugs

A

Metoclopromide: PO and parenteral formulations
Domperidone: greater fast pass metabolism
Short (1-2 hour) duration of action
Hepatic metabolism

78
Q

Indications for prokinetic drugs

A

GERD
Impaired gastric emptying (gastroparesis)
Nausea and vomiting
Postpartum lactation stimulation

79
Q

Contraindications for prokinetic drugs

A

Situations where GI motility is harmful

80
Q

Side effects of prokinetic drugs

A

GI cramping
Diarrhea
Hyperprolactinemia
Metoclopromide crosses blood brain barrier
- dystonias, Parkinson’s-like syndromes, tardive dyskinesia
- drowsiness, restlessness, insomnia, anxiety

81
Q

What does anti-emetic pharmacology target ?

A

Gastric stimuli

Motion sickness

82
Q

Basis for gastric stimuli

A

Based on vagal afferents activating brain stem “vomiting centre” and/or chemoreceptor trigger zone

83
Q

Anti emetic drug that targets gastric stimuli

A

Ondansetron

84
Q

Drugs used to target motion sickness

A

Dimenhydrinate

Scopolamine

85
Q

Ondansetron mechanism of action

A

Agonist of serotonin 5-HT3 receptors

—> vagal afferents, chemoreceptor trigger zone, and vomiting centre

86
Q

Indications for ondansetron

A

Chemo induced nausea and vomiting

Post-op and post radiation nausea and vomiting

87
Q

Side effects of ondansetron

A

Headache
Dizziness
Constipation

88
Q

Dimenhydrinate mechanism of action

A

Antagonist of histamine H1 receptors
- some anticholinergic activity
Relatively weak anti-emetic activity

89
Q

Indications for dimenhydrinate

A

Motion sickness

90
Q

Side effects of dimenhydrinate

A

Dizziness
Sedation/drowsiness
Dry mouth
Urinary retention

91
Q

Scopolamine mechanism of action

A

Antagonist of muscarinic receptors

92
Q

Indications of scopolamine

A

Motion sickness

93
Q

Side effects of scopolamine

A

Anti muscarinic when given orally or parenterally

94
Q

3 primary functions of the stomach

A

Mixing and mechanical breakdown of stomach contents
Storage of ingested food and regulated delivery of processed stomach contents to the duodenum
Secretion of HCl and enzymes involved in protein digestion

95
Q

What lines the fundus and body of the stomach ?

A

Oxyntic mucosa

96
Q

What lines the antrum of the stomach ?

A

Pyloric gland area (PGA)

97
Q

Exocrine glands of the stomach

A

Mucous cells
Chief cells
Parietal cells

98
Q

What do mucous cells secrete ? What stimulates this ? What is the function ?

A

Alkaline mucous
Mechanical stimulation by contents
Protects mucosa against mechanical, pepsin and acid injury

99
Q

What do Chief cells secrete ? What stimulates this ? What is the function of the secreted product ?

A

Pepsinogen
Ach, gastrin
When activated begins protein digestion

100
Q

What do parietal cells secrete ? What stimulates this ? What is the function of the secreted product ?

A

HCl
ACh, gastrin, histamine
Activates pepsinogen, breaks down CT, denatures proteins, kills microorganisms

Intrinsic factor —> facilitates absorption of vitamin B12

101
Q

What are the endocrine/pans rinse cells

A

Enterochromaffin- like (ECL) cells
G cells
D cells

102
Q

What do ECL cells secrete ? What stimulates this? What is the function of the secreted product ?

A

Histamine
Ach, Gastrin
Stimulates parietal cells

103
Q

What do G cells secrete ? What stimulates this ? What is the function of the secreted product ?

A

Gastrin
Protein products, ACh
Stimulates parietal, chief and ECL cells

104
Q

What do D cells secrete ? What stimulates this ? What is the function of the secreted product ?

A

Somatostatin
Acid
Inhibits parietal, G and ECL cells

105
Q

Where are mucous cells, parietal cells and chief cells located ?

A

All gastric pits
Oxyntic mucosa
Oxyntic mucosa

106
Q

Where are ECL cells, G cells and D cells located ?

A

Gastric glands of:

  • oxyntic mucosa
  • PGA
  • PGA
107
Q

How do parietal cells secrete HCl ?

A

Actively

- ionic pumps move H+ and Cl- ions against their concentration gradients into the lumen

108
Q

What 4 functions does HCl perform that assist in GI activity ?

A
  1. Converts pepsinogen into active pepsin
  2. Breaks down CT and muscle fibres of ingested food
  3. Breaks the tertiary structure of proteins
  4. Protection: kills some ingested microorganisms
109
Q

What activates pepsin

A

HCl

110
Q

What is the function of Pepsin?

