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Sandra phase 1 > GI physiology > Flashcards

GI physiology Flashcards

1
Q

What are the extrinsic salivary glands

A

Parotid gland
Sub lingual
Sub mandibular

Account for 90% of saliva secreted

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2
Q

What are the intrinsic salivary glands

A

Labial
buccal
palatine

secrete saliva at a constant rate
accounts for 10% of saliva secretion

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3
Q

Where does the parotid gland secrete saliva

A

Via parotid duct into 2nd maxillary molar

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4
Q

Where does the submandibular gland secrete saliva

A

via Wharton’s duct into the lingual frenulum

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5
Q

Where does the sublingual gland secrete saliva

A

10-20 sublingual ducts
into floor of oral cavity

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6
Q

What cells make up salivary glands

A

serous cells
mucous cells

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7
Q

cells making up parotid gland

A

serous cells

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8
Q

cells making up submandibular gland

A

serous and mucous cells

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9
Q

cells making up sublingual gland

A

mucous cells do contain a small amount of serous cells

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10
Q

Intrinsic salivary glands are made up of what kind of cells?

A

Mucous

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11
Q

What cranial nerves supplies the sublingual and submandibular gland

A

CN7 Facial nerve (parasympathetic)
Deep petrosal nerve (symp)

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12
Q

What cranial nerves supplies the parotid gland

A

CN9 Glossopharyngeal nerve (parasymp)
Deep petrosal nerve )symp

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13
Q

What receptors can stimulate salivation, what else?

A

Chemoreceptors (acidic)
Mechanoreceptors (chewing)

Sight of food
Smell of food
Thought of food

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14
Q

Difference in saliva produces in parasymp and symp nervous system

A

Parasymp: volume of saliva increases: water and electrolyte-rich
Symp: Saliva that is protein-rich, thicker viscous saliva

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15
Q

What is found in saliva (ions etc)

A

Ions: Na+ K+ Cl- HCO3-
H20
IgA
Cystatin
Proline-Rich proteins
Lysozymes

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16
Q

How does water enter and leave acinus

A

Acinar cells contain:
Aquaporin 3+5

Pericellular transport

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17
Q

How does water enter acinus

A

peri cellular transport

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18
Q

Oral cavity boundaries

A

Anterior: Oral vestibule
Posterior: Palatoglossal arch

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19
Q

Purpose of mastication and salivation

A

Increase SA for chemical digestion
Decrease abrasion of G.I lining

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20
Q

What muscles are involved in elevation of tongue?

A

Extrinsic muscles of tongue

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21
Q

What muscles are involved in forming central trough?

A

Intrinsic muscles of tongue

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22
Q

Mandibular depression

A

Lateral pterygoid (CNV3)
Digastric (anterior belly) (CNV3)
Mylohyoid (CNV3)
Geniohyoid (C1) (Cervical plexus)

Let’s Dance Monkey Grooves

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23
Q

Mandibular elevator

A

Masseter
Temporalis
Medial pterygoid

CNV3

Move more trees

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24
Q

Oral phase

A

Oral cavity boundaries:
A: Oral vestibule
O: Palatoglossal arch

Mastication process:
Lat & Med pterygoid
Masseter
Temporalis
ALL INNERVATED BY CNV3

Salivation
chemical digestion
soften food

The downward slope of the tongue
Intrinsic & Extrinsic muscles of the tongue (CN XII)

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25
Q

Pharyngeal phase

A

Prevent bolus from going into the nasopharynx

Prevents bolus from going into the larynx

Prevents bolus from going into the pharynx

The upper oesophageal sphincter relaxes (Cricopharyngeus)

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26
Q

Prevent bolus from going into the nasopharynx how?

A

Uvula elevates

Levator Veli palatial contract

Tensor Veli palatini contract

Lifts soft palate

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27
Q

Prevents bolus from going into the larynx how?

A
  1. Approximate vocal cords adducts
  2. Retroversion of epiglottis
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28
Q

Prevents bolus from going into the pharynx HOW?

A
  1. Outer longitudinal layer - elevates pharynx and larynx
  2. Inner longitudinal layer - pharyngeal peristalsis
  3. Suprahyoid muscle - larynx elevated and moved anteriorly
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29
Q

Oesophageal phase

A

Primary peristalsis is a continuation of pharyngeal peristalsis (Lower oesophageal sphincter relaxes)

Secondary Peristalsis (Local reflexes). If the bolus is stuck

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30
Q

Is stage 1 of swallowing voluntary or involuntary?

A

Voluntary.

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31
Q

What happens in stage 1 of swallowing?

A

Food is compressed against the roof of the mouth and is pushed to the oropharynx by the tongue.

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32
Q

Is stage 2 of swallowing voluntary or involuntary?

A

Involuntary.

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33
Q

What happens in stage 2 of swallowing?

A

The nasopharynx closes off due to soft palate elevation. The trachea is closed off by the epiglottis. Elevation of the hyoid bone shortens and widens the pharynx.

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34
Q

Is stage 3 of swallowing voluntary or involuntary?

A

Involuntary.

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35
Q

What happens in stage 3 of swallowing?

A

The pharyngeal constrictor muscles sequentially contract to produce peristaltic waves. This propels the bolus of food down the Oesophagus. This is followed by depression of the hyoid bone.

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36
Q

Name 6 muscles/groups of muscles that are involved in swallowing.

A
  1. Buccinator.
  2. Suprahyoids.
  3. Muscles of the palate.
  4. Muscles of the floor of the mouth.
  5. Infrahyoids.
  6. Pharyngeal constrictor muscles.

