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year 1 flash cards > GI strand > Flashcards

GI strand Flashcards

1
Q

What is the gastrointestinal tract also referred to as?

A
  • digestive tract

- alimentary canal

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2
Q

How long is the GI tract?

A

8-9 metres long

  • pharynx - stomach = 1m
  • small bowel = 6m
  • large bowel = 1.5m
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3
Q

What is the function of the GI tract?

A

to provide the body with a continual supply of water, electrolytes and nutrients through:

  • motor function: move food along the GI tract at the appropriate rate
  • digestion: secrete digestive juices
  • absorption: absorb the digested food, water and various electrolytes
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4
Q

What lines the abdominal cavity?

A

Parietal peritoneum

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5
Q

What lines organs?

A

Visceral peritoneum

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6
Q

What is the role of mesenteries?

A
  • suspension of organs
  • prevention of gut loops becoming tangled
  • carry blood vessels, nerves and lymphatics
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7
Q

Why does the peritoneum secrete fluid?

A

Provides lubrication to allow organs to move against each other without friction

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8
Q

What does the coeliac artery supply?

A
  • stomach
  • spleen
  • gall bladder
  • pancreas
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9
Q

What does the superior mesenteric artery supply?

A
  • pancreas
  • small bowel
  • proximal region of the large intestine
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10
Q

What does the inferior mesenteric artery supply?

A
  • distal large intestine

- rectum

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11
Q

Where does the majority of blood from the GI tract drain to?

A

hepatic portal vein

- carries absorbed nutrients to the liver for processing

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12
Q

What are the major motor functions of the GI tract?

A
  • accomplish propulsion
  • mix gut contents with digestive secretions and expose to absorptive surface
  • facilitate temporary storage
  • prevent retrograde movement
  • dispose of residues
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13
Q

What generates the cyclical electrical activity of the gut?

A

Interstitial Cells of Cajal

- cyclical electrical activity is referred to as slow wave activity

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14
Q

What stimulates depolarisation of muscles in the GI tract?

A

stretching
acetylcholine
parasympathetic nervous system

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15
Q

From where do phasic contractions of the gut originate?

A

from these electrical
spikes, and as slow-wave frequency differs along the gut, so does the frequency of contractions (e.g. 3 per min in the stomach, 7-12 per min in the s. bowel, & 1- 12 per min. in colon)

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16
Q

What causes hyper polarisation and relaxation of the gut?

A

adrenaline

sympathetic nervous system

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17
Q

Where does tonic contraction of the gut originate from?

A

actin and myosin interaction

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18
Q

What symptoms does oesophageal motor dysfunction lead to?

A
  • heartburn
  • dysphagia
  • regurgitation
  • chest pain
  • difficulty swallowing
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19
Q

What does fast gastric emptying lead to?

A

nausea, vomiting, cramps, bloating, diarrhoea, dizziness

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20
Q

What does slow gastric emptying (gastric resus) lead to?

A

nausea, vomiting, bloating, tummy pain, feeling full quickly

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21
Q

What symptoms does colon motor dysfunction lead to?

A
  • abdominal pain
  • bloating
  • diarrhoea
  • constipation
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22
Q

What is the enteric nervous system?

A

The intrinsic nervous system of the gut

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23
Q

Where is the myenteric plexus found?

A

between longitudinal and circular muscle layers

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24
Q

Where is the submucosal plexus found?

A

the submucosa

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25
Q

What is the role of the myenteric plexus?

A

control of GI movement

  • excitatory fibres: cholinergic, secreting acetylcholine
  • inhibitory fibres: purinergic, secreting ATP
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26
Q

What is the role of the submucosal plexus?

A

control of secretion and sensory functions- receives signals from gut epithelium and stretch receptors in gut wall

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27
Q

What is the role of the parasympathetic nervous system in the gut?

A
  • main sensory and motor control
  • vagus controls the foregut and midgut
  • pelvic splanchnic nerves control hindgut
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28
Q

What is the role of the sympathetic nervous system of the gut?

A

inhibition of gut activity

- innervates all parts of the gut

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29
Q

What are nerves with cell bodies in the submucosal plexus stimulated by?

A
  • irritation of gut mucosa
  • excessive distension of the gut
  • chemical substances in the gut
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30
Q

What percentage of vagal fibres are afferent?

A

80%: cell bodies in submucosa and terminate in myenteric plexus

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31
Q

What is the effect of gastrin on the gut?

A
  • increases stomach motility
  • increases lower oesophageal sphincter tone
  • increases small intestine/gall bladder motility
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32
Q

What is the effect of cholecystokinin on the gut?

A

increases gall bladder motility

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33
Q

What is the effect of secretin on the gut?

A

inhibits motility

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34
Q

What is the effect of gastric inhibitory peptide on the gut?

A
  • decreases stomach motility

- slows emptying of stomach contents into the duodenum

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35
Q

What does reduction in parasympathetic or vagal tone lead to?

A
  • motor dysfunction
  • gut inflammation
  • abdominal pain
  • bloating
  • altered bowel habit
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36
Q

What digestion occurs in the mouth?

A

carbohydrates by alpha-amylase

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37
Q

What digestion occurs in the stomach?

A

protein by pepsin and a small amount of fat

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38
Q

What digestion occurs in the small intestine?

A

carbohydrates, proteins and fats by pancreatic and epithelium enzymes

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39
Q

What is trans cellular absorption and secretion?

A

Through epithelial cell

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40
Q

What is the paracellular route?

A

Through tight junctions

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41
Q

What can cause a leaky gut?

A
  • stress
  • immune response
  • changes in the gut microbiome
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42
Q

What are symptoms of a leaky gut?

A
  • abdominal pain
  • bloating
  • diarrhoea
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43
Q

what are the 5 parts of the stomach

A
  • cardia
  • funds
  • body
  • pylorus
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44
Q

what are the 3 parts to the pylorus

A

pyloric antrum
pyloric canal
pyloric sphincter

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45
Q

what kind of muscles form the smooth muscle of the stomach

A

longitudinal muscle layer

circular muscle layer

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46
Q

what demarcates the stomach from the duodenum

A

pyloric sphincter

and overlying rugae

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47
Q

what is rugae

A

demarcates stomach from duodenum
allows stomach to expand
has a variety of secretory cells

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48
Q

what is the secretion and motility action of the lower oesophageal sphincter and cardia

A

secretes:
mucus and HCO3

motility:
prevention of reflex
entry of food
regulation of belching (burping)

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49
Q

what is the secretion and motility action of the fundus and the body of the stomach

A 
secretions:
H+
intrinsic factor 
mucus 
HCO3
pepsinogens 
lipase

motility:
reservoir
tonic force during emptying

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50
Q

what is the secretion and motility action of the antrum and pylorus

A

secretions:
mucus
HCO3

motility:
mixing 
grinding 
sieving 
regulation and emptying
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51
Q

what are the roles of gastric motility

A

accepting and holding food (accommodation and relaxation) - fudus and body
churning and grinding food - antrum
emptying - antrum and pylorus

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52
Q

what stops the stomach from distending too much

A

parasympathetic innervation from the vagus nerve

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53
Q

what kind of innervation does accommodation of the gastric motility in the stomach require

A

vagal

- stretch signals from vagal nerves allows for dilatation of stomach, allowing 1L of food into stomach

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54
Q

what defects gastric motility

A

different consistencies of food

eg. liquid is allowed to pass through the pyloric sphincter but thicker material is churned more first

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55
Q

what are the 2 dumping signals

A

late dumping syndrome

early dumping syndrome–> rapid gastric emptying (dizziness and palpitations)

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56
Q

in what 3 ways is gastric emptying controlled

A

1) size of the particles in the stomach (>1-2mm cannot pass P sphincter)
2) delivery of acids, AA and lipase sensed and so hormones CCK, secretin and GIP (gastric inhibitory peptidase), released to decrease motility
3) enteric nervous system

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57
Q

what is a gastric pit and gastric gland made from

A 
gastric pit: 
lamina propria 
mucous cells 
neck--> gastric glands:
parietal cells/ oxyntic cells 
smooth muscle cell 
G cell 
Chief cells/peptic cells
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58
Q

what do parietal/oxyntic cells secrete

A

HCL and intrinsic factor to funds and body

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59
Q

what do G cells secrete

A

gastrin into bloodstream

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60
Q

where are G cells mainly found

A

antra/pyloric glands

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61
Q

what do chief/peptic cells secrete

A

pepsinogen

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62
Q

what are the 2 forms go gastrin released

A

G17 - mainly from antrum

G34- mainly from duodenum

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63
Q

what other hormone is gastrin homologous with

A

CCK-PZ - can share the same receptors

also known as CCK-B receptor

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64
Q

what is gastrin release stimulated by

A
  • lumen proteins/AA

- parasympathetic input

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65
Q

what is gastrin release inhibited by

A

lumen H+- NEGATIVE FEEDBACK

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66
Q

what are the main actions of gastrin on the stomach

A

stimulate acid secretion

promote mucosal growth

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67
Q

what are the 2 forms of somatostatin

A

14 and 28 aa forms

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68
Q

what is somatostatin released by

A

D cells of stomach, duodenum and pancreas

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69
Q

what stimulates and inhibits somatostatin release

A

stimulated by lumen H+

inhibited by ACh

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70
Q

what are the effects of somatostatin

A

acts on G cells to inhibit gastrin

inhibits CCK and secretin

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71
Q

what directly and indirectly effects acid secretion of parietal cells

A
  • direct:
    gastrin and ACh stimualte
    somatostatin inhibits

-Indirect:
histamine

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72
Q

what is intrinsic factor? where is it released? why is it essential

A

binds to cobalamin /B12 in small intestine
released from parietal cells in the stomach
essential for B12/cobalamin uptake in ileum

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73
Q

other than the secretion of pepsingogen what do parietal cells release and what are the effects of this?

