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HYMS Block 3 > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

1
Q
  1. Name the function of the mouth and how its anatomical components achieve this function
  2. what are the boundaries of the mouth:
    a) roof
    b) floor
    c) lateral walls
    d) anterior
    e) posterior
  3. what structures form the hard palate?
  4. what is the oral vestibule?
  5. what is the oral cavity proper?
A
  1. process and break down food to form a bolus
    - secretion of saliva helps moisten food and contains digestive enzymes
    - chewing helps break down food
    - tongue movements help shape the bolus

2a) hard and soft palate
b) mylohyoid muscle
c) cheeks
d) lips
e) palatoglossal fold

  1. maxillae and palatine bones
  2. space bounded externally by the cheeks and lips and internally by teeth and gums
  3. gums and teeth to fauces
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2
Q
  1. how is the innervation capsule and the gland of salivary glands different?
  2. what are the borders of the parotid salivary gland?
    a) anterior
    b) inferior/posterior
    c) superior border
  3. what muscle does the parotid duct
    a) transverse across?
    b) pierce?
  4. what type of fluid does the parotid gland produce?
  5. what is the shape of the submandibular gland?
  6. where does the submandibular gland enter the oral cavity?
  7. what type of fluid does the submandibular gland prodice?
  8. where does the sublingual duct enter the oral cavity?
  9. what type of saliva does it produce?
  10. what type of innervation controls salivary production
A
  1. capsule is innervated by somatic nervous system. Gland is innervated by the autonomic nervous system
    2a) posterior aspect of mandible and posterior aspect of masseter
    2b) sternocleidomastoid
    2c) external acoustic meatus
    3a) masseter
    3b) buccinator
  2. serous
  3. hook shaped
  4. either side of sublingual papilla
  5. serous and mucous fluid
  6. papillae either side of the lingual frenulum
  7. mucous
  8. parasympathetic
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3
Q
  1. what artery supplies the
    a) maxillary teeth
    b) mandibular teeth
  2. what nerve supplies the:
    a) maxillary teeth
    b) mandibular teeth
A

1a) maxillary artery
b) inferior alveolar artery
2a) maxillary nerve
2b) branch of mandibular nerve

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4
Q
  1. what artery and nerve supply all muscles of mastication?
  2. what is the origin and attachment of temporalis? What is its action?
  3. what is the origin and attachment of the masseter? What is its action?
  4. what is the origin and attachment of the lateral pterygoid muscle? What is its action?
  5. what is the origin and attachment of the medial pterygoid muscle? what is its action?
  6. what nerve supplys the buccinator? Why does it differ to that of other masticatory muscles?
A
  1. maxillary artery and mandibular nerve
  2. temporal line > coronoid process. Closes jaw
  3. zygomatic arch > angle of mandible. Closes jaw
  4. lateral aspect of lateral pterygoid plate > condyle of mandible. Opens Jaw
  5. medial aspect of lateral pterygoid plate > gonial angle. Opens jaw
  6. facial nerve. It is primarily a muscle of facial expression
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5
Q
  1. what is the role of the constrictor muscles?
  2. what are they innervated by?
  3. what is the glossopharyngeal plexus?
  4. describe the voluntary phase of swallowing
  5. describe the pharyngeal phase of swallowing
  6. describe the oesophageal phase of swallowing
A
  1. contraction to push food into the oesophagus
  2. vagus nerve
  3. a neural plexus formed by pharyngeal branches of the glossopharyngeal nerve and the vagus nerve.
    glossopharyngeal innervation is sensory; vagal innervation is motor. This mediates a reflex
  4. bolus is passed from mouth into oropharynx
  5. involuntary movement of bolus from pharynx to oesophagus. Involves upward movement of uvula and soft palate, closure of epiglottis and vocal folds and ascent of pharynx
  6. involuntary passage of bolus from oesophagus into stomach
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6
Q
  1. what does the oesophagus extend to and from (vertebral levels)
  2. what type of muscle forms the upper oesophageal sphincter?
  3. what type of muscle forms the lower oesophageal sphincter?
A
  1. C6-T10
  2. skeletal
  3. smooth
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7
Q
  1. what is the histology of the mouth > oesophagus?
  2. what is the histology of the stomach?
  3. Name the 4 types of exocrine gland cells that are found in the stomach and what they secrete
  4. what is the oesophageal-gastric junction?
  5. what is barrett’s oesophagus?
A
  1. stratified squamous non-keratinising epithelium
  2. simple squamous
  3. Mucous Neck Cells - mucus
    Parietal Cells - Intrinsic Factor and HCl
    Chief Cells - pepsinogen and gastric lipase
    G cells - gastrin (enteroendocrine)
  4. change in histology found at the junction of the oesophagus and stomach
  5. condition caused by significant acid reflux whereby simple collumnar epithelium expands up the oesophagus.
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8
Q
  1. what is the lymphatic supply of the stomach?