A

Cleaves peptide bonds between certain amino acids

111
Q

Where is pepsinogen stored

A

In inactive form in zymogen granules within chief cells

112
Q

What 3 main components of the gastric mucosal barrier protect the epithelial layer from acid injury ?

A
  1. Acid cannot penetrate hydrophobic epithelial membrane
  2. Tight junctions: prevent acid from diffusing out of lumen
  3. Mucous from mucous cells lining gastric pits is protective.
    - lubrication of luminal contents —> decreased friction
    - inhibits pepsin to protect against auto-digestion of stomach wall
    - neutralizes gastric acid at the epithelial surface
113
Q

Mechanism of H.pylori induced peptic ulcers

A

H.pylori and its toxins —> weaken mucosal barrier —>
Acid and pepsin penetrate mucosal barrier —> histamine is released from damaged epithelium —> enhance gastric acid and pepsin production

Chronic alcohol use, NSAIDs and stress can also contribute

114
Q

What is B12 needed for ?

A

DNA replication (mitosis) in RBC formation

115
Q

What 4 chemical messengers regulate the secretion of gastric juices ?

A

Acetylcholine
Gastrin
Histamine
Somatostatin

116
Q

What does acetylcholine stimulate ?

A

Parietal, chief, ECL, and G cell secretions

117
Q

What does gastrin stimulate ?

A

Parietal, chief and ECL cell secretions

118
Q

What is the primary factor responsible for increasing gastric secretions during the ingestion of a meal ?

A

Gastrin

119
Q

What does gastrin promote the growth of ?

A

The gastric and duodenal mucosa

120
Q

What type of substance is histamine ?

A

Paracrine

121
Q

What does histamine stimulate ?

A

Parietal cell H+ production

122
Q

What is the function of somatostatin ?

A

Acts in a negative feedback manner to turn off gastric H+, pepsinogen and histamine production

123
Q

What are the 3 phases of secretion of gastric juice during the ingestion of a meal

A

Cephalic
Gastric
Intestinal

124
Q

What happens during the cephalic phase of gastric secretions ?

A

Secretion of pepsinogen and H+ in response to sight, smell or thought of food and the process of swallowing
Initiated in the hypothalamus and mediated by vagal efferents
Vagal input —> G cell production of gastrin

125
Q

Describe the gastric phase of gastric secretions

A

Begins when food enters the stomach
Proteins and peptides within lumen are most potent stimuli
Receptors in ENS —> short reflexes —> gastrin release from G cells
Long reflexive loop —> activate H+ and gastrin secretion via vagal and ENS activity
Histamine release is also stimulated —> H+ secretion
Distension/caffeine/alcohol can also stimulate gastric juice production

126
Q

Describe the intestinal phase of gastric secretion

A

Inhibitory
Begins when chyme empties into duodenum
As protein is removed from stomach —> stop secretions in gastric pits and glands
Somatostatin is released from D cells in PGA gastric glands in response to drop in pH —> inhibit parietal, chief and HCl cell activity

127
Q

What happens during the intestinal phase of gastric secretions when there is fat, acid, hypertonic chyme and distension in the duodenum ?

A

Negative feedback:
Influence on gastric secretions via enterogastric reflexes and the enterogastrones CCK and secretin
These factors decrease gastric emptying

128
Q

Typical history of presenting illness for patient with heartburn

A

Character: vague discomfort vs burning vs pain
Onset: often post-prandial
Location: retrosternal
Intensity: variable
Duration: minutes to hours
Aggrevating: supine position, foods which relax lower esophageal sphincter or delay gastric emptying
Relieving: antacids

129
Q

Associated symptoms with heartburn

A

Sour taste
Water brash
Odynophagia
Dysphagia

130
Q

Historical clues for heartburn

A 
Meds
- opioids 
Social history 
- smoking
- alcohol
131
Q

Red flags with heartburn

A 
Vomiting 
Weight loss
Bleeding 
Anorexia 
Dysphagia
132
Q

What is reflux esophagitis and what are the possible causes ?

