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Medicine Year 1 > Case 11 SBA > Flashcards

Case 11 SBA Flashcards

1
Q

What are the three paired salivary glands?

A

Parotid, submandibular, sublingual

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2
Q

What percentage of saliva is secreted from the main three glands?

A

90%

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3
Q

Describe the parotid glands

A

side of face by ears. Parotid duct passes through buccinator muscle and opens into the oral cavity on the inner surface of the cheek opposite the maxillary second molar. Mumps can cause swelling of this gland

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4
Q

Describe the submandibular glands

A

under mandible. Submandibular duct (Wharton duct) travels between sublingual gland and genioglossus. Drains into the mouth through the sublingual caruncles located either side of the frenulum of the tongue

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5
Q

Describe the sublingual glands

A

under tongue. 8-20 ducts of Rivinus drain the sublingual glands. Some form the sublingual duct of Bartholin and join the submandibular duct. Others drain into the mouth separately at the sublingual folds either side of the frenulum of the tongue

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6
Q

Sialolithiasis

A

Salivary stones - calcified deposits that can block ducts causing pain and swelling of the affected gland. Can lead to inflammation and/or infection

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7
Q

Who and where do salivary stones affect most?

A

Male
30-60
Submandibular gland (less common in parotid, rare in sublingual and other smaller glands)

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8
Q

Treatments for sialolithiasis

A

hydration and stimulation of secretion to flush out smaller stones
massage to encourage stone expulsion
sialendoscopy
surgical removal of stones or gland

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9
Q

Functions of saliva

A

Lubrication to facilitate mastication, swallowing, and speech
Digestion and absorption
Protection, oral and dental health

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10
Q

Contents of saliva for lubrication

A

Fluid, mucus, proline-rich proteins

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11
Q

Contents of saliva for digestion and absorption

A

alpha amylase - initiation of starch digestion
lingual lipase - initiation of lipid digestion
r-protein - haptocorrin, role in b12 absorption

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12
Q

Contents of saliva for protection, oral and dental health

A

lysozyme breaks down bacteria walls
lactoferrin sequesters iron to stop bacterial growth and makes cell walls more permeable
slows down viral replication
IgA
thiocyanate
proline-rich proteins
mucus
fluid
HCO3-

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13
Q

Why do bacteria proliferate overnight in the mouth?

A

Low rate of saliva production

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14
Q

Xerostomia

A

dry mouth

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15
Q

What causes salivary gland hypofunction?

A

decreased blood supply, secretory function, stimuli
Sjögren’s syndrome
Nerve damage
Drugs

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16
Q

What can salivary gland hypofunction lead to?

A

dental caries, ulceration, infections, discomfort, speech difficulties, taste, chewing, swallowing

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17
Q

Treatments of xerostomia

A

stimulate residual saliva, artificial saliva, and sugar free gum

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18
Q

What are the secretory units in the salivary glands?

A

Acini - produce all the fluid

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19
Q

Pathway from acinus to main duct in salivary glands

A

Acinus → intercalated duct → striated duct → intralobular duct → interlobular duct → lobar duct → main duct

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20
Q

Histology of submandibular glands

A

acinar/serous cells and mucus secreting cells

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21
Q

Histology of parotid glands

A

lots of serous/acinar cells

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22
Q

Parotid saliva type and percentage secreted

A

Serous, 20-25%

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23
Q

Sublingual saliva type and percentage secreted

A

Mucus/serous, <5%

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24
Q

Submandibular saliva type and percentage secreted

A

Serous/mucus, 60-65%

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25
Q

Other smaller salivary glands saliva type and percentage secreted

A

Mucus, 10%

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26
Q

Functional unit of saliva glands and contents

A

Salivon
acinus, mucus cell, myoepithelial cells, serous cells

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27
Q

Phases of saliva secretion

A

primary secretion from acini and secondary ductular modification

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28
Q

Is saliva hypertonic, isotonic, or hypotonic compared to plasma?

A

Hypotonic

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29
Q

What is secreted in primary secretion of saliva?