2. what is the stomach innervated by?

A
  1. celiac nodes
  2. vagus nerve - secretomotor function.
    Sympathetic innervation - somatic pain and vasculature
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9
Q
  1. which parts of the duodenum are
    a) peritoneal
    b) retroperitoneal
  2. what structures are found laterally to the superior duodenum
  3. what does the descending duodenum receive?
  4. what structures lie anterior and posterior to the horizontal duodenum?
  5. what is found at the ascending duodenum?
A

1a) superior
1b) descending, horizontal and ascending
2. common bile duct and gastroduodenal artery
3. common bile duct and pancreatic duct via hepatopancreatic ampulla of vater at the major duodenal papilla
4. anterior - superior mesenteric artery and vein
posterior - IVC and aorta
5. duodenojejunal flexture. Ligament of treitz supports this flexture

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10
Q
  1. what is a peptic ulcer?
  2. name 7 symptoms of peptic ulcers
  3. when does pain due to a stomach ulcer usually start?
  4. when does pain due to a duodenal ulcer usually start?
  5. how is stomach acid normally prevented from accessing the deeper layers of the stomach/small intestine wall?
  6. what is required for peptic ulcer healing?
A
  1. a break in the lining of the stomach or duodenum, leading to ulceration
    • pain in abdomen, neck, back
      - bleeding
      - indigestion
      - heartburn
      - loss of appetite
      - vomiting
      - can no longer tolerate fatty foods
  3. soon after eating a meal
  4. 2-3 hours after eating
  5. by mucosa
  6. a pH >3
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11
Q
  1. what are gastric glands?
  2. name the 3 exocrine cells contained in gastric glands and their role
  3. name the endocrine cells contained in gastric glands and its role
  4. describe the location of these cells within the stomach
A
  1. columns of secretory cells that extend into the lamina propria
  2. mucous neck cells - secrete mucus
    parietal cells - secrete intrinsic factor and HCl
    chield cells - secrete pepsinogen and gastric lipase
  3. g cells - secrete gastrin into the blood stream
  4. neck cells - cardia, pylori, fundus
    chief cells - fundus
    parietal cells - fundus
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12
Q
  1. describe the process of HCl secretion
  2. describe the compensatory mechanism involving bicarbonate
  3. what factors stimulate gastric acid secretion (3)
A
  1. H+/K+ ATPase is expressed on apical membrane. pumps H+ into lumen of stomach. K+ is recycled back by K+ channels. Cl is secreted by faciliated diffusion.
  2. secretion of acid raises pH of cell. bicarbonate is secreted across basolateral membrane out of cell by bicarbonate-chloride exchanger
  3. Histamine (released by enterochromaffin like cells in response to high stomach pH)- acts on H2 receptors
    Gastrin
    AcH - Vagal, parasympathetic innervation. Acts on M3 receptors
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13
Q
  1. what type of bacteria are H. Pylori?
  2. How do H. Pylori cause peptic ulcers?
  3. how are peptic ulcers caused by H pylori treated?
  4. What is the role of COX1?
  5. What is the role of COX2?
  6. Which of the COX enzymes is the desired target of NSAIDs?
  7. How do prostaglandins act on the stomach?
  8. How do NSAIDs cause peptic ulcers?
  9. What can be co-administered with NSAIDs to prevent peptic ulcer formation?
A
  1. gram negative
