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HYMS Y1 > Block 3 W1 > Flashcards

Block 3 W1 Flashcards

1
Q

How is the upper and lower GI divided?

A

Upper GI - oesophagus to duodenum + associated structures.

Lower GI - jejunum to anus.

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2
Q

What is the boundaries of the mouth?

A 
Roof - hard and soft palate
Floor - mylohyoid muscle
Lateral walls - cheeks
Anterior - lips
Posterior - palatoglossal fold
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3
Q

What are the contents of the mouth?

A

Vestibule, oral cavity, teeth, gums, tongue and salivary glands.

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4
Q

What are the boundaries of the parotid gland?

A

Superior - zygomatic arch and external acoustic meatus
Inferior - mandible and sternocleidomastoid
Anterior - masseter
Posterior - sternocleidomastoid muscle

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5
Q

Where does the parotid duct open into?

A

Stensen duct, 5cm

Traverses masseter, pierces buccinator and opens into vestibule at 2nd upper molar.

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6
Q

What kind of saliva does the parotid produce?

A

Serous saliva - watery solution rich in enzymes

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7
Q

What is the vasculature of parotid?

A

Posterior auricular and superficial temporal arteries.

Retromandibular vein

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8
Q

What is the innervation of parotid?

A

Sensory - auriculotemporal nerve (mandibular nerve)
Parasympathetic - glossopharyngeal nerve via otic ganglion.
Sympathetic - superior cervical ganglion

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9
Q

What is the lymphatic drainage of parotid?

A

Periauricular/parotid lymph nodes.

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10
Q

Where does the submandibular gland lie?

A

Submandibular triangle

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11
Q

What kind of saliva does the submandibular produce?

A

Mixed serous and mucus.

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12
Q

Where does the submandibular duct open into?

A

Whartons duct, 5cm

Empties from the sublingual papilla - raised bumps in line with lingual frenulum under the tongue.

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13
Q

What is the vasculature of submandibular?

A

Submental arteries - facial artery

Submental veins

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14
Q

What is the innervation of submandibular?

A

Parasympathetic - Chorda tympani (facial nerve) and lingual branch (mandibular nerve)
Sympathetic - superior cervical ganglion

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15
Q

What is the lymphatic drainage of submandibular?

A

Submandibular -> jugulo-digastric lymph nodes

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16
Q

Where does the sublingual gland lie?

A

Sublingual fossa
Inferior to tongue, near medial mandible.
Both sublingual glands unite into sublingual fold.

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17
Q

Where does the sublingual duct open into?

A

Minor sublingual ducts (of Rivinus) into sublingual folds.

Major sublingual ducts (of Bartholin) joins submandibular duct into sublingual papilla.

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18
Q

What kind of saliva is produced by sublingual?

A

Mucus saliva

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19
Q

What is the vasculature of sublingual?

A

Sublingual and submental arteries (lingual and facial arteries)
Sublingual and submental veins.

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20
Q

What is the innervation of sublingual?

A

Same as submandibular

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21
Q

What is the lymphatic drainage of sublingual?

A

Submandibular lymph nodes.

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22
Q

Describe a typical tooth.

A

Crown, neck and root.
Enamel -> dentin -> pulp.
Deciduous (20) and permanent teeth (32)
4 incisors, 2 canine, 4 pre-molars, 6 molar (x2)

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23
Q

What is the innervation of the teeth?

A

Maxillary - maxilla nerve

Mandible - mandibular nerve

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24
Q

What is the vasculature of the teeth?

A

Maxillary - maxillary artery

Mandibular - inferior alveolar artery

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25
Q

Describe the TMJ.

A

Synovial joint - separated into upper and lower by articular disc.
Enables mandible to articulate with cranium for large range of movement.

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26
Q

What is the innervation of all muscles of mastication?

A

Mandibular branch of trigeminal nerve, V3

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27
Q

What is the vasculature of all muscles of mastication?

A

Maxillary artery and superficial temporal.

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28
Q

Describe the attachment and insertion of temporalis.

A

Attachment - temporal fossa

Insertion - coronoid process of mandible

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29
Q

Describe the attachment and insertion of masseter.

A

Attachment - zygomatic arch

Insertion - angle of mandible

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30
Q

Describe the attachment and insertion of lateral pterygoid.

A

Attachment - lateral surface of lateral pterygoid plate

Insertion - infra temporal fossa and crest of greater wing of sphenoid.