B SIMMP

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37
Q

Which muscle(s) manipulate food in chewing. Elevate the hyoid bone and flatten the floor of the mouth?

A

Buccinator and Suprahyoids.

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38
Q

What is the function of the muscles of the soft palate in swallowing?

A

They act to tense and elevate the soft palate.

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39
Q

What is the function of the muscles of the floor of the mouth in swallowing?

A

They raise the hyoid bone and larynx.

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40
Q

What is the function of the infrahyoids?

A

To depress the hyoid bone and larynx.

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41
Q

What is the function of the pharyngeal constrictor muscles?

A

They contract sequentially producing peristaltic waves which drive food into the oesophagus.

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42
Q

Do parotid glands have mainly serous or mainly mucous acini?

A

Mainly serous acini.

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43
Q

What is serous acini secretion composed of?

A

alpha amylase - this is needed for starch digestion.

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44
Q

Do sublingual glands have mainly serous or mainly mucous acini?

A

Mainly mucous acini.

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45
Q

What is mucous acini secretion composed of?

A

Mucin - needed for lubrication.

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46
Q

Do submandibular glands have mainly serous or mainly mucous acini?

A

They have serous and mucus acini.

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47
Q

Which of the main salivary glands is constantly active?

A

Submandibular.

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48
Q

What is the function of saliva?

A

It acts as a lubricant for chewing, swallowing and speech. It is important in oral hygiene; has a role in immunity, wash and it can also act as a buffer.

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49
Q

What is the optimum oral pH?

A

7.2

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50
Q

What is the pH range of saliva?

A

6.2 - 7.4

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51
Q

Name 4 factors that can affect the composition of saliva.

A
  1. Stimulus.
  2. Age.
  3. Gender.
  4. Drugs.
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52
Q

Are serous acini dark staining or pale staining on a histological slide?

A

Dark staining.
(Mucus acini = pale staining).

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53
Q

What is the epithelium lining of intercalated ducts?

A

Simple cuboidal epithelium.

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54
Q

What is the function of intercalated ducts?

A

They connect acini to larger striated ducts.

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55
Q

What ions are reabsorbed at striated ducts?

A

Na+ and Cl-

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56
Q

Is saliva hypotonic or hypertonic?

A

Hypotonic - water reabsorption and ion secretion.

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57
Q

What is the importance of the striated duct basal membrane being highly folded?

A

It is folded into microvilli for the active transport of HCO3- against its concentration gradient.

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58
Q

What organelle is abundant in striated ducts and why?

A

Mitochondria. For the active transport of ions.

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59
Q

Name 2 ions that striated ducts secrete.

A

K+ and HCO3-

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60
Q

Name 2 ions that striated ducts reabsorb.

A

Na+ and Cl-

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61
Q

What ducts do striated ducts lead on to?

A

Interlobular (excretory) ducts.

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62
Q

What is the epithelium lining of interlobular ducts?

A

Simple columnar epithelium.

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63
Q

What is the parasympathetic innervation of the Parotid gland?

A

Cn 9 - glossopharyngeal.

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64
Q

What is the parasympathetic innervation of the Sublingual gland?

A

Cn 7 - facial.

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65
Q

What is the parasympathetic innervation of the Submandibular gland?

A

Cn 7 - facial

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66
Q

What nerve passes through the parotid gland but does not innervate it?

A

The facial nerve (Cn 7) gives rise to its 5 terminal branches in the parotid gland.

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67
Q

What artery ascends through the parotid gland?

A

The external carotid artery.

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68
Q

Does parasympathetic innervation stimulate or inhibit salivary secretion?

A

Stimulates.

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69
Q

What stimulates the cephalic phase of gastric secretions?

A

Sight of food
thought of food
smell of food
taste of food

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70
Q

Cephalic phase what happens (para)

A

Stimulus stimulates structures within the cerebral cortex to the hypothalamus

Stimulus sent to the vagus nerve to the stomach to trigger the secretion of HCl and pepsin, more is produced

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71
Q

What inhibits the cephalic phase of gastric secretions?

A

Anything that stimulates the sympathetic nervous system
Stress, emotional upset e.t.c

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72
Q

cephalic phase sympathetic

A

Nerve impulses travel down splanchnic nerve to inhibit the secretion of HCL + pepsin

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73
Q

what happens when the gastric phase is stimulated due to gastric distension

A

Activates stretch receptors go through either vago vagal reflex or enteric reflex

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74
Q

What cells are within the gastric glands of the antrum that either stimulate/inhibit gastric phase secretion

A

enteroendocrine G cells

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75
Q

What do enteroendocrine G cells release

A

Gastrin

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76
Q

What is gastrin responsible for

A

Binds to chief cells receptors and secretes pepsinogen which gets converted to pesin
Binds to parietal cell receptors and secretes HCL

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77
Q

What pH is necessary for pepsinogen to be converted to pepsin

A

1.8-3.5

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78
Q

What inhibits/stimulates gastric phase

A

Stimulates:
Distension
Partially digested protein-pH related

Inhibits:
S.N.S
Somatostatin

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79
Q

What can inhibit/stimulate the parietal cell

A

Stimulates:
Gastrin
Ach
Histamine

Inhibits
prostaglandin
somatostatin

PPS HAG

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80
Q

What can inhibit/stimulate the chief cell

A

Stimulates
Ach
Secretin
Histamine

Inhibits
Gastrin

CASH G

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81
Q

What does the enterochromaffin cell secrete

A

Histamine
(Stim: Ach, Gastrin)
(Inhibit: Somatostatin)

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82
Q

What is the purpose of the mucosal barrier?