  2. secrete urease which causes inflammatory response. Inflammation disrupts stomach lining therefore enabling acid to infiltrate and cause ulceration
  3. antibiotics (amoxycillin with clarythromycin or metronidazole) with a PPI
  4. produce prostaglandins and thromboxanes. Housekeeping roles
  5. produce prostaglandins and prostacyclins to promote inflammation
  6. COX2
  7. activation of prostaglandin receptors decreases stomach acid secretion and increases mucous and bicarbonate secretion
  8. Decrease prostaglandin production therefore reduce mucous secretion and increase acid secretion
  9. Misoprostol - decreases cAMP activity in the parietal cell thus decreases proton pump activity (mimicks prostaglandins)
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14
Q
  1. How do PPIs work?
  2. what are they administered as?
  3. How long do their effects persist and why?
  4. name 4 examples
  5. how do H2 antagonists work?
  6. Name 3 examples
A
  1. antagonise the proton pump therefore decrease stomach acid secretion
  2. prodrugs - at acidic pH they are converted to sulphenamides, which covelently bond the proton pump
  3. half life is 0.5-2 hours however their effects can persist up to 2 days because of irreversible covalent binding
  4. omeprazole, lanzoprazole, pantorazole, rebeprazole
  5. antagonise the H2 receptors, which decreases stomach acid secretion (normally, histamine activation of H2 receptors promotes acid secretion via a cAMP dependent mechanism)
  6. ranitidine, cimetidine, nizatidine
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15
Q
  1. what CNS centre controls the vomiting response?
  2. describe the vomiting response
  3. What are the roles of these inputs into the vominting centre and what neurotransmitters/receptors do they use
    a) cerebral cortex
    b) peripheral inputs
    c) chemoreceptor trigger zone
    d) vestibular input
A
  1. medullary vomiting centre
  2. deep inspiration to avoid aspiring vomit
    retroperistalsis starts from middle of small intestine and proceeds through relaxed pyloric sphincter
    decreased intrathoracic pressure and increased abdominal pressure propels stomach contents into oesophagus

3a) anxiety and raised Intracranial pressure - GABA and H1
3b) relay info re state of GI tract. chemoreceptors and mechanoreceptors. 5-HT3 and 4, D2
3c) Drugs and hypercalcemia. D3, 5-HT3 and NK1
3d) vestibular problems/motion sickness. mAcHr and H1

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16
Q
  1. what 2 classes of drugs are used to treat motion sickness? Name examples and side effects of these drigs
  2. how does chemotherapy induce vomiting (2 ways)
  3. what drugs are used to reduce chemotherapy induced vomiting?
  4. how does metoclopramide work?
  5. how does domperidone work?
  6. what is phenothiazine used for?
A
  1. muscarinic antagonists such as hycosine
    - side effects include blurred vision, dry mouth and gut relaxation
    histamine antagonists such as promethazine.
    - side effects include drowsiness and dry mouth
    - also used to treat morning sickness
  2. stimulates chemoreceptor trigger zone (Dopamine and 5-HT)
    irritates the GI mucosa (5HT)
  3. 5HT3 antagonists such as ondanestron and graniestron
  4. acts on chemoreceptor trigger zone and increases motility of digestive tract
  5. acts on gut and chemoreceptor trigger zone
  6. used after nausea induced by chemotherapy/radiotherapy/cytotoxic drugs

HYMS Block 3 (4 decks)

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