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31
Q

Describe the attachment and insertion of medial pterygoid.

A

Attachment - medial surface of lateral pterygoid plate.

Insertion - pyramidal process of palatine, tuberosity of maxilla and mandibular ramus.

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32
Q

What is accessory muscle of mastication?

A

Buccinator (muscle of facial expression), supplied by facial nerve. Keeps food in oral cavity.

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33
Q

What are the closers of the mandible?

A

Masseter, temporalis and medial pterygoid.

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34
Q

What are the openers of the mandible?

A

Lateral pterygoid

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35
Q

What are the grinders of the mandible?

A

Medial and lateral pterygoid.

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36
Q

List the extrinsic muscles of tongue.

A

Hyoglossus
Styloglossus
Palatoglossus
Genioglossus - mental symphysis to glossus

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37
Q

List the intrinsic muscles of tongue.

A

Superior longitudinal
Inferior longitudinal
Transverse
Vertical

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38
Q

Describe the innervation of tongue.

A

Motor - all -> hypoglossal nerve, except palatoglossal -> vagus nerve.
General sensory:
- posterior 1/3 glossopharyngeal nerve
- anterior 2/3 lingual nerve
Special sensory:
- posterior 1/3 glossopharyngeal nerve
- anterior 2/3 facial nerve via chorda tympani.

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39
Q

Describe the vasculature of tongue.

A

Lingual artery and vein.

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40
Q

Describe the pharynx.

A

Funnel-shaped fibromuscular tube beginning at base of skull to the inferior border of cricoid cartilage (C6).
Comprised of nasopharynx, oropharynx and laryngopharynx.

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41
Q

What are the circular muscles of the pharynx?

A

Superior constrictor (mandible), middle constrictor (hyoid) and inferior constrictor (cricoid) muscles (median raphe).

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42
Q

What are the longitudinal muscles of the pharynx?

A

Stylopharyngeus, palatopharyngeus and salpingopharyngeus.

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43
Q

What are the innervations of the pharynx?

A 
Pharyngeal plexus (sits middle constrictor).
Formed by pharyngeal branch of glossopharyngeal (sensory), vagus nerves and sympathetic fibres of superior cervical ganglion.
Vagus innervates all muscles of pharynx except stylopharyngeus (glossopharyngeal).
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44
Q

What are the vasculature of the pharynx?

A

External carotid artery

Pharyngeal venous plexus

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45
Q

How does the oropharynx prevent the food going to nasopharynx?

A

Uvula and levator veil contract, pulling soft palate up.

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46
Q

What is the automatic swallowing reflex?

A

When food touches back of pharynx, involuntary reflex occurs due to vagus contracting the muscles for soft palate to lift and close nasopharynx.

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47
Q

Outline the 3 phases of swallowing.

A
  1. Oral - bolus pushed backward by elevating tongue by styloglossus and palatoglossus.
  2. Pharyngeal:
    - soft palate -> lifts and closes nasopharynx
    - vocal fold ->shuts to prevent movement into trachea
    - larynx and epiglottis -> tilts down and closes trachea
    - upper oesophageal sphincter -> opens
  3. Oesophageal - sequential contraction of the 3 constrictor muscles, peristalsis.
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48
Q

Describe the oesophagus.

A

Fibromuscular tube, 25cm
From inferior border of cricoid cartilage (C6) to cardiac orifice of stomach (T11).
Cervical, thoracic and abdominal parts.

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49
Q

Describe the muscles of the oesophagus.

A

Internal circular and external longitudinal muscles.
External longitudinal:
- superior third -> voluntary striated muscle
- middle third -> voluntary striated and smooth muscle
- inferior third -> smooth muscle
Moves bolus by peristalsis

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50
Q

Describe the upper oesophageal sphincter.

A

Voluntary striated skeletal muscle - made of cricopharyngeus and inferior constrictor.
Relaxes during swallowing.

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51
Q

Describe the lower oesophageal sphincter.

A

Smooth muscle located at gastro-oesophageal junction (T11) - normally closed.
Weak sphincter that prevents gastro-oesophageal reflux.
Right crus of diaphragm has ‘pinch-cock’ effect.

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52
Q

What are the anatomical constrictions on the oesophagus?

A
  • Pharyngeal-oesophageal junction
  • Tracheal bifurcation
  • Gastro-oesophageal junction.
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53
Q

What is the innervation of oesophagus?