A

Prevents corrosive damage by HCl + pepsin

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83
Q

Where do the most powerful contractions in the stomach take place?

A

Pylorus

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84
Q

What happens when the pylorus contract

A

Retropulsion (chyme back up stomach)
Chyme pumped into duodenum

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85
Q

What do S cells secrete

A

Secretin

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86
Q

What does secretin stimulate/inhibit

A

Stimulates the liver to turn cholesterol into bile synthesis
Inhibits G cells to secrete Gastrin
Stimulate ductal epithelial cells of the pancreas to secrete HCO3-

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87
Q

What do I cells secrete

A

Cholecystokinin

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88
Q

what does Cholecystokinin stimulate

A

Stimulates the liver to break down cholesterol into bile
Stimulates the gallbladder to secrete conc bile
Binds to the sphincter of Oddi to relax
Binds to pancreatic acinar cells to excrete pancreatic digestive enzymes contents via exocytosis

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89
Q

Pyloric sphincter purpose

A

Lets small amounts of chyme into duodenum, the ensures that H+ doesn’t get too high and damage duodenum

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90
Q

What is the mucosal barrier made-up of

A

Gel layer (Top): H2O, Phospholipid, High amount of mucins: HCO3-)

HCO3- layer

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91
Q

What converts pepsin into pepsinogen

A

HCO3-

If pepsin wants to escape the gel layer of the mucosal barrier then it reacts with HCO3- of the mucosal barrier
H+ + HCO3- —> H20 + CO2

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92
Q

Diff between tonic and rhythmic contractions

A

Tonic is a sustained contraction
Rhythmic is alternating contractions

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93
Q

What are the interstitial cells of Kajal

A

Pacemaker cells
They spontaneously depolarise that cause other smooth muscle of GI tract to contract

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94
Q

Explain spike potential

A

Every time a wave is produced above the subthreshold it generates spike potential. The bigger the wave above subthreshold the more spike potential is formed. This means that a bigger force of contraction will be produced.

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95
Q

Fundamentals of motility

A

Segmentation (Rhythmic)

  • mix chyme with digestive juices
  • increases absorption of nutrients

Propulsion/Peristalsis (Rhythmic)
-move G.I content along the G.I tract

Resovoir functions (storage functions)(Tonic)
-Sphincter
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96
Q

What is peristalsis

A

alternating wave of contraction and relaxation

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97
Q

Zenkers diverticulum

A

Outpouching just above UES
Dysphagia
Cough/Regurgitation
Halitosis

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98
Q

Primary function of oesophagus in G.I motility

A

Peristalsis

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99
Q

What is receptive relaxation

A

It is when the vagus nerve relaxes the fundus of the stomach as its getting ready to receive the food prior to food being in the stomach

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100
Q

What do receptive & adaptive relaxation play a role in

A

Gastric accommodation

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101
Q

What is gastric accommodation

A

When the bolus is in the stomach the intra-gastric volume increases
But the intragastric pressure stays the same as long as it’s not above 1.5l

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102
Q

What stimulus plays and important role in segmentation/peristalsis

A

distension
PSNS
SNS
Irritants

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103
Q

Segmentation in small intestine

A

-Sluggish short-lived contractions
-mixing chyme + BILE+ pancreatic enzymes + intestinal/pancreatic fluid ( HCO3- & mucous)
Mixing chyme enhances absorption
-anterograde (->anal) and retrograde (-> oral)
-Increases contact time with the chyme and mucosal surfaces to stimulate absorption

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104
Q

Role of stomach?

A

Storage (reservoir)
Mixing
emptying

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105
Q

Peristalsis in small intestine

A

Propulsive action (oral –> anal)

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106
Q

Migrating mobility complex

A

Occurs between meals (Fasting State)
Peristalsis starts at stomach to ileum
2 hours typical duration
Pulls food residue, dead cells, undigested substances
stimulated by motilin

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107
Q

What opens the ileocecal valve as its always closed and what is the purpose of this

A

Increase in gastrin
Gastrocecal reflex

=relax ileocecal valve & contraction of distal ileum

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108
Q

Haustral contractions

A

segmentation
triggered by distension
occurs in ascending & descending colon
mainly driven by Teniae Coli
Absorption: electrolytes, water, complex B vitamins

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109
Q

Mass movement (Peristalsis) of large intestine

A

Propulsion of rectum
primarily occurs in transverse & descending colon
Primary stimulants: stretch, irritants, the gastrocolic reflex
Occurs 3-5 times per day
During meals or after
Contractions over 20cm of a portion of large intestine

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110
Q

Defaecation Reflex

A
  1. Stretch of sigmoid colon and rectum
  2. stimulates sensory fibres and travel to CNS
  3. Stimulates parasympathetic motor fibres
  4. Contraction of the sigmoid colon and rectum
    5, Relax the internal anal sphincter
  5. Relax the external anal sphincter (voluntarily)
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111
Q

What nerve innervates the external anal sphincter

A

pudendal nerve

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112
Q

What innervates the internal anal sphincter

A

Pelvic nerve

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113
Q

Describe the internal anal sphincter

A 
smooth muscle 
involuntary reflex (muscle) 
innervated by the autonomic nervous system
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114
Q

Describe the external anal sphincter

A

Skeletal muscle
voluntary
innervated by the somatic nervous system

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115
Q

G.I Motility of oesophagus is primarily

A

Peristalsis

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116
Q

G.I Motility of small intestine is primarily

A

Peristalsis
Segmentation
Ileocecal valve plays a role as well

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117
Q

G.I Motility of large intestine is primarily

A 
Haustral contractions (segmentation)
Mass movement (peristalsis)
Defaecation reflex
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118
Q

What enzyme digests carbohydrates secreted by salivary glands

A

salivary alpha-amylase

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119
Q

What enzyme digests carbohydrates secreted by pancreatic acinar cells

A

pancreatic amylase secreted in the duodenum

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120
Q

What enzymes are secreted in the aid of digesting lipids

A

Sublingual and parotid secreting lingual lipase
Chief cells in the stomach secreting gastric lipase
Pancreas secreting bile, pancreatic lipase, PLA2, Cholesterol Ester Hydrolyse

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121
Q

What is the volume of an empty stomach?

