Week 10-12: Gastrointestinal Tract Flashcards Preview

Med 1 UBC Fall 2019 > Week 10-12: Gastrointestinal Tract > Flashcards

Flashcards in Week 10-12: Gastrointestinal Tract Deck (245)
Loading flashcards...

Which Inflammatory Bowel Disease is characterized by bloody stool?

Ulcerative Colitis. In contrast, Crohn's Disease does not present with bloody stool.


Symptoms of ulcerative colitis, alleviating factors

Crampy lower abdominal pain, relieved by bowel movement; Bloody stool; No mass; Confined to mucosa; Continuous from rectum (colon only); No granulomas;


4 basic GI processes

- Motility - muscular contractions that mix and move forward the contents of the GIT

- Secretion - glands located along the GIT that secrete their contents into the tract, assisting in motility, digestion and absorption

- Digestion - the biochemical breakdown of large particles and molecules into smaller, absorbable particles

- Absorption - small particles are absorbed from the GIT into the blood or lymph


2 broad categories of movement (motility) in GI

1) Mixing movements: Redistribute luminal contents locally, enhancing the exposure to digestive secretions; expose luminal contents to GIT epithelium for absorption.

2) Propulsive movements: Move luminal contents forward. Rate of propulsion varies with specific function of region (e.g., esophagus = rapid; small intestine = slow)


What layers make up the small intestine?

  • Muscularis externa is the major smooth muscle layer of the GIT. It has two layers:
    • - Inner circular layer - responsible for restriction of the lumen
    • - outer longitudinal layers - responsible for shortening of the GIT
  • Myenteric plexus lies underneath, coordinating muscularis externa contractions.
  • Inner most layer is the Muscularis Mucosae, which is a thin layer of smooth muscle between the mucosal and submucosal layers.


Explain the role of Ca2+ and Myosin Light Chain Kinase in GI smooth muscle contraction

- increased intracellular Ca2+ leads to binding of Ca2+ and calmodulin.

- the Ca-Calmodulin complex activates Myosin Light Chain Kinase (MLCK)

- MLCK phosphorylates myosin, which can now bind actin and perform shortening of muscle fibres.

- Contraction is terminated when Myosin Light Chain Phosphatase cleaves phosphate from myosin.


How can a smooth muscle cell increase Ca2+ levels for contraction? (2)

1. Calcium-induced calcium release: Depolarisation of membrane brings Ca into cell via voltage gated calcium channels at base of calveoli (indentation at membrane). The influx of Ca induces sarcoplasmic reticulum to release of Ca .

2. Pharmaco-mechanical coupling: IP3 receptor in SR responds to elevated cytosolic levels of IP3 by releasing Ca2+


Describe the role of the Interstitial Cells of Cajal (ICC) as 'pacemaker' cells for GI smooth muscle contraction

These are specialized smooth muscle cells of GIT that act as pacemakers for contraction! The undergo spontaneous, transient membrane depolarisations that are propagated to adjacent smooth muscle cells via gap junctions, resulting in SLOW WAVES. Greater # of APs sent along, increases the strength of contraction.


How are the duration and amplitude of slow waves modulated?

By enteric motor neurons in the walls of the GIT.


List the components of ENS

1) Sensory neurons (including mechanoreceptors, chemoreceptors and osmoreceptors)

2) Interneurons (excitatory and inhibitory)

3) Secretomotor cells, which influence… - Smooth muscle - Epithelial cells that secrete or absorb fluid/electrolytes - Enteric endocrine cells


Describe the role of the enteric NS in the regulation of GI motility

The enteric NS can operate entirely in the GI wall without external input (it's reflexive). Moderate contraction by sending NTs to ICCs and smooth muscle cells in the circular and longitudinal muscle layers, which result in increased intracellular Ca levels and consequent contraction.


Autonomic Nervous System regulation of GI motility

En Passant Innervation: motor axons have multiple varicosities containing NT that can be released into smooth muscle to reach targets The ANS communicates with the ENS


Describe the 3 phases of swallowing

1) ORAL PHASE: pushing food bolus toward the back of oral cavity and up against the palate. Requires tongue.