A

Cervical - recurrent laryngeal nerve
Thoracic - vagus and greater splanchnic nerve
Abdomina - vagus plexus

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54
Q

What is the vasculature of oesophagus?

A

Arteries:
Cervical - inferior thyroid artery
Thoracic - oesophageal branches of aorta and bronchial arteries
Abdominal - left inferior phrenic and left gastric arteries.
Veins:
Cervical - vertebral, brachiocephalic and inferior thyroid vein
Thoracic - azygous and hemiazygous veins (systemic circulation)
Abdominal - left gastric (portal circulation)

55
Q

Describe the lymphatic drainage of oesophagus.

A

Cervical - deep cervical nodes
Thoracic - tracheobronchial and posterior mediastinal nodes
Abdominal - left gastric and coeliac nodes.

56
Q

Describe the histology of digestive tract.

A

Mouth, oropharynx, laryngopharynx and oesophagus -> non-keratinised stratified squamous.
- Becomes keratinised from smoking.
Stomach -> changes to simple columnar at the gastro-oesophageal junction.
- seen as colour change
- has goblets and parietal cells.

57
Q

Define Barrett’s oesophagus.

A

Consistent reflux -> simple columnar epithelium grows upwards into oesophagus.

58
Q

Describe the location of stomach.

A

Muscular bag with variable size and lies on stomach bed.

Left hypochondriac and epigastric regions.

59
Q

Describe the anatomy of the stomach.

A

4 main regions:
- cardia -> superior opening to stomach
- fundus -> most superior part
- body -> large central part inferior to fundus
- pylorus -> entry point to duodenum, divided into Antrum and canal.
Greater curvature -> cardiac to pyloric Antrum.
Lesser curvature -> concave medial surface of stomach.

60
Q

Describe the histology of the stomach.

A

Rugae - overproduction of epithelium, allows expansion.

Oblique, circular, longitudinal muscles.

61
Q

Describe the pyloric sphincter.

A

Circular smooth muscle.
Lies on transpyloric plane.
Controls exit of chyme (3ml/wave)

62
Q

Describe the vasculature of the stomach.

A

Coeliac trunk:
Lesser curvature - left and right gastric arteries
Greater curvature - short gastric and left + right gastroepiploic arteries.
Veins mirrors the arteries.

63
Q

Describe the lymphatic drainage of the stomach.

A

Coeliac nodes

64
Q

Describe the innervation of the stomach.

A

The coeliac plexus (T6-T9) supplies sympathetic fibres. SNS - greater splanchnic nerve.
Vagus supplies parasympathetic fibres (secretomotor) -> peristalsis and secretory action.
- left vagus supplies anterior vagal trunk
- right vagus supplied posterior vagal trunk

65
Q

Describe the duodenum.

A

C-shaped tube, 25cm

Receives chyme from stomach.

66
Q

What are the 4 parts of the duodenum?

A
  1. Superior - peritoneal
    - duodenal cap
    - common bile duct and gastroduodenal artery lies posterior
  2. Descending - retroperitoneal
    - junction of foregut and midgut
    - receives fluid from CBD and main pancreatic duct via hepatopancreatic ampulla (of Vater) at major duodenal papilla
    - sphincter of oddi surrounds this
    - minor duodenal papilla -> entry point of accessory pancreatic duct
  3. Transverse (horizontal) - retroperitoneal
    - superior mesenteric artery and vein anterior
    - aorta and IVC posterior
  4. Ascending - retroperitoneal
    - joins jejunum at duodenojejunal flexure supported by ligament of Treitz from right diaphragmatic crus.
67
Q

Describe the vasculature of the duodenum.

A

Foregut - coeliac axis

Midgut - superior mesenteric axis

68
Q

Describe the lymphatic drainage of the duodenum.

A

Duodenal lymph nodes drains into superior mesenteric and coeliac nodes.

69
Q

Describe the innervation of the duodenum.

A

SNS - coeliac and superior mesenteric plexus

PNS - vagus

70
Q

Describe the digestion of carbohydrates.

A

Only monosaccarides are absorbed so starch/glycogen is broken down.
Starts in mouth by salivary amylase and lingual lipase.

71
Q

What does alpha-amylase (salivary and pancreatic) form?

A

Hydrolyses 1,4-glycosidic bonds in starch -> maltose, maltotriose and alpha-limit dextrin (oligosaccharide)

72
Q

Where do maltase, alpha-dextrinase and sucrase work?

A

Intestinal brush border - hydrolyse oligosaccharides to glucose.