A

50ml

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122
Q

What is the maximum volume of the stomach?

A

1.5L

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123
Q

What is receptive relaxation?

A

Smooth muscle in the body and fundus of the stomach relaxes prior to the arrival of food, this allows the stomach volume to increase. There is afferent input from Cn 10. NO and serotonin also influence relaxation.

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124
Q

Where do peristaltic waves begin in the stomach?

A

In the gastric body.

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125
Q

Where in the stomach are peristaltic contractions the most powerful?

A

In the gastric antrum.

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126
Q

Why is the pyloric sphincter closed as the peristaltic wave reaches it?

A

This prevents chyme entering the duodenum and so the gastric contents are forced back and mixed together in the body of the stomach.

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127
Q

On average, how many peristaltic waves are there a minute?

A

3 (slow repol/depol cycles).

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128
Q

Name 2 factors that can increase the strength of peristaltic contractions.

A
  1. Gastrin.
  2. Gastric distension.
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129
Q

Name 5 factors that can decrease the strength of peristaltic contractions.

A
  1. Duodenal distension.
  2. Low pH in duodenum lumen.
  3. Increased duodenal osmolarity.
  4. Increased sympathetic action.
  5. Decreased parasympathetic action.

ID LID

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130
Q

What do parietal cells secrete?

A

H+ and intrinsic factor.

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131
Q

What cells secrete Gastrin?

A

Enteroendocrine cells / G cells.

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132
Q

What cells secrete somatostatin?

133
Q

What cells secrete histamine?

A

Enterochromaffin like cells.

134
Q

On average, how much gastric acid do we secrete a day?

135
Q

What is the hydrogen ion concentration of gastric acid?

136
Q

Where does the H+ come from in gastric acid?

A

In parietal cells: H2O + CO2 = HCO3- + H+

137
Q

What is the mechanism of the H+/K+ ATPase proton pump?

A

It pumps H+ into the stomach lumen and K+ into the parietal cell.

138
Q

What ions are exchanged on the side of the parietal cell in contact with the capillaries?

A

Cl- is pumped into the parietal cell and HCO3- moves out of the parietal cell into the capillary.

139
Q

What is the importance of HCO3- being exchanged for Cl-?

A

HCO3- moving out of the cell increases the rate of the forward reaction and so more H+ are produced. Cl- moving into the cell then moves into the stomach lumen via Cl- channels and combines with H+ to form HCl.

140
Q

What are the 4 phases important in regulating gastric acid secretion? Do these phases turn secretion on or off?

A
  1. Cephalic phase - turning ON.
  2. Gastric phase - turning ON.
  3. Gastric phase - turning OFF.
  4. Intestinal phase - turning OFF.
141
Q

Regulating gastric acid secretion: What stimuli are involved in the cephalic phase?

A

Sight, smell, taste of food. Chewing.

142
Q

Regulating gastric acid secretion: What stimuli are involved in the gastric ON phase?

A

Gastric distension, presence of peptides and amino acids in the stomach.

143
Q

Regulating gastric acid secretion: What stimuli are involved in the gastric OFF phase?

A

Low pH in the gastric lumen.

144
Q

Regulating gastric acid secretion: What stimuli are involved in the intestinal phase?

A

Low pH in duodenal lumen, duodenal distension, presence of amino acids and fatty acids in the duodenum.

145
Q

Briefly describe the cephalic phase.

A

The parasympathetic nervous system is triggered by stimuli. This releases Ach. Ach acts on parietal cells and on gastrin and histamine. HCl secretion increases.

146
Q

Briefly describe the gastric ON phase.

A

Gastrin is released in response to the stimuli. This acts on parietal cells and triggers release of histamine (histamine then acts on parietal cells too). HCl secretion increases.

147
Q

Briefly describe the gastric OFF phase.

A

Gastrin is inhibited in response to stimuli and histamine is therefore indirectly inhibited. Somatostatin is also released and this inhibits parietal cells. HCl secretion decreases.

148
Q

Briefly describe the intestinal phase.

A

The enterogastrones secretin and CCK are released in response to stimuli. Secretin inhibits gastrin and stimulates further somatostatin release. HCl secretion decreases.

149
Q

What neurotransmitter is involved in regulating gastric acid secretion?

150
Q

What hormone is involved in regulating gastric acid secretion?

151
Q

What paracrine factors are involved in regulating gastric acid secretion?

A

Histamine and Somatostatin.

152
Q

What enterogastrones are involved in regulating gastric acid secretion?

A

Secretin and CCK.

153
Q

Name the 4 main defence mechanisms against gastric acid secretion.

A
  1. Alkaline mucous.
  2. Tight junctions between epithelial cells.
  3. Replacing damaged cells.
  4. Feedback loops.
154
Q

Define ulcer.

A

A breach in a mucosal surface.

155
Q

Name 3 things that can cause peptic ulcers.