A

ACh - stimulates parietal cells to release H+

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74
Q

what is pepsingoen released in response to from chief/peptic cells?

A

in response to ACh

minor effects of secretin, CCK and gastrin

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75
Q

how is pepsinogens released and what happens to them

A

released as pro hormones- pepsinogens

  • cleaved spontaneously at low pH
  • cleaved by pepsin - autolysis
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76
Q

what is pepsin

A

endoprotease - cut within peptide chain rather than terminal AA

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77
Q

what is the optimum pH for pepsin and at what point are they denatured

A

pH 2-3 optimum

denatured above 5-7- ie. once in small bowel

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78
Q

what are gastric lipase. what is their optimum pH

A

initial digestion of triglycerides
cleave outer fatty acids of triglycerides = diacyl glycerol

ph 4

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79
Q

what is ptyalin a-Amylase. what is its optimum pH and when is it denatured

A

initial digestion of polysaccharides

optimum ph 7
denatured at ph 4

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80
Q

how is vomit controlled

A

centrally controlled by area postrema = chemoreceptor trigger zone:
- vagal afferents in response to irritants in and around bowel
- pain
motion sicknesss
- drugs or toxis
- pregnancy

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81
Q

what are the consequences of vomitting

A 
salavation 
sweating 
hyperventilation 
retching (involuntary contractions of diaphragm) 
displacement of cardia to thorax 
emptying of gastric content
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82
Q

what happens during vommiting

A

inhibition of respiration
reflex closure of glottis and soft palate
opening of lower and upper oesphageal sphincter
stomach and pyloric sphincter relax
abdominal musvcles contract
increase in intra gastric pressure

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83
Q

name the general structure of the muscular layer of the small intestine from inner to outer layers

A

muscosa –> submucosa –> muscular externa –> serosa (visceral peritoneum)

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84
Q

what structures are in the submucosa

A

lymphatic vessels
arteries and viens
submucosal plexus

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85
Q

what structures are in the muscular externa

A

circular muscular layer
myenteric plexus
longitudinal muscle layer

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86
Q

what are crypts of lieberkuhn

A

the spaces/ crevices between each villi

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87
Q

what do crypts of lieberkuhn secrete

A

bicarbonate rich fluid

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88
Q

what are brush border enzymes? where are they found? what’s their function?

A

integral membrane proteins
surfaces of intestinal microvilli
break down materials in contact with

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89
Q

what is the first stage of small bowel motility

A

peristalsis

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90
Q

what is peristalsis? and what are the 3 stages of muscular contraction in peristalsis

A

peristalsis is the waves of muscular contractions which move contents along the GI tract

3 stages:
1- circular muscular contractions - contract behind bolus while circular muscles ahead of bolus relax
2- longitudinal muscular contractions - ahead of bolus contract, shortening adjacent segments
3- wave of contraction - in circulation muscles forces bolus forward

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91
Q

what is the second stage of small bowel motility

A

segmentation

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92
Q

what is the happens during the segmentation stage in small bowel motility ? what’s the significance of this

A

alternate contractions of neighbouring segments

churn and fragment the bolus mixing it with intestinal secretions

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93
Q

what is the 3rd stage of small bowel motility

A

migrating motor complex-MMC

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94
Q

What happens during the MMC stage of small bowel motility? how often does this occur?

A

when gut is empty- series of strong, slow peristaltic waves sweep down from stomach to small bowel
pyloric sphincter is relaxed = large things can pass
= help clean out the gut
happens every 90 mins

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95
Q

why is MMC of small bowel important

A

prevents reflex and reduces bacterial growth

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96
Q

what id the MMC of the small bowel stimulated by? what is it suppressed by

A

motilin - released by M cells

suppressed by feeding

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97
Q

where are the APUD cells located and what is their function

A

crypts of lieberkuhn

release hormones

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98
Q

what cells do the APUD cells contain? what hormones do each of these cells secrete?

A

I cells –> CCK
S cells –> secretin
M cells –> motilin
G cells –> Gastrin

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99
Q

what do the pancreatic duct cells release in the small intestine

A

bicarbonate secretion

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100
Q

what do the goblet cells release in the small intestine

A

mucus secretion

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101
Q

what enzymes break down carbohydrates

A
  • soluble amylase –> breaks internal bonds a1,4

- short chain carbohydrates then broken down by specific brush border enzymes

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102
Q

how are glucose, galactose and fructose absorbed

A

glucose and galactose absorbed activity by SGLT1

fructose absorbed passively by Glut5

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103
Q

by what process are proteins broken down? where does this start and by what

A

proteolysis

starts in stomach by pepsin

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104
Q

what is the protein which drives proteolysis? how is it formed

A

trypsin

formed from trypsinogen becoming active by enterokinase on epithelial cells

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105
Q

what cells secrete enterokinase

A

crypt cells

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106
Q

what proenzymes does trypsin activate and into what?

A

trypsinogen into trypsin
chymotrypsinogen into chymotrypsin
proelastase into elastase
procarboxypeptidase A into carboxypeptidase A
procarboxypeptidase B into carboxypeptidase B

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107
Q

name the 3 endopepdases involved in protein digestion

A

trypsin
chymotrypsin
elastase

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108
Q

name the exopepetidases involved in protein digestion

A

the carboxypeptidases ( A and B)

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109
Q

how are small peptides mad soluble in order to diffuse across the brush border

A

membrane bound peptidases chop them up into AA and dipeptides

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110
Q

how are AA taken up in the kidney

A

by sodium linked secondary active transporters

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111
Q

how are the dipeptides taken up by cells?

A

by proton linked secondary active transporters

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112
Q

how is the proton gradient across cells maintained

A

by Na+/H+ Exchange (which depends on sodium gradient )

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113
Q

what is the first stage to fat digestion? what is the significance of this stage

A

bile salts break up lipid droplets

increase SA

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114
Q

why is the amiphatic nature of bile important

A

allows it to interact with fatty environment and watery environment

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115
Q

what is the 2nd stage of fat digestion

A

pancretic lipase cleaves outside fatty acids = monoglycerdie and 2 free fatty acids

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116
Q

explain the 3rd stage of fat digestion? what happens when they are inside the cell

A

monoglycerides and fatty acids form a complex with bile salts which soluble them = mixed micelles = cross brush border
once inside triglycerides are resynthiesed and packaged to chylomicra which are exocytosed into intersitium

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117
Q

do chylomicra empty into the capillaries of lymphatic system

A

into he lymphatic system - lymphatic lacteals

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118
Q

what is happens to conjugated bile salts

A

actively absorbed in distal ileum and recycled

5% ,ost in faces

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119
Q

where is calcium reabsorbed? what kind of process is this ? what is it regulated by

A

reabsorbed in the duodenum
ACTIVLEY
regulated by vit D

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120
Q

name the fat soluble vitamins

A

AKED

absorbed with lipids

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121
Q

how are water soluble vitamins absorbed

A

alongside transport proteins -usualy Na+

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122
Q

how is B12 /cobalamin absorbed

A

by intrinsic factor

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123
Q

where does most digestion and absorption take place

A

small bowel

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124
Q

what is the importance of the colon

A

electrolyte balance and water reabsorption

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125
Q

how are NA+ and K+ secretion in the colon controlled

A

aldosterone

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126
Q

what divides the liver into R and L lobes

A

falciform ligament

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127
Q

how many segments is the liver divided into? what are they divided by

A

8 segemts

by vasculature/blood vessles

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128
Q

where does the intrahepatic and extra hepatic billary drainage drain into?

A

intrahepatic into common hepatic duct

extra hepatic drainage into cystic and pancreatic ducts

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129
Q

what does one acini structured pancreatic cell contain

A
  • digestive enzyme secreting cells
  • pancreatic islet - islets of langerhans
  • capillary
  • hormones secreting islet cells
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130
Q

what surrounds the pancreas?