A

Na, Cl, mucin glycoprotein, proline-rich protein, IgA

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30
Q

What is primary saliva secretion mainly driven by?

A

Na/K/2Cl transporter - the movement of chloride ions

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31
Q

How are chloride ions secreted in primary saliva secretion?

A

Down the concentration gradient through chloride channels that are mostly calcium controlled or ligand-gated. the opening of the channels is mostly controlled by ACh

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32
Q

What is secreted in secondary modification of saliva?

A

Lysozyme and potassium in intercalated duct
Potassium and HCO3 in striated and other ducts

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33
Q

What is reabsorbed in secondary modification of saliva?

A

Chloride and sodium ions in striated and other ducts

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34
Q

How are Na and Cl reabsorbed in secondary modification of saliva?

A

Na through ENaC, Cl through paracellular route

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35
Q

How does cystic fibrosis impact on saliva secretion and compositon?

A

CFTR involvement so cystic fibrosis would reduce the concentration of HCO3 in saliva but does not affect volume of saliva

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36
Q

Parasympathetic control of saliva production (which nerves and neurotransmitters)

A

CNVII (facial) controls sublingual and submandibular, CNIX (glossopharyngeal) controls parotid. Profuse secretion of watery saliva. ACh and VIP (vasoactive intestinal peptide) used.

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37
Q

Sympathetic control of saliva production

A

small volume of saliva rich in proteins and mucus. Norepinephrine

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38
Q

Cephalic control of saliva production

A

unconditioned and conditioned. Food or irritating substance in the mouth (reflex) or thought, sight, and smell of food (Pavlov)

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39
Q

Sympathetic and parasympathetic control of blood supply to salivary glands

A

parasympathetic vasodilation via ACh and VIP,
sympathetic vasoconstriction via norepinephrine, vasodilation via bradykinin

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40
Q

Intrinsic pacemaker in the stomach

A

Interstitial cells of Cajal generate a sub-threshold oscillating membrane potential (need stimuli to get contraction)

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41
Q

Gastro-gastric reflexes (antrum and reservoir)

A

enteric nervous system.
distention of reservoir stimulates antral contraction, distension of antrum leads to prolonged relaxation of reservoir

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42
Q

Major excitatory neurotransmitters in gastric emptying

A

ACh and gastrin

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43
Q

Major inhibitory neurotransmitters in gastric emptying

A

NO, VIP, and ATP

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44
Q

Intestinal brake mechanism

A

gastric emptying inhibited by stomach contents entering small intestine. controlled by release of intestinal hormones and entero-gastric reflexes.

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45
Q

Hormones involved in intestinal brake mechanism

A

Increased secretin from acid, increased CCK from fats, decreased gastrin from acid

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46
Q

Increase and decrease of which nervous systems leads to delayed gastric emptying?

A

Increased sympathetic activity and decreased parasympathetic activity leads to decreased gastric emptying. Enteric and vagus involvement.

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47
Q

Motility functions of the stomach

A

reservoir for ingested foodstuffs (upper stomach), initial breakdown/digestion of foodstuffs, controlled emptying of contents into intestines (lower stomach)

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48
Q

Mechanisms involved in stomach acting as a reservoir

A

Receptive relaxation and gastric accommodation. Both involve relaxation of fundus and proximal corpus

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49
Q

Receptive relaxation mechanism

A

LOS and proximal stomach relax in anticipation of contents. Vagovagal reflex.

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50
Q

Where is the vagovagal reflex and what does it control ?

A

afferent and efferent fibres of vagus nerve coordinate responses to gut stimuli via dorsal vagal complex in brain. Controls contraction of GI muscle layers in response to distension of the tract by food and allows for accommodation of large amounts of food in tract

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51
Q

Stages of mixing and emptying of stomach contents

A

Propulsion, grinding, retropulsion and then repeat

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52
Q

Stomach propulsion

A

peristaltic contraction propels material towards antrum and occlusion of pylorus

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53
Q

Stomach grinding

A

churning of trapped material in antrum, only particles <2mm can pass through

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54
Q

Retropulsion of stomach

A

most of the bolus is returned to gastric body to be broken down

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55
Q

Which type of meal leads to a feeling of satiety for longer and why?