A
  1. Helicobacter pylori.
  2. NSAIDS.
  3. Chemical irritants.

Hairy Nasal Cavity

156
Q

Why do NSAIDS cause peptic ulcers?

A

They inhibit cycle-oxygenase 1.
Cycle-oxygenase 1 is needed for prostaglandin synthesis, prostaglandins stimulate mucus secretion. Without cycle-oxygenase 1 there is less mucus and so the mucosal defence is reduced.

157
Q

Why does helicobacter pylori cause peptic ulcers?

A

Helicobacter pylori lives in gastric mucus. It secretes urease. Urease breaks into CO2 and NH3. The NH3 combines with H+ to form NH4+. NH4+ damages the gastric epithelium, an inflammatory response is triggered and mucosal defence is reduced.

158
Q

Name 2 drugs that can be used to reduce gastric acid secretion.

A
  1. Proton pump inhibitors.
  2. H2 receptor antagonists.
159
Q

If water input is 9L, how much is reabsorbed and how much is excreted in the faeces?

A

8.8L is reabsorbed and 0.2L is excreted in the faeces.

160
Q

How does water move across the small intestine?

A

It moves freely by osmosis and also via aquaporins.

161
Q

How does Na+ move across the small intestine?

A

Na+ is actively transported from the lumen by pumps located in the cell membranes in the ileum and jejunum.

162
Q

How does K+ move across the small intestine?

A

Via passive diffusion. Movement is determined by the potential difference between lumen and capillaries.

163
Q

Where does Cl- and HCO3- reabsorption mainly take place?

A

In the ileum and colon.

164
Q

What is the mechanism for Cl- and HCO3- reabsorption?

A

Cl- is actively reabsorbed in exchange for HCO3-. The intestinal contents therefore become more alkaline.

165
Q

What enzyme digests starch in the small intestine?

A

Pancreatic amylase.

166
Q

What bonds does pancreatic amylase break?

A

alpha 1-4 linkages.

167
Q

What are the end products of starch digestion?

A

Maltose!
Also maltotriose, glucose polymers and alpha-dextrins.

168
Q

Where in the small intestine are bile salts absorbed?

169
Q

What enzyme(s) hydrolyse peptide bonds in the stomach?

170
Q

What is the optimum pH for pepsins?

171
Q

Why is pepsin action terminated in the small intestine?

A

The pH in the small intestine is too alkaline and so it denatures.

172
Q

What enzyme(s) further break down peptides in the small intestine?

A

Pancreatic proteases.

173
Q

What is the precursor molecule for pepsin?

A

Pepsinogen.

174
Q

What activates pepsinogen?

175
Q

What 2 groups can pancreatic proteases be divided into?

A
  1. Endopeptidases e.g. trypsin.
  2. Exopeptidases e.g. carboxy dipeptidases.
176
Q

How do amino acids get absorbed into the blood?

A

Passive diffusion.

177
Q

What enzyme(s) hydrolyse cholesterol esters in the intestinal lumen?

A

Pancreatic esterases.

178
Q

What emulsifies lipids?

A

Bile salts.

179
Q

What is the advantage of emulsifying lipids?

A

It increases the SA for digestion and so digestion is more efficient.

180
Q

What digests lipids in the small intestine?

A

Pancreatic lipases.

181
Q

Are lipids hydrophobic or hydrophilic?

A

Hydrophobic

182
Q

What are the end products of fat digestion?

A

Free fatty acids and monoglycerides.

183
Q

What triglyceride bonds is pancreatic lipase able to hydrolyse with ease?

A

1 and 3 bonds (the 2 bond is hydrolysed at a slower rate).

184
Q

What protein binds pancreatic lipase to the surface of the lipid?

A

Co-lipase. This is essential, pancreatic lipase can not work without it.

185
Q

The end products of fat digestion combine with bile salts and cholesterol to form what?

A

Mixed micelles.

186
Q

What is the function of mixed micelles?

A

Lipid transport systems.

187
Q

How are chylomicrons formed?

A

Triglycerides, phospholipids and cholesterol combine with proteins inside the epithelial cell forming chylomicrons.

188
Q

Is vitamin A fat or water soluble?

A

Fat soluble.

189
Q

What are the functions of vitamin A?

A

Vitamin A is needed for cellular growth and differentiation. It is also important for eyesight and lymphocyte production.

190
Q

Name 3 sources of vitamin A.

A
  1. Oily fish.
  2. Dairy.
  3. Liver
191
Q

What is the recommended daily intake of vitamin A for men and women?

A

Women - 600µg. Men - 700µg.

192
Q

What are the consequences of vitamin A deficiency?

A

Night blindness, growth retardation, increased susceptibility to infection.

193
Q

What are the consequences of vitamin A toxicity?

A

Anorexia, vomiting, headache, reduced bone density, conjunctivitis.

194
Q

Is vitamin C fat or water-soluble?

A

Water soluble (easily lost when boiled).

195
Q

What are the functions of vitamin C?

A

Synthesis of collagen, neurotransmitters and carnitine. It has an antioxidant ability and can absorb non-haem iron.

196
Q

Name 4 sources of vitamin C.

A
  1. Citrus fruits.
  2. Green leafy veg.
  3. Potatoes.
  4. Kidney.
197
Q

What is the recommended daily intake of vitamin C?

198
Q

What are the consequences of vitamin C deficiency?

A

Weakness, shortness of breath, aching, bleeding gums, thickening of skin.

199
Q

What are the consequences of vitamin C toxicity?

A

Diarrhoea, nausea, renal stone formation.