A

many tubes: enteric, billary and vascular

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131
Q

why is it hard to operate on the pancreas

A

lots of blood vessels surround it

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132
Q

how is the pancreas regulated

A

by the neuroendocrine system

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133
Q

what nerves are involved in the neuroendocrine system of the pancreas? what are their effects

A
  • vagus nerve –> releases acetylcholine

- splanchnic nerve –> smooth muscle release noradrenaline and decrease AcH

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134
Q

what two cells and so hormones does the duodenum have and release?

A

I cells –> CCK

S cells –> secretin

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135
Q

what’s stimulates motilin release in the intestine

A

neural stimulus

fasting

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136
Q

what are the 3 phases of pancreatic juice secretion

A

1- cephalic phase
2- gastric phase
3- intestinal phase

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137
Q

what percent of pancreatic juice secretion is the cephalic phase responsible for and what is it stimulated by? what’s another thing the cephalic phase stimualtes?

A

20%
sight, smell, taste of food –> sends signals via vagal nerve to the pancreas –> enzyme release and decrease bicarbonate

also stimulates apetite

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138
Q

what percent of pancreatic juice secretion is the gastric phase responsible for and what is it stimulated by?

A

10%
continuation of the cephalic phase
rich in enzymes and decrease bicarbonate

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139
Q

what percent of pancreatic juice secretion is the intestinal phase responsible for and what is it stimulated by?

A

70%
produces gastric chyme - partially rich in broken down fat and protein

juices rich in bicarbonate to neutralise chyme

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140
Q

what stimulates the release of CCK

A

lipids and peptides in small intestine (introduction of chyme)

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141
Q

what are the 2 types of CCK receptors and what hormones are they best adapted to ?

A

CCK A - best for CCK

CKK B - best for gastrin

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142
Q

what are the 2 main effects of CCK

A

stimualtion of:

  • gall bladder emptying
  • pancreatic secretion
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143
Q

what mechanism switches CCK off

A

negative feedback loop - as pH falls levels of secretin release decrease

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144
Q

what is secretin stimulated by? what are its main effects?

A

stimulated by acid in small intestine

main effects:

  • stimulate bicarbonate secretion by ductal cells in pancreas and liver (pancreatic and bile fluid)
  • modest inhibition of gastric secretion
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145
Q

does secretion have an effect on a appetite and if so what?

A

yes - decreases appetite

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146
Q

why are proteases formed as inactive precursors?

A

they are dangerous to ells if activated in wrong place at the wrong time

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147
Q

what is a trypsin inhibitor and where is to found ?

A

stops activation. of trypsin

found in secretory vesicles and diluted out via exocytosis

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148
Q

name the 3 pancreatic lipases

A

pancreatic lipase
nonspecific esterase
prophospholipase A2

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149
Q

name the 2 nucleases

A

deoxyribonuclease

ribonuclease

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150
Q

what do pancreatic ducts secrete and what is this stimulated by?

A

bicarbonate release

stimulated by secretin and increased by CCK (via vagus)

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151
Q

in CF what are pancreatic secretions like and why?

A

thick and sticky due to pancreatic failure

NB-give pancreatic enzyme supplementation

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152
Q

is bile recycled?

A

yes- up to 8 times a day

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153
Q

what does bile consit of?

A 
bile salts 
phospholipids 
cholesterol 
bile pigmanets
inorganic ions
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154
Q

where do we get bile pigments from?

A

breakdown of Hb to bilirubin

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155
Q

what kind of charged inorganic ions does bile contain

A

more anions than cations as bile ha negative charge

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156
Q

during synthesis of bile acids and salts what does conjugation do?

A

makes them more water soluble and less toxic

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157
Q

what are hepatocytes sandwiched between?

A

blood supply (hepatic and portal branch) and bile duct

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158
Q

what are canaliculus and what do they secrete ?

A

spaces between 2 hepocytes

secrete:

  • bile acids
  • conjugated bilirubin
  • xenobiotics (foreign molecules)
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159
Q

what is added to bile as it moves down the bile duct? what is this process stimulated by

A

bicarbonate
sat
water

stimulated by secretin

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160
Q

during the fasting state, what state are the bile slats in and how is this maintained?

A

bile salts remain dissolved as gallbladder undergoes tonic contraction

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161
Q

how does bile back up into the gall bladder

A

sphincter of Oddi closed so bile backs up

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162
Q

during digestive period how is bile secreted into duodenum

A

strong Gallbladder contractions and relaxation of sphincter of Oddi

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163
Q

what nerves regulate Gallbladder function

A

vagal nerve

splanchnic nerve

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164
Q

how is the risk of gallstones reduced

A

(gallbladder reabsorbs salt and water and the bile components form micelles and so meaning the fluid remains isotonic )
the net proton secretion acidifies bile reducing the risk of precipitation of Ca and other salts = reducing the risk

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165
Q

are maxillary or mandibular dental arcade on the bottom or top?

A

maxillary top half of mouth

mandibular = bottom half of mouth

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166
Q

what is mastication

A

chewing

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167
Q

what are the muscles of mastication involved in?

A

closing of jaw

slide/rock jaw from side to side

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168
Q

what are the 3 major salivary glands, from largest to smallest

A

parotid gland (largest)
submandibular
sublingual

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169
Q

what are the roles of saliva ?

A
  • lubrication of mouth and food and cleaning
  • facilitation of taste
  • protection against acid and bacteria
  • digestion
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170
Q

how does saliva lubricate the mouth?

A

through serous and mucus fluid

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171
Q

how does saliva protect against acid and bacteria

A
  • antibacterial enzymes (lysozyme, IgA)
  • bicarbonate
  • Ca2+
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172
Q

how is saliva involved in digestion

A
  • salivary amylase (ptyalin)

- lingual lipase

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173
Q

how is saliva production regulated

A

neural control : both parasympathetic and sympathetic

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174
Q

what kind of secretion does is the parasympathetic nervous system responsible for in saliva

A

watery secretion

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175
Q

what kind of secretion does is the sympathetic nervous system responsible for in saliva

A

mucoid secretion

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176
Q

how is the parasympathic secretion of saliva controlled? what’s this driven by?

A

by salivatory centre in the brain stem
driven by:
- local stimuli (taste and touch in mouth)
- central stimuli (smell and sight of food)
- learned reflex (pavlova dogs)

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177
Q

why is it importnant to always have a background production of saliva?

A

prevents glands from becoming stagnant and makes sure bacteria that runs through is spat out or swallowed- infection prevention

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178
Q

what is the 2 stage production of saliva ?

A

1) initial isotonic fluid containing mainly NaCl, protein and mucus
2) passes along duct = salt reabsorption and HCO3- and K+ = leads to hypotonic and alkaline fluid

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179
Q

why is flow rate importnant in production of saliva ?

A

decrease flow rate = decrease amount of absorption of salts

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180
Q

what is the parotid gland responsible for?

A
  • serous secretion
  • 50% of saliva
  • main source of salivary amylase
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181
Q

what innervation is the parotid gland under?

A
  • parasympathic supply via glossopharyngeal (CN VI)

- sympathy supply from superior cervical ganglion

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182
Q

what is the submandibular gland responsible for?

A

serous and mucous secretion

  • 45% saliva
  • main source of lysozyme and lactoperoxidase
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183
Q

what innervation is the submandibular gland under?

A
  • parasympathic supply facila nerve (CN VII)

- sympathetic supply from superior cervical ganglion

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184
Q

what is the sublingual gland responsible for?

A
  • mucous secretion
  • 5% saliva
  • main source of lingual lipase
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185
Q

what innervation is the sublingual gland under?

A
  • parasympathetic supply of facial (CN VII)

- sympathetic from superior cervical ganglion

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186
Q

what is ptyalin a amylase involved in and how does it work?

A

involved in initial digestion of polysaccharides - eg. starch
a amylases can only cute a-1,4 sites (not 1,6)

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187
Q

what pH is ptyalin a amylase denatured ? Whats its optimum

A

4

optimum- 4

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188
Q

what is lingual lipase involved in and how does it work?

A

initial digestion of triglycerides

- cleaves outer fattty acids of triglycerides - diacyl glycerol

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189
Q

what is the optimum pH is lingual lipase ? how is it denatured

A

optimum - pH4

- stable in stomach but denatured by pancreatic proteases

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190
Q

what are papillae

A

taste buds

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191
Q

name the 3 types of papillae from tip of the tongue to back ?

A

tip:
fungiform
circumvallate
follate

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192
Q

what type of cells are taste sensors

A

specialised epithelial cells:

  • Ion channel-based sensors
  • GPCR- based sensors
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193
Q

what type of cells are odour sensors

A

nerve cells (part of olfactory nerve)

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194
Q

how does mucous get secreted into the oesophagus?