A

Acid damage to esophagus

  • increased abdominal pressure
  • increased volume of regurgitant
  • decreased esophageal clearance
133
Q

Describe the stepwise treatment of reflux esophagitis

A

Correct the underlying cause
- reduce or stop meds that drop LES pressure

Lifestyle changes

  • smoking cessation
  • alcohol cessation
  • weight reduction

Medications
Surgery

134
Q

Medications for treating reflux esophagitis

A

Antacids
Sucralfate
H2RAs
PPIs

135
Q

Complications of esophagitis

A 
Pain 
Bleeding
Stricture 
Barrett’s esophagus 
Adenocarcinoma
136
Q

GI causes of retrosternal burning

A

GERD
Esophagitis
Esophageal spasm
Esophageal cancer

137
Q

Cardiac causes of retrosternal burning

A

MI
Pericarditis
Aortic dissection

138
Q

Different types of esophagitis

A

Infectious: herpes, cytomegalovirus, candida
Inflammatory: eosinophilic
Trauma: pill

139
Q

Presentation in patients with herpes and CMV esophagitis

A

Odynophagia - typically very painful

Often immunosuppressed

140
Q

Candida esophagitis presentation

A 
Dysphagia 
May or may not have thrush 
Usually Immunosupressed
- diabetic 
- HIV 
-chemo
141
Q

Presentation of eosinophilic esophagitis

A

Dysphagia
History of atopy
Furrows, rings, exudates
Often in younger population

142
Q

Treatment for eosinophilic esophagitis

A

Viscous budesonide and PPI

Six food elimination diet (wheat, milk, eggs, soy, nuts, shellfish)

143
Q

Common causes of pill esophagitis

A

NSAIDs
K+
Alendronate
Antibiotics such as tetracycline and doxycycline

144
Q

Rome iii definition of dyspepsia

A

One or more of:

  • post prandial fullness
  • epigastric pain or burning
  • early satiety
145
Q

Associated symptoms of dyspepsia

A

Nausea
Bloating
Anorexia

146
Q

Causes of dyspepsia

A 
Functional (60%): no obvious cause 
- non-ulcer dyspepsia 
     - ulcer-like symptoms 
     - dysmotility-like symptoms 
Organic (40%) - detectable etiology
147
Q

Etiology of functional dyspepsia

A

Impaired gastric motor function
Visceral sensitivity
Psychosocial factors

148
Q

Gastritis vs gastropathy

A

Gastritis- inflammation of gastric mucosa associated with injury
Gastropathy- epithelial cell damage and regeneration without inflammation

149
Q

Two main patterns of gastritis

A

Antral based

Corpus predominant

150
Q

Describe antral based gastritis

A

Infection increases gastrin secretion —> increased parietal acid production —> duodenal damage —> gastric metaplasia in duodenum —> +/- H. Pylori moves into duodenum —> duodenal ulcers
Low pH —> H.pylori don’t move into body as readily

151
Q

Describe corpus-predominant atrophic gastritis or pangastritis

A

Genetically lower acid production —> easier for H.pylori to move into body —> pangastritis —> risk factor for gastric ulcers as well as intestinal metaplasia —> dysplasia —> gastric carcinoma

152
Q

What is peptic ulcer disease

A

Damage to the mucosal lining of the intestinal surface where acid is implicated in pathogenesis
Ulcer: damage extends into the muscularis mucosa

153
Q

Causes of peptic ulcer disease

A 
Ischemia 
H.pylori 
Smoking, alcohol 
Zollinger-Ellison syndrome, carcinoid 
Chron disease, radiation, chemo 
Adenocarcinoma 
NSAIDs 
ICU
154
Q

Complications of peptic ulcer disease

A

Pain
Penetration / perforation
Bleeding
Obstruction

155
Q

Management of peptic ulcer disease

A 
Correct underlying cause
Lifestyle changes 
Pharmacological: PPI 
Endoscopic 
- injection 
- coagulation 
- clipping 
Radio graphic 
Surgical
156
Q

Possible investigations for patients presenting with dysphagia

A

Labs: serology, urea breath test, stool studies
Radiology: X-rays, upper GI series, fluoroscopy, CT, MRI
Endoscopy: gastroscopy (esophagogastroduodenoscopy), enteroscopy, ERCP, cholangioscopy, colonoscopy
Endoscopic ultrasound
Manometry

157
Q

What conditions would give an abnormal AXR ?

A

Ileus, SBO, LBO
Volvulus
Constipation
Severe colitis

158
Q

Pros and cons of UGI series (barium swallow)

A 
Pros: 
Easy 
Cheap 
Good test in dysphagia 
Cons: 
Low sensitivity 
Low specificity
159
Q

What is the best test for severe abdominal pain ?

A

CT abdomen

160
Q

What is CT enterography

A

Same as CT abdomen, but with negative PO contrast and with IV contrast

161
Q

What can be used for distinguishing between motility disorders of esophagus ?

A

Esophageal manometry

162
Q

What are the major structures of the exocrine pancreas ?

A

Ductal cells

Acinar cells

163
Q

What is the function of acinar cells ?

A

Produce digestive enzymes

~15-100 grams of protein secreted per day

164
Q

What is the function of ductal cells ?

A

Produce basic bicarbonate fluid

—> about 1.5 L of fluid per day

411 (16 decks)

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