200
Q

Are B vitamins fat or water soluble?

A

Water soluble.

201
Q

How many B vitamins are there?

202
Q

What are B vitamins important for?

A

Cell metabolism and energy production.

203
Q

How long do glycogen stores in a 70Kg adult last?

A

About 12 hours.

204
Q

How long do lipid stores in a 70Kg adult last?

205
Q

What percentage of BMR do these organs use?
a) Brain.

b) Liver.
c) Muscle.

A

a) 20%.
b) 21%.

c) 22%.

206
Q

What fuels does the brain use?

A

Glucose and ketone bodies.

207
Q

What fuels does the liver use?

A

Glucose, amino acids, fatty acids.

GAF

208
Q

What fuels does muscle use?

A

Glucose, ketone bodies, amino acids and triacylglycerol.

209
Q

What are free sugars and starch associated with effecting?

A

They can cause shifts in blood glucose and insulin due to their rapid absorption. This can strain the pancreas.

210
Q

What type of starch is the most desirable and why?

A

Slowly digestible starch. It is slowly digested and absorbed and so has little influence on blood glucose and insulin.

211
Q

What is the cause of lactose intolerance?

A

A deficiency in lactase.

212
Q

Give 3 symptoms of lactose intolerance.

A
  1. Bloating.
  2. Diarrhoea.
  3. Pain.
213
Q

Explain the mechanism that produces the symptoms of lactose intolerance.

A

Lactose intolerance has an osmotic effect. H2O and fermentable sugars enter the the large intestine lumen and cause diarrhoea, bloating and pain.

214
Q

Why might someone with enterocyte loss be unable to break down lactose?

A

Enterocytes at villi contain lactase. If the enterocytes are lost they may have lactase deficiency.

215
Q

Define BMR.

A

The energy needed to stay alive at rest, usually 24kcal/kg/day.

216
Q

Where does the foregut begin and end?

A

Mouth to the major duodenal papilla. (In the embryo - oropharyngeal membrane to the liver bud).

217
Q

Where does the midgut begin and end?

A

Major duodenal papilla to 2/3 along the TC. (In embryo - liver bud to 2/3 along with TC).

218
Q

Where does the hindgut begin and end?

A

Distal 1/3 of TC to anal canal. (In embryo - distal 1/3 of TC to cloacal membrane).

219
Q

Why are the foregut, midgut and hindgut divisions different in the adult compared to in the embryo?

A

It changes due to the formation of the ampulla of vater.

220
Q

Are the pharyngeal clefts formed in the endoderm or ectoderm?

221
Q

Are the pharyngeal pouches formed in the endoderm or ectoderm?

222
Q

How many pharyngeal arches are there?

A

5 (4 pharyngeal clefts and pouches).

223
Q

What does the first pharyngeal arch form?

A

Muscles for mastication. Innervation: Cn 5.

224
Q

What does the second pharyngeal arch form?

A

Muscles for facial expression. Innervation: Cn 7.

225
Q

What does the third pharyngeal arch form?

A

Stylopharyngeus muscle. Innervation: Cn 9.

226
Q

What does the fourth pharyngeal arch form?

A

Cricothyroid muscle. Innervation: External branch of superior laryngeal nerve (Cn 10).

227
Q

What does the sixth pharyngeal arch form?

A

Intrinsic Muscles of the Larynx. Innervation: Recurrent laryngeal nerve (Cn 10).

228
Q

Why is the stomach the shape it is?

A

Due to differences in growth rates. The greater curvature grows faster than the lesser curvature.

229
Q

Why does the left vagus nerve become the anterior vagal trunk and the right vagus become the posterior vagal trunk?

A

Due to the 90 degrees clockwise rotation of the stomach in its longitudinal axis.

230
Q

What are the axis of stomach rotation?

A

Longitudinal and anteroposterior.

231
Q

What does the dorsal mesentery become?

A

The greater omentum.

232
Q

What are the 4 layers of the GI tract?

A
  1. An innermost mucosa.
  2. A sub-mucosa.
  3. An external muscle coat (muscularis externa)
  4. A serosa.
233
Q

What is the innermost mucosa layer composed of?

A
  • A folded epithelium.
  • Lamina propria (connective tissue).
  • Muscularis mucosa (ring of smooth muscle).
234
Q

What is the submucosa layer composed of?

A

Loose connective tissue containing glands and lymph tissue. Many blood vessels and a rich plexus of nerves that is part of the enteric nervous system (Meissner’s plexus) are also found in the submucosa.

235
Q

What is the muscular externa composed of? What is its function?

A

Composed of 2 layers of smooth muscle: circular and longitudinal. Nerves that are part of the enteric nerve plexus are also present here (Aurebach’s plexus). Contraction of the muscle helps to break down and food and propel it along the GI tract.

236
Q

What is the serous layer composed of?

A

Composed of a simple squamous epithelium that covers the outside surface of the gut tube facing the peritoneal cavity.

237
Q

What enzyme are parietal cells abundant in?

A

Carbonic anhydrase.

238
Q

Give 5 functions of hepatocytes.

A
  1. Creation and storage of energy in the form of glycogen.
  2. Synthesise and secrete plasma proteins.
  3. Remove amino groups from amino acids for the production of urea. (Deamination).
  4. Uptake, synthesis and excretion of bilirubin and bile acids.
  5. Detoxification and inactivation of drugs and toxins.
239
Q

What are the 2 key stages for fat digestion?

A
  1. Emulsification.
  2. Triglyceride hydrolysis.
240
Q

What clinical feature would you see in a patient with fat malabsorption?