A

submucosal oesophageal glands secrete mucous

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195
Q

what is the oesophagus innervated by

A

oesophageal plexus

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196
Q

what are the 2 flexures in the large bowel?

A

hepatic flexure

splenic flecxure

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197
Q

what are haustra in the large intestine

A

divides the colon into little segments along its whole length

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198
Q

what is layers is the haustra made of from outer layers to inner layers?

A
  • muscularis externa
  • submucosa
  • muscularis mucosae
  • intestinal gland
  • mucous cells
  • simple columnar epithelium
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199
Q

what is the muscularis externa of the haustra made of?

A
  • longitudinal layer- taenia coli

- circular layer

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200
Q

where is the ileoceacal valve?

A

in the terminal iluem going into the caecum

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201
Q

how does the ileoceacal valve work?

A

one way valve :

  • periodic relaxation to allow flow
  • ileal distention = opens the valve
  • caecal distension = closes the valve
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202
Q

is the large bowel designed to move contents along?

A

no

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203
Q

what is haustration ?

A

slow contractions in the circular muscles to squeeze contents to and fro (like segmentation)

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204
Q

what is mass movement in the large bowel? how often does it occur

A
  • a peristaltic wave

- a few times a day

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205
Q

how is the large bowel regulated ?

A
  • intrinsic activity: enteric nervous activity
  • some parasympathetic control
  • enteroendocrine and neurocrine influences
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206
Q

where do we get the enteroendocrine and neurocrine influences for the large bowel coming form?

A

cells releasing 5-HT and Peptide YY

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207
Q

what triggers a mass movement in the large bowel

A

gastrocolic and orthocolic reflexes

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208
Q

what is an ‘ileal break’

A

when the presence of undigested lipid in the distal ileum and proximal part of the colon releases peptide YY and so slows gastric emptying and small bowel peristalsis =. designed to stop you eating

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209
Q

how is digestion carried out in the large colon?

A

by bacteria (not human enzymes)

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210
Q

what do bacetria digest in the large bowel and consequently what do thyey produce?

A
  • fiber –> short chain fatty acids (eg. butyric acid, hyrogen and methane)
  • Urea and AA –> amonia
  • billirubin –> urobilingoen and stercobilins
  • cysteine and methonine –> hydrogen sulphide
  • conjugated bile acids –> secondary bile acids
  • primary bile acids –> secondary bile acids
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211
Q

what can happen if we dont have bacteria in the large bowel to digest the foods?

A

weight loss

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212
Q

how are short chain fatty acids absorbed in the colon? why is it important these get digested ?

A
  • secondary active transport with Na linked transporter

- importnant energy source for coloncytes

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213
Q

how does salt absorption happen in the colon ?

A

endothelial Na channels allow trnascellular Na transport
K+ in by Na/K pump
this is followed by paracellular Cl flux
followed by water

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214
Q

what is salt absorption in the colon stimulated by?

A

aldosterone (controls Na/K pump in kidneys and large colon)

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215
Q

how do Ecoli and Cholera effect salt secretion in the colon ? what other bacteria works in a similar way?

A

increase the amount of cAMP
= increases the amount of K+ and Cl lost through the channels into the lumen
= affects Na/K pump and increases amount Na lost
= leading to diarrhoea as water follows

C.Difficile works similar but instead increases Ca2+ in cell not cAMP

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216
Q

how is K+ conc determined in the colon

A

by plasma K+ conc
aldosterone
cAMP

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217
Q

what is the rectosigmoid junction

A

a sharp angle as the sigmoid colon enters the rectum

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218
Q

does the rectum contain valves?

A

yes

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219
Q

what are the 2 sprinters in the anus and what muscles are they comprised of?

A

1- internal anal sphincter : smooth muscle

2- external anal sphincter : skeletal muscle

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220
Q

what is the pectinate line? where is it ?

A

in the anal canal

where epithelium becomes stratified squamous : what you squeeze to defecate

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221
Q

how are we able to defecate

A

faeces enter rectum and pressure rises triggering the internal anal sphincter to relax and the urge to defecate , anal sampling occurs and then the external sphincter and the pelvic floor relax = open way

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222
Q

what is anal sampling

A

anal canal determines if the substance is solid/liquid/gas and tells your brain = you decide what to do with it

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223
Q

why does sitting or squatting facilitate the passage of faeces ?

A

increases the rectosigmoid angle

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224
Q

what is rectal peristalsis?

A

triggers colonic mass movement + raised abdominal pressure (valsalva manoeuver/ grunting) providing motive force

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225
Q

What does metabolism enable?

A
  • extraction of energy from the environment

- synthesis of essential carbohydrates, proteins and lipids

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226
Q

What is catabolism?

A

Breakdown of energy rich compounds such as carbohydrates, fats and proteins

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227
Q

What are examples of catabolic pathways?

A

glycolysis
proteolysis
lipolysis
glyconeogenesis

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228
Q

What is anabolism?

A

The synthesis of complex molecules from simpler ones. These reaction pathways require ATP

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229
Q

What are examples of anabolic pathways?

A

glyconeogenesis
lipogenesis
gluconeogenesis

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230
Q

What are the metabolic forms of carbohydrates?

A

Glucose and fructose

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231
Q

What is the storage form of carbohydrates?

A

Glycogen

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232
Q

How long does the store of liver glycogen last?

A

8-10 hours

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233
Q

What is the store of glycogen in the liver used to support?

A

Glucose concentration in the blood

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234
Q

What is the store of glycogen in the blood used for?

A

Localised energy

- rapid, but short-lived energy storage

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235
Q

What is the metabolic form of lipids?

A

Free fatty acids

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236
Q

Why do fats provide a very dense energy store?

A

They do not bind much water and contain little oxygen

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237
Q

What is the storage form of lipids?

A

Triglycerides

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238
Q

Where are triglycerides stored?

A

Adipose tissue

239
Q

What are the disadvantages of lipids as a metabolic fuel compared to carbohydrates?

A
  • it takes longer to re-release the energy from lipids

- lipids cannot be synthesised back to glucose

240
Q

What does the liver convert lipids to during starvation?

A

Ketone bodies

241
Q

Why are proteins not an ideal energy source?

A
  • they are mainly stored as functional proteins

- catabolism of functional proteins impairs cellular function

242
Q

How can proteins be used as a metabolic fuel?

A

Most amino acids can be converted to glucose in gluconeogenesis by the liver

243
Q

What are the 4 phases of energy metabolism?

A
  1. Absorptive
  2. Post-absorptive
  3. Fasting
  4. Intense exercise
244
Q

What is the average fat storage of the body?

A

4000MJ

245
Q

What is the average usable protein store of the body?

A

100 MJ

246
Q

What is the average liver glycogen store of the body?

A

2.4 MJ

247
Q

What is the average blood glucose level of the body?

A

0.16 MJ

248
Q

What is the average daily energy need of the body?

A

12 MJ

249
Q

How many molecules of ATP are produced from aerobic respiration?

A

36

250
Q

How many molecules of ATP are produced from glycolysis (anaerobic respiration)? (net)

A

2

251
Q

What are the 3 levels of metabolic control?

A
  1. Hormonal
  2. Substrate
  3. Allosteric
252
Q

How does insulin effect:

  1. sugars?
  2. glycogen?
  3. proteins?
  4. lipids?
A
  1. glycolysis
  2. synthesis
  3. synthesis
  4. synthesis
253
Q

How does glucagon/adrenaline effect:

  1. sugars?
  2. glycogen?
  3. proteins?
  4. lipids?
A
  1. gluconeogenesis
  2. breakdown
  3. breakdown
  4. lipolysis
254
Q

How does growth hormone effect:

  1. sugars?
  2. glycogen?
  3. proteins?
  4. lipids?
A
  1. glujconeogenesis
  2. synthesis
  3. synthesis
  4. lipolysis
255
Q

How does cortisol effect:

  1. sugars?
  2. glycogen?
  3. proteins?
  4. lipids?
A
  1. gluconeogenesis
  2. redistribute to muscle
  3. breakdown
  4. redistribute to abdomen
256
Q

How does TNF-alpha and IL-1 effect:

  1. sugars?
  2. glycogen?
  3. proteins?
  4. lipids?
A
  1. glycolysis
  2. breakdown
  3. breakdown
  4. breakdown
257
Q

What is the key factor for regulating metabolism in the fed and fasted states?

A

Blood glucose concentration (and insulin)

258
Q

Why do the metabolic requirements of the brain differ to elsewhere in the body?

A

The blood-brain barrier limit what can get across

259
Q

What is the brain reliant on?

A

Plasma glucose concentration and can use ketone bodies during times of fasting or starvation

260
Q

Why do the metabolic requirements of erythrocytes differ?