73
Q

What does alpha-dextrinase work?

A

Acts on alpha-dextrin - removes one glucose at a time.

74
Q

What does sucrase form?

A

Sucrose -> glucose/fructose

75
Q

What does lactase form?

A

Lactose -> glucose/galactose

76
Q

What does maltase form?

A

Maltose -> 2x glucose

77
Q

Describe the absorption of glucose and galactose.

A

Transported from intestinal lumen into absorptive cells by Na+-dependent glucose symporter (SGLT) at the apical membrane.
Glucose transported to blood by facilitated diffusion (GLUT2).
Na+/K+ ATPase pumps Na+ into blood to maintain low intracellular Na+.

78
Q

Describe the absorption of fructose.

A

Facilitated diffusion.

79
Q

Define resistant starch.

A

Remains of plant cell wall that are resistant to digestion so passes through SI to LI where it is broken down into short chain fatty acids (dietary fibre) by bacteria.

Acetate, propionate and butyrate.

80
Q

What are the benefits of resistant starch?

A

Absorbs - cholesterol (increase clearance), bile acids (tumour-promoting action) and potential carcinogens.
Increase viscosity of gut contents to slow down absorption.
Butyrate has anti-proliferative action, propionate has anorectic effect.

81
Q

What is the role of pepsin and where is it secreted?

A

Pepsin - proteolytic enzyme that digests protein.

Secreted as pepsinogen by gastric chief cells and activated to pepsin by gastric H+.

82
Q

What are pancreatic proteases and their role?

A

Pancreatic enzymes - typsin, chymotrypsin, elastase, carboxypeptidase A and B.
Break down proteins into di/tripeptides (60%) and free AAs (40%).

83
Q

Describe the absorption of free AAs

A

Na+-dependent AA cotransporter in the apical membrane transports AA from lumen to absorptive cells.
AA transported to blood by facilitated diffusion.
4 separate carriers for neutral, acidic, basic and imino AAs.

84
Q

Describe the absorption of di/tripeptides.

A

Absorbed faster than free AAs.
H-dependent cotransport on apical membrane transports them into the absorptive cells.
Cytoplasmic peptidases hydrolyses into free AAs -> transported into blood by facilitated diffusion.

85
Q

Define zymogens.

A

Digestive enzymes are released as precursor (inactive) cells then activated after secretion.

86
Q

What is the components of saliva?

A

Water, ions, enzymes and lysozyme - 1.5L/day

87
Q

What are the phases of gastric secretion?

A
  1. Cephalic phase (1/3)
  2. Gastric phase (2/3)
  3. Intestinal phase
88
Q

What are the stimulators of cephalic phase?

A

Sight, thought, smell and taste -> stimulate vagus nerve (PNS) to activate parietal and chief cells -> increase HCl and pepsin.

89
Q

What are the different cell types in the stomach?

A

Mucus cells - secrete mucus to protect epithelial (cardiac and pyloric).
Parietal cells - secrete HCl and intrinsic factor (fundus, body and pyloric).
Chief cells - secrete pepsinogen (cardiac).
Enteroendocrine cell - secrete protein hormones e.g. somatostatin. G cells - secrete gastrin (pyloric Antrum)
Stem cells - throughout.

90
Q

What are the stimulators of the gastric phase?

A
  1. Distention - chemo/stretch receptors activated -> increases HCl and pepsin.
  2. Increased peptones -> enters-endocrine Antrum G cells releases gastrin -> binds parietal cells to release H+ via pump. Gastrin binds chief cells -> vesicles exocytose to release pepsinogen.
91
Q

What are the inhibitors of the gastric phase?

A
  1. SNS -> stress, depression and anxiety
  2. Somatostatin - responds to high H+ by antral D cells (chemoreceptor). SST -> reduces gastrin secretion on antral G cells.
92
Q

What inhibits somatostatin?

A
  • Vagus stimulation reduces D cell activation and SST

- gastrin binds D cells and inhibits it.

93
Q

What are the stimulators of gastric H+ secretion?

A
  1. Vagal stimulation - releases ACh, which binds M3 receptor on parietal cell -> activates H+,K+-ATPase.
  2. G cells - releases gastrin -> binds CCK2 receptors. Second messenger IP3/Ca2+. Also stimulates histamine release from ECL cells.
  3. Enterochromaffin-like cell - releases histamine, which binds H2 receptors on parietal cell. 2nd messenger cAMP.
94
Q

Describe the formation of HCl from parietal cell.