A

Pale and smelly faeces.

241
Q

What clinical feature would you see in a patient with vitamin K malabsorption?

242
Q

What clinical feature would you see in a patient with protein malabsorption?

A

Swollen ankles.

243
Q

Where in the layers of the GI tract would Meissner’s plexus be found?

A

In the submucosa.

244
Q

Where in the layers of the GI tract would Auerbach’s plexus be found?

A

In the muscularis externa between the circular and longitudinal layers of muscle.

245
Q

Name the abdominal retroperitoneal organs.

A

Supradrenal glands, Aorta, IVC, Duodenum (except cap), Pancreas (except tail), Ureters, Colon (ascending and descending), Kidneys, Oesophagus, Rectum.

246
Q

Name the abdominal intraperitoneal organs.

A

Spleen, Small intestine, Appendix, Liver, Transverse colon, Stomach, Sigmoid colon.

247
Q

What is the arcuate line?

A

The lower limit of the posterior rectus sheath.

248
Q

What happens to the posterior rectus sheath below the arcuate line?

A

It is absent. The rectus abdominis is in direct contact with the transversalis fascia.

249
Q

What envelopes the rectus abdominis above the arcuate line?

A

It is enveloped by the internal oblique aponeurosis.

250
Q

What is the anterior layer of rectus sheath formed from?

A

External oblique aponeurosis and the anterior lamina of the internal oblique aponeurosis.

251
Q

What is the posterior layer of the rectus sheath formed from?

A

The posterior lamina of the internal oblique aponeurosis and the transversus abdominis aponeurosis.

252
Q

What forms the anterior rectus sheath below the rectus abdominis?

A

The external oblique, internal oblique, and transversus abdominis aponeurosis forms the anterior rectus sheath. There is no posterior rectus sheath.

253
Q

What vertebral level does the umbilicus mark when lying down?

254
Q

What abdominal plane would you refer to when carrying out a lumbar puncture?

A

The intercristal plane. It joins the highest points of the pelvis posteriorly and marks the space between L4 and L5.

255
Q

Describe 2 ways in which the transpyloric plane can be drawn.

A
  1. The midpoint between the suprasternal notch and the pubic symphysis.
  2. Connects the two points marked by the insertion of the rectus sheath into the costal margin.
256
Q

Name 3 structures that cross the transpyloric plane.

A
  1. The pylorus of the stomach.
  2. The gall bladder.
  3. The pancreas.
257
Q

At what vertebral level is the transpyloric plane?

258
Q

What is the intercristal plane?

A

It connects the highest points of the pelvis at the lower back.

259
Q

At what vertebral level is the intercristal plane?

260
Q

What is the intertubercular plane?

A

A line that joins the tubercles of the iliac crests.

261
Q

At what vertebral level is the intertubercular plane?

262
Q

What is the subcostal plane?

A

A plane parallel to the lowest points of the costal margins.

263
Q

At what vertebral level is the subcostal plane?

264
Q

Where is the swallowing centre found?

A

Medulla oblongata.

265
Q

What molecule is responsible for the activation of pepsinogen into pepsin?

266
Q

Give 3 functions of HCl in the stomach.

A
  1. Solubilisation of food particles.
  2. Kills microbes.
  3. Activates pepsinogen forming pepsin.
267
Q

Histamine is secreted by enterchromaffin like cells. What are enterochromaffin cells?

A

Enterchromaffin cells are located in the intestine and secrete serotonin, not histamine.

268
Q

What type of cells are secretin and CCK?

A

Enterogastrones.

269
Q

Chief cells secrete pepsinogen and and an enzyme. What is the enzyme?

A

Gastric lipase.

270
Q

Name 3 monosaccharides.

A
  1. Glucose.
  2. Fructose.
  3. Galactose.
271
Q

Name 3 disaccharides.

A
  1. Sucrose (glucose and fructose).
  2. Lactose (glucose and galactose).
  3. Maltose (glucose and glucose).
272
Q

Name 3 polysaccharides.

A
  1. Starch.
  2. Cellulose.
  3. Glycogen.
273
Q

Where does the majority of complex polysaccharide digestion occur?

A

In the large intestine via gut bacteria.

274
Q

Where is the first site of starch digestion?

A

In the mouth via salivary amylase.

275
Q

Briefly describe starch digestion.

A

Begins in the mouth via salivary amylase. In the small intestine pancreatic amylases catalyse alpha 1-4 linkages forming maltose. The end products are further broken down by enzymes e.g. maltase on the luminal membrane; this forms monosaccharides. The products diffuse into the blood.

276
Q

What are proteins digested into?

A

Dipeptides, tripeptides and amino acids.

277
Q

What enzyme is responsible for protein digestion in the stomach?

278
Q

What is the optimum pH for pepsin action?

279
Q

What does pepsin break proteins into?

A

Peptide fragments.

280
Q

What enzymes are responsible for protein digestion in the small intestine?

A

Pancreatic proteases.

281
Q

What are the 2 types of pancreatic proteases?

A
  1. Endopeptidases.
  2. Exopeptidases.
282
Q

Give 2 examples of an endopeptidase.

A
  1. Trypsin.
  2. Chymotrypsin.
283
Q

Give 2 examples of an exopeptidase.

A
  1. Carboxypeptidases.
  2. Aminopeptidases.
284
Q

What is the function of endopeptidases?

A

They break peptide bonds between non-terminal amino acids.

285
Q

What is the function of exopeptidases?

A

They break peptide bonds between terminal amino acids and so form monomers.

286
Q

Which type of pancreatic protease can form monomers?

A

Exopeptidases.