A

They have no mitochondria so only anaerobic respiration can occur. This is inefficient

261
Q

Describe adipose tissue

A
  • major site of lipid storage in the form of triglycerides (TGs)
  • it is sensitive to both insulin and glucagon
  • HIGH GLUCOSE: insulin promotes uptake of glucose and conversion and TGs
  • LOW GLUCOSE: glucagon promotes the release of free fatty and glycerol from stored TGs
262
Q

Describe the metabolic requirements of type 1 muscle

A
  • highly aerobic
  • adapted to prolonged, modest activity
  • main energy source: fatty acids
263
Q

Describe the metabolic requirements of type 2b muscle

A
  • Fast twitch muscle
  • Explosive performance
  • Quickly fatigue
  • Few mitochondria
  • Rely mainly on anaerobic glycolysis with glucose coming from their glycogen store
264
Q

Describe the metabolic requirements of type 2a muscle

A
  • intermediate between type 1 and 2b
  • contain some mitochondria
  • glycogen provides energy
  • at lower exercise levels, fatty acids are the main energy source
265
Q

Describe the metabolic requirements of cardiac muscle

A
  • highly aerobic tissue
  • 40% mitochondria
  • main energy source is fatty acids
  • can also use lactate bodies
266
Q

What is metabolism?

A

Sum of all of the chemical reactions in the body

267
Q

Why must plasma glucose levels be tightly controlled?

A

to be fairly tightly controlled to avoid
damage to the brain (at low levels) or a variety of other organs (at
high levels).

268
Q

Describe the blood supply to the liver

A
  • portal vein 75%

- hepatic artery 25%

269
Q

What are the contents of the portal vein?

A

Blood from the small intestine, stomach, pancreas and spleen

270
Q

What is contained in the hepatic artery?

A

Oxygenated blood

271
Q

What is the blood output from the liver?

A

The hepatic vein

272
Q

Where does the hepatic vein drain?

A

The inferior vena cava

273
Q

Describe the internal structure of the liver

A

Lobular structure
Made up of specialised cells and structures including Kupffner cells, hepatocytes, sinusoid cells, bile canaliculi and bile ducts

274
Q

How is the efficiency of exchange increased in the liver?

A

Blood from tea hepatic portal vein and hepatic artery mixes

275
Q

Describe hepatocytes

A
  • make up 60% of lung tissue

- carry out most metabolic functions

276
Q

Describe endothelial cells

A
  • lining of sinusoids

- contain fenestrations so do not form a barrier for small molecules entering hepatocytes

277
Q

Describe Kupffer cells

A
  • located with the sinusoidal lining - macrophages
  • phagocytose bacteria and old erythrocytes
  • protect the lover from gut derived bacteria
278
Q

Describe pit cells

A

Natural killer cells - help protect from viruses/tumour cells

279
Q

Describe hepatic stellate cells

A
  • lipid-filled cells
  • primary site of vitamin A storage
  • control turnover o connective tissue, synthesise collagen and regulate contractibility of sinusoids
280
Q

What are the functions of the liver?

A
  • carbohydrate, lipid and protein metabolism
  • bile formation
  • detoxification of xenobiotics
  • removal of internal waste
  • degradation of bilirubin
  • storage of glucose, iron copper and vitamin A, D, K and B12
  • nitrogen metabolism
  • synthesis of blood components
  • detoxification (haem, drugs, alcohol)
  • immunological function (pit and Kupffer cells)
281
Q

What are bile salts formed from?

A

Cholesterol

282
Q

What percentage of bile salts are recirculated?

A

95%

283
Q

What reduces blood cholesterol levels?

A
  • increasing dietary fibre

- drugs

284
Q

What is cholestyramine (questran)?

A 
Drug that 
- binds bile acids in the gut
- prevents recirculation of bile
- increases bile acid synthesis
so decreases blood cholesterol
285
Q

Why may gallstones form?

A

If more cholesterol enters bile than can be solubilised by bile salts, precipitation of cholesterol occurs. This leads to the formation of gallstones

286
Q

Where do gallstones become lodged?

A

The common bile duct

287
Q

What are xenobiotics?

A
  • potentially toxic and of no nutritional value

- include drugs and food additives or toxins present in food

288
Q

What waste products are processed by the liver?

A
  • hormones such as insulin and GH
  • bilirubin (from breakdown of erythrocytes)
  • urea
289
Q

How are xenobiotics metabolised?

A
  • Phase 1 reactions to form the primary metabolite
    (Oxidation, hydrolysis, hydroxylation or reduction)
  • Phase 2 reactions to form the secondary metabolite (conjugation eg sulphation or glucuronidation)
290
Q

Why are xenobiotics metabolised?

A
  • To inactivate them

- It makes molecules easier to excrete as metabolites are usually more pharmacologically inactive or hydrophilic

291
Q

What enzymes are involved in phase 1 metabolism by the liver?

A

cytochrome P450 enzymes (CYP)

292
Q

Descrive cytochrome P450 enzymes

A
  • large family of haem proteins - mono-oxygenases
  • found in smooth endoplasmic reticulum
  • inducible
  • there is individual variation - important in therapeutics
293
Q

Describe phase 2 metabolism by the liver

A

⮚ Conjugation – addition of glucuronyl, sulphate, methyl, acetyl, glycyl groups to reactive group on molecule
⮚ Various enzymes involved
⮚ Many of these reactions occur in liver, but also lung, kidney

294
Q

Define prodrug

A

A prodrug is an inactive (or less active) compound which is metabolised to produce the therapeutically active form in the body

295
Q

Why use prodrugs?

A
  • to improve absorption in the gut

- to allow an alternative route of administration

296
Q

What is an example of a prodrug?

A

Tamoxifen is a prodrug used in the treatment of hormone-sensitive breast cancer
It is activated to produce endoxifen, 100 x more potent than tamoxifen

297
Q

Give an example that shows why individual variation in cytochrome P450 enzymes is important in therapeutics

A
  • The breast cancer drug tamoxifen is activated by cytochrome P450 enzymes.
  • There are different levels of 2D6 enzymes in different women meaning tamoxifen has a different efficacy in different women as the drug is differentially activated
298
Q

Why may the use of alcohol alongside other drugs increase toxicity?

A
  • Chronic use of alcohol induces synthesis of the cytochrome P450 enzymes
  • This means that certain drugs are more greatly metabolised and so have a greater effect
299
Q

Describe what happens in a paracetamol overdose in terms of metabolism

A
  • paracetamol is primarily metabolised via phase 2 pathways
  • a normally minor route for paracetamol metabolism becomes overwhelmed in paracetamol overdose
  • depletion of glutathione allows free NAPQI to react with membranes
  • this results in hepatic necrosis and liver failure
300
Q

What is the average lifespan of an erythrocyte?

A

120 days

301
Q

Where are red blood cells phagocytosed?

A

In the Kupffer cells of the liver, spleen and bone marrow.

302
Q

What are the stages of haem breakdown?

A

Haem -> Biliverdin -> Bilirubin

303
Q

How is bilirubin transported to the liver?

A

Attached to albumin

304
Q

How is bilirubin metabolised in the liver?

A
  • conjugation (mainly with glucuronic acid)

- Secretion into billiard canalicular - an active process

305
Q

How is bilirubin metabolised in the gut?

A
  • further metabolised by bacteria in the gut to urobilinogen

- urobilinogen is then converted to urobilin or stercobilin

306
Q

Problems with haem metabolism can lead to…

A

Haemolytic anaemia (preheptaic jaundice)

307
Q

Problems with bilirubin metabolism can lead to…

A

Liver damage
Gilbert’s syndrome
(Intrahepatic jaundice)

308
Q

Problems with bile secretion can lead to…

A

blockage - gallstones/pancreatic carcinoma

extra hepatic jaundice

309
Q

What is weight bias?

A

Discrimination based on one’s weight

- many people who are obese experience discrimination as a result

310
Q

What diseases does obesity lead to an increased risk of?

A
  • type 2 diabetes
  • hypertension
  • coronary heart disease
  • certain cancers such as colon
  • osteoarthritis
  • depression
311
Q

How is BMI calculated?

A

weight (kg) / height (m^2)

312
Q

What is a healthy BMI?

A

20-25

313
Q

In which group are obesity related deaths highest?

A

Men and those aged above 40

314
Q

What percentage of the population is obese?

A

27-29%

315
Q

What is another measure of weight independent of BMI?

A

Waist circumference

316
Q

What has been the trend in prevalence of obesity over the last 30 years?

A

Increasing

317
Q

Why is the prevalence of obesity increasing?

A
  • obesogenic environment
  • people are locked not lifestyles which is toxic for energy balance and in which the pace of technological advancement has overtaken human development
318
Q

How did the foresight report 2007 define an obesogenic environment?

A

a normal response to an abnormal environment

319
Q

What is the link between families and obesity?