A

Within parietal cell, CO2 and H2O -> H+ and HCO3- catalysed by carbonic anhydrase.
H+ secreted into lumen by H+,K+-ATPase. Cl- secreted alongside -> HCl.
HCO3- absorbed into blood in exchange for Cl- -> pH of blood increases (alkaline tide).

95
Q

What are the inhibitors of gastric H+ secretion?

A
  1. Low pH (<3) in stomach - inhibits gastrin secretion and therefore H+.
  2. Somatostatin - binds receptors on parietal cell that are coupled to adenyl cyclase via Gi protein -> decreasing cAMP and H+. Also Inhibits release of histamine and gastrin secretion.
  3. Prostaglandins - activates Gi protein.
96
Q

What are the major GI hormones?

A

Gastrin, secretin, CCK and GIP

97
Q

What are the actions of gastrin?

A
  1. Increases H+ secretion by gastric parietal cells.

2. Stimulates growth of gastric mucosa by RNA and protein synthesis.

98
Q

What are the stimulators of gastrin?

A
  1. Small peptides and AAs in the lumen of stomach.
  2. Distention of stomach
  3. Vagal stimulation mediated by gastrin-releasing peptide.
99
Q

What are the inhibitors of gastrin?

A
  1. H+ in lumen of stomach

2. Somatostatin

100
Q

What are the actions of CCK?

A
  • Stimulates contraction of gallbladder and relaxation of sphincter of oddi for secretion of bile
  • Stimulates pancreatic enzyme secretion
  • Potentiates secretin-induced stimulation of pancreatic HCO3- secretion
  • Stimulates growth of exocrine pancreas
  • Inhibits gastric emptying
  • Inhibits H+ secretion
101
Q

What are the stimulators of CCK?

A
  • Small peptides and AA
    -Fatty acids and monoglycerides
    in duodenum and jejunum.
102
Q

What are the actions of secretin?

A
  • Stimulates pancreatic HCO3- secretion -> neutralises H+ in intestinal lumen
  • Stimulates HCO3- and H2O secretion by liver and increases bile production
  • Inhibits H+ secretion by parietal cells.
103
Q

What are the stimulators of secretin?

A
  • H+ in duodenum

- Fatty acids

104
Q

What are the actions of glucose-dependent insulinotropic polypeptide (GIP)?

A
  • Stimulates insulin release

- Inhibits H+ secretion

105
Q

What are the stimulators of GIP?

A

Fatty acids, AAs, orally administered glucose.

106
Q

What stimulates gastric secretion in the intestinal phase?

A

Gastrin and entero-oxyntin:

  • peptones stimulate duodenal G cells to release gastrin -> travels back to stomach via vessels and activates parietal cells -> H+ release
  • gastrin also activates chief cells to release pepsinogen.
107
Q

What are the inhibitors of gastric secretion in the intestinal phase?

A

Intestinal S cells -> release secretin.
Entero-endocrine I cells -> release CCK
Endocrine cells i.e. PYY and neurotensin -> reduces proton pump
K cells -> release GIP

108
Q

How does stomach not digest itself?

A

Mucosal barrier:

  • gel layer rich in mucin, H2O and phospholipids
  • HCO3-, which converts pepsin to pepsinogen and with H+ forms H2O and CO2 -> burp.
109
Q

What is absorbed in the stomach?

A
  • Alcohol

- Aspirin

110
Q

What is absorbed in the small intestine?

A 
Alcohol
Water
Fats
AAs
Glucose
Water-soluble vitamins C, B
Fat-soluble vitamins A, D, E, K
Minerals (Na, K, Mg, Ca, Fe)
Bile
111
Q

What is absorbed in the large intestine?

A

Acids and bases
Water
Remainder of Na and K

112
Q

Define peptic ulcer.

A

Disruption of the epithelium due to loss of protective mucus barrier or excessive H+ and pepsin secretion.
Causes acid to corrode tissue -> pain and bleeding.

113
Q

What are the symptoms of peptic ulcers?

A 
Pain in abdomen/neck/navel/back
Bleeding
Indigestion
Heartburn
Loss of appetite
Vomiting
Can't tolerate fatty food.
114
Q

Within gastric pits, what do gastric glands produce?

A

Gastric juice - HCl, enzymes and mucus (parietal, chief and neck cells).

115
Q

Give an overview of gastric secretion targets.