A

Fat-rich as fatty acids trigger a strong intestinal brake response

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56
Q

Peristalsis

A

movement of contents along the oesophagus caused by a wave of relaxation followed by contraction of smooth muscle

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57
Q

Triggers of primary and secondary peristalsis

A

Primary = swallowing, secondary = presence of luminal contents

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58
Q

Voluntary swallowing reflex

A

voluntarily forming bolus in the mouth –> move tongue back and up –> tips bolus into the pharynx

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59
Q

Involuntary swallowing reflex

A

triggered by bolus exerting pressure on pharyngeal wall –> soft palate elevation –> inhibition of respiration as larynx raised and glottis closed –> upper oesophageal sphincter relaxes/opens –> oesophageal peristalsis –> lower oesophageal sphincter opens, and bolus enters stomach

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60
Q

Primary and secondary peristalsis of upper oesophagus

A

striated muscle so controlled by vagus nerve. excitatory ACh (nicotinic)
Primary = result of sequential activation of lower motor neurons in nucleus ambiguous
Secondary = mediated by central reflex

61
Q

Peristalsis of lower oesophagus

A

smooth muscle
Primary = vagal nerves via enteric nervous system. Excitatory pathway originates in rostral dorsal motor nucleus of vagus (DMN), inhibitory in caudal DMN
Secondary = local reflex

62
Q

Peristalsis local reflex

A

sensory neurons (mechanical and chemical) detect contents –> stretch receptors receive message and stretch –> firing of inhibitory motor neurons causing smooth muscle relaxation (oesophagus after area of detection) OR firing of excitatory motor neurons causing smooth muscle contraction (oesophagus before area of detection) –> stretch in next section of oesophagus and cycle repeats

63
Q

Retching

A

dry heaves, chyme into oesophagus followed by immediate backflow, relaxation of distal and contraction of proximal oesophagus

64
Q

Vomiting

A

forceful expulsion of GI contents, associated with contraction of intercostal muscles and increased intrathoracic pressure

65
Q

What contracts to cause retching and vomiting?

A

Skeletal muscle, not the stomach

66
Q

What is the vomiting reflex preceded by?

A

Retrograde peristaltic contractions originating in the jejunum

67
Q

Vomiting reflex steps

A

Chyme forced from proximal small intestine into relaxed stomach through widely opened pylorus –> rhythmic respiratory movements against a closed glottis produce negative oscillations in intrathoracic pressure –> abdominal muscles and diaphragm contract, increasing intra-abdominal pressure –> contents moved out

68
Q

Vomiting receptors in brain

A

Higher sensors - e.g. excessive stress
Chemical trigger zone - floor of fourth ventricle in medulla oblongata, afferent fibres that reach blood brain barrier and detect harmful substances in blood

69
Q

What is the vomiting mechanism?

A

A defence mechanism

70
Q

Labyrinthine receptors

A

In inner ear, play a part in motion sickness and vertigo. Vertigo can be caused by drugs and toxins which triggers vomiting

71
Q

Vomiting receptors in GI tract

A

Touch in throat - stop swallowing harmful substances
Chemo in stomach - sense harmful substances

72
Q

Vomiting receptors in GI tract

A

Touch in throat - stop swallowing harmful substances
Chemo in stomach - sense harmful substances
Mechano in stomach - detect abrasive substances

73
Q

If the vomiting centre decides vomiting is the appropriate response, where does it send the signals?

A

Abdominal muscles, oesophageal muscles, oesophageal sphincters, and respiratory muscles.

74
Q

Which muscles are involved in the elevation of the mandible?

A

temporalis, masseter, medial pterygoid

75
Q

Which muscle is involved in retraction of the mandible?

A

Temporalis

76
Q

Which nerve is responsible for taste on the anterior 2/3 of the tongue?