A

Shared environment and shared genetics mean that it is common for multiple members of the same family to be classed as obese

320
Q

How is obesity managed for those with a BMI of 25-29.9?

A
  • general advice

- diet, physical activity

321
Q

How is obesity managed for those with a BMI of 25-29.9 and high waist circumference and co-morbidities?

A
  • diet
  • physical activity
  • consider drugs (orlistat)
322
Q

How is obesity managed for those with a BMI of 30-39.9?

A
  • diet
  • physical activity
  • consider drugs (orlistat)
323
Q

How is obesity managed for those with a BMI of 40 and above?

A
  • diet
  • physical activity
  • consider drugs (orlistat)
  • consider bariatric surgery
324
Q

How is weight managed in practice?

A
  • motivation established
  • goals set such as 5-10% reduction of initial weight
  • being realistic eg in rate of weight loss and lifetstyle and behavioural changes
325
Q

How does obesity link to COVID-19 health risk?

A 
people living with obesity are twice as
likely to be hospitalized if tested
positive for COVID-19
◼an increased susceptibility to respiratory
problems, inflammation, and
immunological disturbances
326
Q

What are the social determinants of health?

A
  • racial and ethnic discrimination
  • access to healthy food
  • access to health care
  • location and physical environment
  • socioeconomic status
  • education
  • social and community context
327
Q

what 3 muscles form the anterolateral abdominal wall? what supports these anteriorly and posteriorly

A

external oblique
internal oblique
transervous abdominous

supported anteriorly: rectus abdominous
supported posteriorly by : quadratus lumborum

328
Q

what sheet separates abdominal and pelvic cavity?

A

there is no sheet

329
Q

at what point does the oesophagus pierce the diagphram

A

T10

330
Q

what does it mean if an organ is reteroperitoneal

A

situated outside the peritoneum, in contact with the body wall but not fully invested in peritoneum (eg.kidneys)

331
Q

what does it mean if an organ is intraperitoneal

A

suspended from the abdominal wall by double layered peritoneum/mesentery (eg. GI tract)

*in general structures that change size and shape (eg.stomach) are intraperitoneal *

332
Q

what is a mesentery

A

double layered fold of peritoneum

333
Q

during development why does the whole gut tube have a dorsal mesentery

A

separates the gut tube from the body wall allowing it to grow longer than the body cavity, yet while still being attached to the body wall

334
Q

other than the gut tube what other structures have this dorsal mesentery ?

A

Aorta
IVC
spinal chord
sympathetic chain

335
Q

what structures of the gut retain a mesentery after development ? what are these mesenteries called?

A

small intestine: the mesentery of the small intestine

transverse colon: transverse mesocolon

336
Q

how is the transverse mesocolon separated and what are these called?

A

separated by mesocolic shelf into supracolic and infracolic compartments

337
Q

what does it mean if something is secondarily retroperitoneal? name some structures like this

A

it used to have a mesentery but lost it

ascending and descending colon

338
Q

what are the 2 sacs of the abominla cavity

A

greater and lesser sac

339
Q

what is the greater sac? what is the greater sac split into

A

main part of peritoneal cavity

supra and infra colic compartments

340
Q

what is the lesser sac

A

recess of the peritoneal cavity between the stomach and the abdominal wall

341
Q

how are the greater and lesser sacs connected?

A

epiploic foramnen (of winslow)

342
Q

during development what structure of the gut has both ventral and dorsal mesenteries ? does it stay after devlpoment

A

fore gut
yes remains attached to the lesser curvature of the stomach, distal oesophagus and proximal part of the duodenum after development

343
Q

which mesenteries do the liver and spleen develop in?

A

liver in the ventral mesentery

spleen in the dorsal mesentery

344
Q

during development how is the:

  • liver attached to the ventral wall
  • liver attached to the stomach
  • stomach attached to the spleen
  • spleen attached to the dorsal wall
A
  • liver–>ventral wall= falciform ligament (ventral mesentery)
  • stomach –> liver = lesser omentum (ventral mesentery)
  • stomach–> spleen = gastrosplenic ligament (dorsal mesentery)
  • spleen–> dorsal wall = lienorenal ligament (dorsal mesentery)
345
Q

what do the dorsal and ventral mesenteries turn into after development

A

dorsal mesentery- greater omentum

ventral mesentery- lesser omentum

346
Q

what are the features of the supra colic compartment

A 
falciform ligament 
subphrenic recess
coronary ligaments 
hepatorenal recess - Morrison's recess 
lesser omentum 
epiploic foramen 
gastrosplenic ligament 
lienorenal ligament
347
Q

what are the features of the infra colic compartment

A

paracolic gutters

the mesenteries

348
Q

When is the primitive gut tube formed?

A

During embryonic folding

349
Q

Describe the location of the primitive gut tube

A

Extends from the oropharyngeal membrane to the cloacal membrane

350
Q

What are the three parts of the primitive gut tube?

A

Foregut
Midgut
Hindgut

351
Q

What is the foregut?

A

Primitive gut tube from mouth to 1st half of the duodenum

352
Q

What is the midgut?

A

Primitive gut tube from 2nd half of duodenum to 2/3 along transverse colon

353
Q

What is the hindgut?

A

Primitive gut tube from distal 1/3 transverse colon to superior 2/3 rectum

354
Q

At what point is the midgut continuous with the yolk sac?

A

The vitelline duct

355
Q

What is the epithelial lining of the primitive gut tube derived from?

A

Endoderm

356
Q

What is the smooth muscle and connective tissue of the primitive gut tube derived from?

A

Visceral mesoderm

357
Q

What gives rise to the visceral and parietal mesoderm?

A

Visceral and parietal peritoneum

358
Q

What suspends the primitive gut tube from the posterior abdominal wall??

A

The dorsal mesentry

359
Q

What is a mesentery?

A

A double fold of peritoneum that encloses an organ and connects to the body wall. They carry blood supply, lymphatics and nerve supply to and from organs.

360
Q

What is an organ surrounded by a mesentery called?

A

Intraperitoneal

361
Q

What is an organ not surrounded by a mesentery called?

A

Retroperitoneal

362
Q

Where is the dorsal mesentery found?

A

From lower oesophagus to the cloaca

363
Q

Where is the ventral mesentery found?

A

From lower oesophagus to 1st part of dudenum

364
Q

What does the ventral mesentery form?

A

Lesser momentum and falciform ligament

365
Q

What do the vitelline arteries give rise to?

A

The arteries of the gastrointestinal tract

- after going under remodelling ad losing their connection to the gastrointestinal tract

366
Q

What three arteries supply the gastrointestinal tract?

A

Coeliac trunk - foregut
Sup. mesenteric - midgut
Inf. mesenteric - handgut

367
Q

How is the definitive gut lumen formed?

A
  • week 6: proliferation of endoderm derived epithelial lining occludes the gut tube
  • apoptosis of the epithelium occurs over the next two weeks creating vacuoles - recanalisation
  • vacuoles coalesce to fully recanalise the gut tube by week 9
  • during this process the epithelium undergoes further differentiation
368
Q

What three conditions can be caused by abnormal recanalisation?

A
  • duplication eg cyst
  • stenosis
  • atresia
369
Q

Which part of the small intestine is most commonly affected by abnormal recanalisation?

A

ileum

followed by duodenum

370
Q

What is intersuception?

A

Part of the gut tube folds in on itself leading to narrowing

371
Q

What does the foregut give rise to?

A

The respiratory diverticulum

372
Q

How does the foregut separate from the respiratory diverticulum?

A

By forming a tracheoesophageal septum - pharynx and oesophagus

373
Q

What is an oesophageal atresia?

A
  • displacement of the tracheoesophageal septum separates proximal and distal end of oesophagus
  • prevents the foetus from swallowing amniotic fluid and returning it to the mother through the placental circulation
374
Q

What is polyhydraminos?

A

the excessive accumulation of amniotic fluid — the fluid that surrounds the baby in the uterus during pregnancy

375
Q

Why is oesophageal atresia problematic?

A

There is a large foetal sac due to an increased amount of amniotic fluid. This can push on baby and stop devlopment. Also, the mother’s stomach can only stretch so far.

376
Q

When does the oesophagus form?

A

Week 4

377
Q

What makes up the oesophagus?

A
  • Endodermal epithelial lining and smooth muscle from visceral mesoderm
  • Skeletal muscle derived from paraxial mesoderm
378
Q

What is a congenital hiatal hernia?

A
  • oesophagus lengthens rapidly in week 4-7 as stomach descends into the abdomen
  • insufficient elongation results in part of the stomach positioned supradiaphragmatically
  • it is irreducible
379
Q

When is the stomach developed?

A

Appears in week 4 as a dilation of the foregut

380
Q

Where is the stomach suspended from?

A

The ventral and dorsal mesentries

381
Q

What forms the greater curvature?