A
  • cholinergic muscarinic receptors
  • prostaglandin receptors
  • histamine receptors
  • gastrin receptor
  • proton-pump inhibitor
  • antibiotics
116
Q

What are two potential causes of peptic ulcers?

A

Helicobacter pylori
NSAIDs
Smoking and alcohol

117
Q

What is Helicobacter pylori and its mech of action?

A 
G negative bacteria
Once infected, remains in stomach for life
MoA:
- urease (makes stomach alkaline
- induces inflammation -> gastritis
- disrupts lining of stomach -> ulcer
118
Q

Outline the treatment for H.pylori.

A

Amoxicillin + clarithromycin/metronidazole

PPI

119
Q

Describe the mech of action of PPI.

A

Blocks H+,K+-ATPase pump -> prevents proton secretion into lumen by parietal cells -> raises stomach pH.
Prodrug - initially inactive.
Once taken up by parietal cell, converts to sulphonamide intermediate -> this irreversibly binds pump -> non-functional, must be degraded and replaced by new pump to restore function.

120
Q

Why does the PPI remain in system when its half life is short?

A

Half-life - 2hours
Single dose persists for 3 days:
- accumulation of drug in parietal cell
- irreversible nature of drug

121
Q

Describe the mech of action of H2 antagonists.

A

Normally, histamine binds receptor -> activates Gs -> activates adenyl cyclase -> cAMP -> activates protein kinase A -> allows H+ to extrude from parietal cell.
H2 antagonist blocks the histamine-2 receptor -> reduces H+ secretion.

122
Q

Give examples of PPI.

A

Omeprazole, lansoprazole, pantoprazole

-zole

123
Q

Give examples of H2 antagonists.

A

Cimetidine, ranitidine

-idine

124
Q

Why do NSAIDs cause peptic ulcers?

A

NSAIDs target COX1 and 2 -> reduces prostaglandin production:

  • increases gastric acid secretion
  • reduces mucus and HCO3- secretion
125
Q

What is the mech of action of misoprostol?

A

Prostaglandin receptor agonist - mimics prostaglandins activity to reduce cAMP in parietal cells and reduce pump activity.

126
Q

What do antacids do?

A

Neutralises gastric acid, increasing pH of stomach for healing.

127
Q

What are the internal and external causes of vomiting?

A

Internal: headaches, viral infections, heart attack, pregnancy
External: motion sickness, alcohol poisoning, food poisoning, medicine

128
Q

What are the dangers of vomiting?

A
  • aspiration
  • physical injury to muscles (over-straining), oesophagus (acid damage) and teeth (acid degradation)
  • retching is the reverse peristalsis of stomach and oesophagus without vomiting
  • electrolyte/fluid imbalance
129
Q

What do triggers of vomiting centre in brain cause?

A
  • respiration stops
  • closure of glottis
  • relaxation of lower oesophageal sphincter (clear tract for vomit cascade)
  • contraction of diaphragm and abdominal muscle + abdominal pressure -> anti peristalsis.
130
Q

Describe higher control of vomiting.

A

Chemoreceptor trigger zone (CTZ) and the vomiting centre in medulla has receptors for:
Dopamine
5-HT
ACh
Histamine
Activation of these receptors -> nausea and vomiting.

131
Q

Describe how muscarinic receptor antagonists work, examples and side effects.

A

Prevents info from vestibular apparatus reaching CTZ.
Used for travel sickness.
e.g. hyoscine
SE: blurred vision, dry mouth, relaxes gut.

132
Q

Describe how H1 receptor antagonists work, examples and side effects.

A

Blocks histamine activity and prevents info from CTZ reaching vomiting centre in medulla.
e.g. promethazine
SE: drowsiness and dry mouth

133
Q

Describe how 5-HT receptor antagonists work, examples and side effects.

A

Blocks 5-HT receptors -> reduces activity of vagus nerve - used to stimulate vomiting centre.
Used for chemotherapy induced sickness.
e.g. ondanestron, granisetron
SE: few

134
Q

Describe how D2-receptor antagonists work, examples and side effects.

A

Blocks D2 receptors - prevents info reaching vomiting centre.
Also used as antipsychotics i.e. chlorpromazine
e.g. Metaclopramide - acts on CTZ and gut, increases motility.
e.g. Domperidone - acts on CTZ and gut, doesn’t cross BBB.
SE: broad, adverse CNS effects (disorders of movement)

HYMS Y1 (25 decks)

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