A

chorda tympani

77
Q

What role do the ducts play in the formation of saliva?

A

Reabsorb electrolytes with the exclusion of water making saliva hypotonic

78
Q

What is the role of R-protein (haptocorrin) produced by the salivary glands?

A

Binds to vitamin B12 protecting it from gastric acid

79
Q

Which muscle is responsible for elevation of the soft palate?

A

Levator veli palatini

80
Q

Which nerve inner ages the levator veli palatini?

A

Vagus

81
Q

Innervation of soft palate muscles

A

All vagus except for tensor veli palatini which is trigeminal

82
Q

Motor innervation of pharynx

A

vagus

83
Q

What is achlorhydria and what can it lead to?

A

Reduced acid secretion
Decreased absorption of iron

84
Q

What has both direct and indirect inhibitory effects on acid secretion by parietal cells?

A

Somatostatin

85
Q

Three phases of gastric juice secretion

A

Cephalic, gastric, intestinal

86
Q

What is the Cephalic gastric juice reflex?

A

Smell, taste, sight, thought, swallowing

87
Q

What is the Cephalic phase of gastric juice secretion mediated by?

A

Vagus nerve and ACh release

88
Q

What does the Cephalic phase of gastric juice secretion stimulate/

A

Insertion of primary vesicles

89
Q

What percentage of gastric acid secretion is the Cephalic phase responsible for?

A

30%

90
Q

What distends the intestines in the gastric phase of secretion?

A

Entry of food

91
Q

What does distension of the intestines in the gastric phase stimulate the release of?

A

ACh (vago-vagal ENS)

92
Q

What do partially digested proteins stimulate in the gastric phase?

A

G-cells and gastrin release

93
Q

What inhibits the gastric phase of secretion?

A

Low intra-gastric pH particularly in natural regions stimulating somatostatin release from D cells

94
Q

What percentage of gastric acid secretion is the gastric phase responsible for?

A

50-60%

95
Q

What is the intestinal phase of gastric juice secretion?

A

Presence of amino acids and peptides in the small intestine

96
Q

What is stimulated in the intestinal phase of gastric secretion?

A

Acid secretion from gastrin via G-cell stimulation

97
Q

What inhibits the intestinal phase of gastric secretion?

A

Stimulation of endocrine cells to release enterogastrones

98
Q

What percentage of gastric juice secretion is the intestinal phase responsible for?

A

5-10%

99
Q

What has stimulatory direct or indirect effects on parietal cells?

A

Gastrin, histamine, ACh, gastrin-releasing peptide

100
Q

Which cells produce gastrin?

A

G-cells

101
Q

Which cells are responsible for histamine release in the GI tract?

A

Enterochromaffin (ECL)

102
Q

What has direct or indirect inhibitory effects on the parietal cells in gastric juice secretion?

A

Somatostatin, cholecystokinin, secretin

103
Q

Which cells produce somatostatin?

A

D cells

104
Q

Which cells produce cholecystokinin in the GI tract?

A

I cells

105
Q

Which cells produce secretin in the GI tract?

A

S cells

106
Q

Describe the stimulation of the parietal cells for the control of gastric juice

A

ACh acts on M3 receptor which triggers insertion of tubular vesicles causing more proton pumps on the luminal surface

107
Q

Describe the stimulation of ECL cells

A

ACh acts on M3 receptors which causes exocytosis of histamine vesicles. The histamine acts on H2 receptors causing more tubular vesicles to be inserted

108
Q

Which receptor does gastrin bind to to stimulate ECL and parietal cells?

A

CCKb

109
Q

Describe the inhibition of gastric juice secretion in the parietal cells

A

Parietal cells secrete acid. The acid inhibits G cells and has a positive effect on D cells - the somatostatin released inhibits the G cells further

110
Q

Describe the inhibition of gastric juice secretion in the endocrine cells

A

Acid acts on the endocrine cells in the duodenum causing the release of enterogastrones which act on D cells increasing somatostatin

111
Q

Name some enterogastrones

A

Secretin, enteroglucagon, cholecystokinin, peptide YY, somatostatin, neurotensin

112
Q

Which cells secrete HCl in the stomach?