A

Differential growth in week 5 - the dorsal wall grows faster

382
Q

When does the stomach undergo rotation?

A

Weeks 7-8

383
Q

Describe rotation of the stomach

A
  • 90 degree clockwise rotation around the craniocaudal axis causes the lesser curvature to move from the ventral position to the right
  • Similarly the greater curvature moves from dorsal position to the left
  • The vagus nerves are initially located on left and right sides of the gut tube but are also
    rotated such that the left vagus trunk becomes anterior and the right becomes dorsal
  • Also rotation around the ventrodorsal axis
384
Q

What does rotation around the ventrodorsal axis mean?

A
  • the greater curvature faces slightly caudally

- the lesser curvature faces slightly cranially

385
Q

What forms the lesser peritoneal sac?

A

Rotation of the stomach around the craniocaudal axis

386
Q

What is the omental bursa otherwise known as?

A

The lesser peritoneal sac

387
Q

What is the epiploic foreman?

A

Connects the greater and lesser sacs

388
Q

How is the greater momentum formed?

A

• The dorsal mesentery attached to the greater curvature of the stomach and the posterior
abdominal wall continues to grow
• Reflects back on itself to form an extension of the lesser sac (omental bursa)
• Ventral and dorsal folds fuse before birth
• The posterior layer of the greater omentum also fuses with the mesentery of the
transverse colon

389
Q

What is congenital pyloric stenosis?

A

Narrowing of the pyloric sphincter caused by hypertrophy of smooth muscle

390
Q

How common is congenital pyloric stenosis?

A
  • affects 1 in 500 births

- more common in males than females

391
Q

What is the complication of congenital pyloric stenosis?

A

Restricts gastric emptying which can lead to dilation of the stomach

392
Q

What are signs of congenital pyloric stenosis?

A
  • palpable pyloric mass
  • projectile vomiting
  • visible peristalsis
393
Q

What is heterotopic gastric tissue?

A

inappropriate differentiation of the gut tube can lead to ectopic gastric tissue

394
Q

What are the complications of heterotopic gastric tissue?

A
  • acid production can cause inflammation and ulceration in the surrounding area
  • damage can leaf to strictures due to scarring or rupture of tissue
395
Q

How is the duodenum formed?

A

The duodenum elongates in week 4 resulting in a ventrally projecting C-shape
• This is then dragged to the right by the rotating stomach
• The dorsal mesentery attached to the duodenum degenerates so that the
(majority) duodenum lies against the posterior abdominal wall – secondarily
retroperitoneal

396
Q

What are the origins of the duodenum?

A

proximal half is foregut, distal half is midgut. The

boundary is distal to the entrance of the common bile duct

397
Q

how do prostaglandin/PGE2 effect parietal cell

A

bind to parietal cells and activate Gi mechanisms, decreasing gastric acid secretions

398
Q

What are the major components of the innate immune system?

A
  • pattern recognition receptors
  • antimicrobial peptides
  • cells
  • complement components
  • cytokines
399
Q

What are examples of pattern recognition receptors (PRR)?

A
  • toll-like receptors (TLRs)
  • NOD-like receptors (NLRs)
  • Rigl-like receptors (RLRs)
  • C-type lectins (CLRs)
  • Scavenger receptors
400
Q

What are examples of antimicrobial pepsins?

A

defensins, cathelin, protegrin, granulsyin, histatin, secretory leukoprotease inhibitor, and probiotics

401
Q

What are examples of innate immune cells?

A

Macrophages, dendritic cells, NK cells, NK-T cells, neutrophils, eosinophils, mast cells, basophils, and epithelial cells

402
Q

What are the complement components of the innate immune system?

A

Classic and alternative complement pathway, and proteins that bind complement components

403
Q

What are the cytokines of the innate immune system?

A

Autocrine, paracrine, endocrine cytokines that mediate host defense and inflammation, as well as recruit, direct, and regulate adaptive immune responses

404
Q

What are pattern recognition receptors?

A

An inclusive term for antigen recognition receptors in the innate immune system

405
Q

What are the two groups of pattern recognition receptors?

A
  • Cell surface and intracellular - TLRs, NLRs, RLR’s and CLR’s
  • Fluid-phase soluble receptors
406
Q

What is the role of macrophages?

A

Phagocytose and kill bacteria; produce antimicrobial peptides; bind (LPS); produce inflammatory cytokines

407
Q

What is the role of plasmacytoid dendritic cells (DCs)?

A

Produce large amounts of interferon- (IFN-) which has antitumor and antiviral activity, and are found in T cell zones of lymphoid organs; they circulate in blood.

408
Q

What are the roles of myeloid dendritic cells?

A

Interstitial DCs are strong producers of IL-12 and IL-10 and are located in T cell zones of lymphoid organs, circulate in blood, and are present in the interstices of the lung, heart, and kidney; Langerhans DCs are strong producers of IL-12; are located in T cell zones of lymph nodes, skin epithelia, and the thymic medulla; and circulate in blood

409
Q

What is the role of natural killer cells?

A

Kill foreign and host cells that have low levels of MHC+ self peptides. Express NK receptors that inhibit NK function in the presence of high expression of self-MHC

410
Q

What is the role of NK-T cells?

A

Lymphocytes with both T cell and NK surface markers that recognize lipid antigens of intracellular bacteria such as M. tuberculosis by CD1 molecules and kill host cells infected with intracellular bacteria.

411
Q

What is the role of neutrophils?

A

Phagocytose and kill bacteria, produce antimicrobial peptides

412
Q

What is the role of eosinophils?

A

Kill invading parasites

413
Q

What is the role of mast cells and basophils?

A

Release TNF-, IL-6, IFN- in response to a variety of bacterial PAMPs

414
Q

Describe the adaptive immune system of the GI tract

A

Evolution in response to changing
pathogen structures
– Variable regions of pathogen that MUTATE at
greater speed than humans • Central feature is UNIQUE antigen
receptor found on each lymphocyte
• In response to infection this lymphocyte
undergoes CLONAL expansion
• High degree of specificity

415
Q

What is the estimated range of antigenic variability?

A

1x10^9

416
Q

What is the role of killer or cytotoxic T lymphocytes? (CD8)

A
  • able to kill

- cellular immunity

417
Q

What is the role of helper T lymphocytes?

A
  • secrete growth factors (cytokines) which control the immune response
  • help B and T lymphocytes
418
Q

What is the role of suppressor T lymphocytes?

A

To damp down immune response

419
Q

What represents the first line of immunological defence in the GI tract? Why?

A

GI tract mucosal surface
• Mucosal surfaces separate the external environment from the internal
sterile environment and therefore represent the first line of defence.

420
Q

What does the gut mucosal barrier encounter?

A

• Harmless antigens eg food.
• Commensal bacterial flora
• Pathogenic organisms which have developed effective methods for
colonisation and invasion

421
Q

An important role of the mucosal immune system is…

A

tolerance

422
Q

The gut immune system is …. compared to the systemic immune system

A

functionally and anatomically different

423
Q

The gut immune system comprises of:

A

Innate defences:
• Commensal bacterial flora
• Epithelial barrier
• Biochemical factors produced by epithelial cells

Specific defences:
• Lymphoid tissue associated with mucosal surfaces - [Gut associated lymphoid tissue; GALT]:

424
Q

Define pre-biotic

A

Food for bacteria- induces growth of beneficial microorganism

425
Q

Define pro-biotic

A

Contains live bacteria

426
Q

Breast milk is a source of…

A

pre-biotics

427
Q

How does the gut microbiome develop over time?

A

Breast milk -> Inulin-type fructans (prebiotic) -> Colonic fermentation -> Acidic pH -> Lactobacillus, Bifidobacteria (probiotics) -> Stimulation of intestinal host defences -> Maturation of mucosal immune system

428
Q

What are the benefits of gut microflora?

A 
Resistance to colonisation by pathogens 
• Stimulate local immunity 
• Oral tolerance 
• Nutrition 
• Epithelial cell turnover 
• Intestinal motility
429
Q

What are diseases of the GI tract?

A
  • Irritable bowel syndrome
  • Ulcers (helicobacter pylori)
  • Extraintestinal disease - septicaemia
  • Autoimmunity - reactive arthritis
  • Allergy
430
Q

What do stem cells of the epithelial bacteria differentiate into?

A

Enterocytes
• Goblet cells
• Enteroendocrine cells
• Paneth cells

431
Q

Describe the epithelial barrier

A

Prevents penetration by microorganisms • Intestinal mucosal barrier is a single cell layer • Self-renewing system undergoing continuous renewal from
stem cells located near the base of the crypts of Lieberkhun

432
Q

What is the role of goblet cells in the epithelial barrier?

A

Produce mucins to provide for
mucus layers that resist
microbial access

433
Q

What is the role of enterocytes in the epithelial barrier?