2) PHARYNGEAL PHASE: Touch and pressure receptors in the pharyngeal nerve (in pharynx) send stimulation to medulla via trigeminal nerve, thus initiating reflexive component of swallowing. Pharyngeal wall contracts, thus pushing food into esophagus. Tongue prevents bolus from travelling backward into mouth. Uvula elevates to seal nasal passages. Vocal cords contract and epiglottis closes over the trachea.

3) ESOPHAGEAL PHASE: swallowing centre relaxes pharyngeoesophageal sphincter and initiates primary peristaltic waves by interacting with ENS, to propagate the bolus toward the stomach. These are paired with secondary peristaltic waves, which are triggered by stretch and act to dislodge bolus. Gastroesophageal sphincter opens when a peristaltic wave pushes food bolus against it.


What coordinates the motion of swallowing?

The swallowing centre in the medulla oblongata. The initiation of swallowing is voluntary, but once it starts, completion of swallowing in reflexive.


Explain the opening of the gastroesophageal sphincter

The vagus nerve mediates reflexive relaxation of the sphincter when a food bolus is pushed up against it.


Describe primary peristalsis

~5-9 seconds of travel along esophagus

- Inner circular layer of muscularis externa contracts, pinching a ring

- Outer longitudinal muscle layer contracts in front of the inched ring, reducing the length of the tube

- This sequence propagates along the length of the esophagus, pushing luminal contents toward the stomach


What initiates the reflexive phase of swallowing?

Pressure of food against the pharyngeal palate stimulate the trigeminal nerve which signals reflexive swallowing to occur.


What are the 2 major motility paradigms in the small intestine?

1. segmentation 2. Migrating Mobility Complex


Explain segmentation

Dominant motility in small intestine right after a meal, responsible for mixing chyme and moving it toward large intestine. Composed of alternating contractions and relaxations of adjacent sections of the intestine.


What initiates segmentation? (3)

distension of the lumen

presence of gastrin

parasympathetic input


What is the migrating mobility complex?

Replaces segmentation following the absorption of a meal. Moves luminal contents along the intestine in periods between meals. Begins at the duodenal-gastric junction and consists of weak peristaltic movements that travel short distances. A second wave begins more distally than the previous to move contents along.


Pathophysiology of achalasia

= functional disorder of the esophagus characterized by increased resting tone and incomplete relaxation of the lower esophageal sphincter, preventing food from entering the stomach. 

can be recognized by the 'bird beak sign' on radiology. 


What is esophagitis (2) and what may cause it (3)?

= inflammation and epithelial damage of esophagus

  • May be caused by reflux (GERD), infection of immunocompromised, eosinophilic esophagitis


What is GERD?

= gastric contents leak backward into the esophagus causing irritation/inflammation of esophagus


Barrett's esophagus: what it is and how it may progress

= distal squamous mucosa of esophagus is replaced by metaplastic columnar epithelium. A response to prolonged injury, columnar epithelium may be more resistance to acid. 

Barrett's esophagus is a complication of GERD that may progress to esophageal adenocarcinoma. 

Premalignant dysplasia does not invade lamina propria. Graded based on histologic assessment. 



Pathophysiology of diaphragmatic (hiatal) hernias

types (2)

possible presenting Sx (2)

= abnormal protrusion of a segment of the stomach above the diaphragm. 

Can be (a) sliding or (b) paraesophageal/nonaxial

Usually asymptomatic, can have reflux or heartburn. 


Gastritis: what is it? Acute vs chronic vs chornic active

= inflammation/irritation of the gastric mucosa

ACUTE: sudden onset; often with erosions or ulcer. Often caused by NSAIDs, alcohol, cocaine, stress, trauma. 

CHRONIC: Ongoing. Often multifactorial and often combined with acute. Due to infection, autoimmunity, reactive. 

CHRONIC ACTIVE: persistent inflammation of the gastric mucosa related to h pylori. Typically affects antrum of stomach and may extend to body. Increased risk of gastric carcinoma and gastric lymphoma. 


Peptic ulcer disease: define, possible complications

= acid-induced ulceration of the mucosa and wall of the stomach or duodenum often associated with h. pylori. 

Complications: perforation, hemorrahage, obstruction (stenosis), penetration


Carcinoma of the esophagus

didn't find this in lecture but it is an objective so check CBL research from the week. 


Gastric Polyps

= abnormal growth of tissue projecting from a membrane in the stomach

Can be neoplastic (benign or malignant) or non-neoplastic (hyperplastic or fundic gland polyp)