A

Parietal oxyntic

113
Q

What actions does HCl have in the stomach?

A

Denatures proteins
Activates pepsinogen to pepsin
Solubilises and maintains iron in ferrous state for absorption

114
Q

What can achlorhydria lead to?

A

Decreased iron absorption and anaemia

115
Q

Which cells secrete pepsinogen?

A

Chief cells

116
Q

What activates pepsinogen to pepsin?

A

Removal of a short peptide in acid conditions

117
Q

What pH is optimal for pepsinogen?

A

3.5

118
Q

What percentage of protein digestion is pepsin responsible for ?

A

<20%

119
Q

Is pepsin essential? Why or why not?

A

No as pancreatic proteases can compensate

120
Q

Which cells secrete gastric lipase?

A

Chief cells

121
Q

What pH is optimal for gastric lipsae?

A

3-6

122
Q

Action of gastric lipase?

A

Contributes to hydrolysis of lipids

123
Q

What can gastric lipase partially compensate for?

A

Decreased pancreatic lipase secretion in pancreatic dysfunction

124
Q

Which cells secrete intrinsic factor?

A

Parietal cells

125
Q

Action of intrinsic factor

A

Binds to B12 and enables its absorption

126
Q

Which cells secrete mucin in the stomach?

A

Mucus-secreting neck cells

127
Q

Purpose of mucus in the stomach

A

Forms a barrier over the mucosal surface to protect it from gastric contents
Lubricates the mucosal surface to protect against abrasive effects of contents

128
Q

Which cells secrete bicarbonate in the stomach?

A

Surface epithelial

129
Q

Where is bicarbonate located in the stomach?

A

Trapped in the unstirred layer between the mucus blanket and the mucosal surface

130
Q

Action of bicarbonate in the stomach?

A

Neutralises acid
Deactivates pepsin

131
Q

What are the aims of the drugs used to treat gastritis, ulcers, and reflux disease?

A

Reduce acidity of stomach contents to prevent further damage and allow time for healing

132
Q

Proton pump inhibitor examples?

A

Omeprazole, lansoprazole

133
Q

Antacid examples

A

Aluminium hydroxide, sodium bicarbonate

134
Q

H2 agonist in gastric disease example

A

Ranitidine

135
Q

Describe the activation of parietal cells in the stomach

A

Tubular vesicles are inserted into the apical membrane and canaliculi are created which increases area exposed to the lumen

136
Q

What do tubular vesicles contain?

A

Proton pumps

137
Q

Anatomical barrier for gastric juice

A

Resistant epithelium - apical ,membrane and tight junctions

138
Q

Physiological barrier for gastric juice

A

Mucus gel layer and bicarbonate microclimate

139
Q

What stimulates mucus in the stomach?

A

Vagus nerve and irritation

140
Q

What stimulates the protection of the gastric mucosa?

A

Presence of acid in the duodenum
Central and enteric nervous systems (ACh and VIP)
Prostaglandins

141
Q

What inhibits the protection of the gastric mucosa?

A

COX inhibitors
H pylori
Alpha 2 adrenergic receptor stimulation

142
Q

Gastritis

A

Inflammation of the lining of the stomach

143
Q

Peptic ulcers

A

Open sores in the lining of the stomach or duodenum >5mm in diameter that extend into the submucosa

144
Q

Erosions

A

Peptic ulcers <5mm or without depth

145
Q

Causes of peptic ulcers and gastritis?

A

H pylori
Alcohol
NSAIDs

146
Q

What causes mast cell damage in the mucosa?

A

Pepsin allowing H+ into the mucosa

147
Q

Sensory innervation of nasopharynx

A

trigeminal

148
Q

Sensory innervation of oropharynx

A

glossopharyngeal

149
Q

Sensory innervation of layrngopharynx

A

vagus

Medicine Year 1 (23 decks)

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