287
Q

What process are protein digestion products absorbed into the intestinal epithelial cells?

A

Secondary active transport coupled to H+ or Na+.

288
Q

What molecules makeup phospholipids?

A

1 glycerol backbone, 2 fatty acids and 1 phosphate group.

289
Q

What are triglycerides broken down into?

A

Monoglycerides and 3 fatty acids.

290
Q

What enzyme is needed for fat digestion?

A

Pancreatic lipase.

291
Q

What mechanism speeds up the digestion of fats?

A

Emulsification - the surface area for lipase action is increased.

292
Q

What substances emulsify lipids?

A

Bile salts and phospholipids.

293
Q

What enzyme anchors lipase to the surface of an emulsified lipid droplet?

294
Q

Name 4 molecules to make up micelles.

A
  1. Fatty acids.
  2. Monoglycerides.
  3. Bile salts.
  4. Phospholipids.
295
Q

What molecule is produced that aids absorption?

296
Q

What is the function of micelles?

A

They are lipid transport systems. They move to the epithelial brush border and release the fatty acids and monoglycerides for absorption.

297
Q

What happens to the fatty acids and monoglycerides inside the intestinal epithelial cells?

A

They are re-synthesised into triglycerides in the smooth ER.

298
Q

Why are fatty acids and monoglycerides re-synthesised into triglycerides inside the intestinal epithelial cells?

A

To maintain the concentration gradient for further absorption of fatty acids and monoglycerides.

299
Q

Inside the intestinal epithelial cell, triglycerides combine with other lipids e.g. cholesterol to form what molecules?

A

Chylomicrons.

300
Q

What are the functions of chylomicrons?

A

Chylomicrons move through the lymphatics and the blood stream to tissues.

301
Q

How is vitamin B12 absorbed?

A

It binds to a protein, intrinsic factor. It is then absorbed in the terminal ileum via endocytosis.

302
Q

What can cause pernicious anaemia?

A

If you have low levels of intrinsic factor you will have B12 deficiency. This will mean fewer RBC’s will be formed leading to pernicious anaemia.

303
Q

What can cause Barrett’s oesophagus?

304
Q

Describe Barrett’s oesophagus.

A

When the stratified squamous oesophageal epithelium changes to a simple columnar one at the lower end of the oesophagus. This can be caused by prolonged acid reflux from the stomach.

305
Q

What is the function of the Vagus nerve in regards to parietal cells?

A

The vagus nerve stimulates the release of Ach which then acts on the parietal cells to increase HCl production.

306
Q

Give 4 risk factors for GORD.

A
  1. Obesity.
  2. Pregnancy.
  3. Hiatal hernia.
  4. Smoking.
    (Sedentary lifestyle is not a risk factor).
307
Q

Where in the stomach are G cells most numerous?

A

In the antrum.

308
Q

Name 2 areas of the body with a low pH to combat bacteria.

A

Stomach and vagina.

309
Q

Name 3 organs that secrete digestive enzymes.

A
  1. Stomach.
  2. Pancreas.
  3. Salivary glands.
310
Q

What structure, visible microscopically, is primarily responsible for absorption?

311
Q

Name 3 physical mechanisms of absorption.

A
  1. Endocytosis.
  2. Diffusion/facilitated diffusion.
  3. Active transport.
312
Q

Name 2 diseases that can cause malabsorption.

A
  1. Crohn’s disease - loss of plicae circulares.
  2. Coeliac disease - vili atrophy.
313
Q

Define malnutrition.

A

A lack of nutrition due to not eating enough, being unable to absorb nutrients, eating the wrong things.

314
Q

Why might an elderly person be at risk of malnutrition?

A
  1. Immobility - unable to cook and eat.
  2. Dental problems meaning its difficult to chew foods.
  3. Decreased appetite.
  4. Not eating the right things.
315
Q

Name 3 physical tests for malnutrition.

A
  1. BMI.
  2. Amount of body fat.
  3. Height.
316
Q

Give 4 complications of malnutrition.

A
  1. Apathy.
  2. Depression.
  3. Increased risk of infection.
  4. Anaemia.
317
Q

Why is endoscopy preferred to a barium meal?

A

Produces a better image and is more accurate. Also prevents exposure to radiation as a barium meal requires an X-ray.

318
Q

What muscles contribute to the upper oesophageal sphincter?

A

Cricopharyngeus.

319
Q

Where are the stem cells that replace the epithelium located?

A

The base of crypts.

320
Q

What are the pacemaker cells of the small intestine called?

A

Interstitial cells of Cajal.

321
Q

Name 2 endocrine secretions from the duodenum?

A
  1. Secretin.
  2. CCK.
322
Q

Why are fatty acids and monoglycerides re-synthesised into triglycerides inside the epithelial cell?

A

To maintain a diffusion gradient allowing for further reabsorption.

323
Q

Which papillae do not bear taste buds?

A

Filiform papillae.

324
Q

Does the oesophagus have a serosa layer?

325
Q

What is refeeding syndrome?

A

Metabolic disturbances (hypokalemia, hypomagnesemia etc) that occur due to the reinstitution of nutrition to patients who are starved/severely malnourished.

326
Q

What is vitamin A

327
Q

What is vitamin E

A

Tocopherol

328
Q

Fat soluble vitamins

329
Q

diff in chylomicrons vs micelles

A

Chylomicrons: lipoproteins composed of triglycerides, cholesterols, phospholipids, proteins and apolipoproteins.

Micelles: spherical aggregates of lipid molecules in an aqueous solution

Sandra phase 1 (16 decks)

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