A 
Mechanical action, cilial action
creates current to remove
microbes that are poorly
adhered • Produce antimicrobial peptides
• Defensins • Cathelicidins
• Produce antimicrobial proteins
• Lysozyme, lactoferrin
434
Q

What is the role of secretory IgA in the epithelial barrier?

A

May be of limited specificity to

bind to microbes

435
Q

How is the specific immune system of the gut organised?

A

• Aggregated follicles in Peyers Patches [lower part of small intestine;
Ileum], appendix.
• Single follicles in along length of GI tract
• Induction of immune responses

436
Q

What is found in the Peyer’s patch?

A 
M-cells [microfold cells] specialised
enterocytes adapted to antigen
uptake
• Pass antigens to professional APCs
[dendritic cells]
• Dendritic cells present antigens to T
-cells and B-cells are activated
• B-cells migrate to mesenteric lymph
nodes
• Differentiated plasma cells migrate
to tissues
• Plasma cells secrete IgA
437
Q

How is oral tolerance achieved?

A

T cells- overwhelming response to antigen is non responsive

438
Q

What are Peyer’s patches?

A

specialised sites of initiation of immune responses

439
Q

why are cells more leaky as you move down the GI tract (ie. from duodenum to colon)

A

structure of tight junctions vary as you move down - increasing leakiness

440
Q

What is the concentration of ATP in most cells?

A

6mM

441
Q

What mass of ATP does the average human body contain?

A

75g

442
Q

What is the average ATP turnover of humans?

A

75kg a day

443
Q

Under aerobic conditions, what percentage of cellular ATP is produced in the mitochondria

A

95%

444
Q

Describe the outer membrane of mitochondria

A
  • smooth and freely permeable to molecules under 5000 Da

- no ionic or electrical gradients

445
Q

Describe the inner membrane of mitochondria

A
  • folded into christae permeable to a small number of molecules only via specific transporters
    • a very good electrical insulator, capable of maintaining large ionic and electrical
    gradients
    • contains more protein than lipid – respiratory enzymes, transporter proteins
446
Q

Describe the matrix space of mitochondria

A

• contains wide range of enzymes – Krebs cycle, fatty acid oxidation, urea cycle
(in liver)
• high concentrations of substrates, cofactors & ions • contains mitochondrial DNA, RNA & ribosomes (these resemble bacterial
components) though few mitochondrial proteins are coded on mitochondrial
DNA

447
Q

Describe the inter membrane space of mitochondria

A
  • has metabolite & ion concentrations similar to cytosol

* contains cytochrome c

448
Q

Summarise the link reaction

A

Pyruvate dehydrogenase catalyses conversion to acetyl CoA

449
Q

What causes the neurological/cardiovascular symptoms of beri-beri?

A

Disruption of PDH function caused by lack of thiamine

450
Q

What causes Wernike-Korsakoff syndrome?

A

Lack of thiamine

451
Q

PDH is inhibited when…

A

energy levels are high

452
Q

What are the two stages of the Krebs/citric acid cycle?

A
  1. Synthesis of 6-C compound (citrate) which then loses 2 C as CO2 to become a 4 C compound (succinylcholine CoA)
  2. Oxidation of a 4 C compound to regenerate oxaloacetate and initiate another round of the cycle
453
Q

What are the main outputs of the Krebs cycle?

A
  • reduces coenzymes NADH & FADH2 - electron carriers
  • CO2 (waste product)
  • 1 GTP = 1 ATP
454
Q

Summarise the control of the Krebs cycle

A
  • entry of pyruvate (glucose) controlled by need for energy and availability of Acetyl CoA from fat oxidation
  • Control of cycle by need for energy as monitored by ATP : ADP and NADH; NAD+ rations
455
Q

What are the three key enzymes of the Krebs cycle?

A
  • citrate synthase
  • isocitrate dehydrogenase
  • alpha-ketoglutarate dehydrogenase
456
Q

How does the Krebs cycle act as an exchange for intermediates for other metabolic pathways?

A
  • Amino acid carbon skeletons feed into the Krebs cycle
  • A number of anabolic (synthetic) pathways use Krebs cycle intermediates as building blocks
  • Synthesis of oxaloacetate from pyruvate is important in replenishing oxaloacetate if needed
457
Q

Why do patients with type 1 diabetes synthesis ketones?

A

Diabetic patients cannot use glucose effectively in the absence of insulin
Glycolysis is inhibited, [pyruvate] low
Gluconeogenesis is NOT inhibited – oxaloacetate & malate being removed to form glucose
In the absence of insulin, fatty acids are mobilised from adipose tissue and oxidised to acetyl CoA – acetyl CoA levels HIGH
But lack of oxaloacetate prevents acetyl CoA from entering the Krebs cycle
So ketones are synthesised instead

458
Q

What are the two parts of oxidative phosphorylation?

A
  • electron transport

- ATP synthesis

459
Q

Summarise electron transport

A 
the energy (reduction potential) of the electrons in
NADH/FADH2 is used to create a proton gradient across the inner mitochondrial membrane – OXIDATION
460
Q

Summarise ATP synthesis in oxidative phosphorylation

A

the energy from the proton gradient is used to phosphorylate ADP to synthesise ATP – PHOSPHORYLATION

461
Q

How does cyanide effect oxidative phosphorylation?

A

Blocks removal of electrons from the chain by the reduction of oxygen to water at complex IV

462
Q

What is the energy produced when electrons are transferred between complexes?

A

To pump protons across the inner mitochondrial membrane creating a H+ gradient

463
Q

Describe the transport of ATP at the inner mitochondrial membrane

A

ADP must be transported into the mitochondria to supply the ATPase
ADP
ATP must be transported out to other areas of the cell Antiporter in the inner mitochondrial membrane allows this exchange Phosphate is also required – its transport into the matrix requires the movement of a Pi proton out of the intermembrane space
H+

464
Q

How many protons are required in the synthesis of 1 molecule of ATP to cross the inner mitochondrial membrane?

A

4

465
Q

NADH … cross the inner mitochondrial membrane

A

cannot

466
Q

Where is NADH oxidised and reduced?

A

Oxidised - cytosol

Reduced - matrix

467
Q

What are uncouplers?

A

Weak acids which are soluble in the membrane

468
Q

How do uncouplers work?

A

When they penetrate the inner mitochondrial membrane they diffuse freely At the inter-membrane space interface they associate with protons – driven by the relatively high [H+]
At the matrix surface they release protons – driven by relatively low [H+]

469
Q

Uncouplers are used to generate … in newborns

A

heat

- non-shivering thermogenesis

470
Q

How do uncouplers generate heat in newborns?

A

Babies possess brown adipose tissue – has more mitochondria/ different appearance to white adipose tissue
Mitochondria in brown adipose tissue contain thermogenin (uncoupling protein-1)
When core body temperature drops, sympathetic nervous system release of noradrenalin leads to increased concentrations of free fatty acids in the cytosol, which activate thermogenin

471
Q

Why may targeting brown adipose tissue be useful therapeutically?

A

To promote triglyceride clearance and weight loss

472
Q

What is DNP?

A

Dinitrophenol
DNP was widely available as a ‘slimming pill’ in the USA during the 1930s
However side effects including hyperthermia, tachycardia, excess sweating, blindness (due to cataracts) & fatalities led to it being withdrawn in 1938

473
Q

what is GALT? what does it contain

A

gut associated lymphocyte tissue

contains: APCs, effector cells and largest reservoir of B and T cells

474
Q

how are the lymphoid elements organised in the gut

A
  • organised mucosal associated lymphoid tissue ( Peters patchers)
  • diffuse mucosal associated comprising widespread leukocytes (intraepithelial lymphocytes, lymphocytes in lamina propria)
475
Q

where are intraepithelial lymphocytes found ? what do they mostly contain

A

between intestinal epithelial cells

mostly contain cytotoxic T cells

476
Q

where are lamina propria lymphocytes found ? what do they mostly contain

A

in loose connective tissue - under epithelium (epithelium and lamina propriety = musocsa)
T helper cells

477
Q

what is the function of IgA’s released from GALT

A
  • neutralises viruses and toxins
  • enhances non-specific defines mechanisms
  • inhibits: bacterial adhesion, macromolecule absorption and inflammtory effects of other Igs
478
Q

Why does a low level of glucose lead to unconsciousness?

A

Glucose is a key energy source for the brain

479
Q

What is glycosuria?

A

Excess sugar in the urine. It is dangerous as it causes more water to leave in urine leading to dehydration.

480
Q

What concentration can glucose reach in the portal vein after a meal?

A

20mM

481
Q

What can the liver use to make glucose?

A

Glycogen, amino acids or ketone bodies from lipids

482
Q

What glucose transporters are important in whole body metabolism?

A

GLUT-2 and GLUT-4

483
Q

What are the two types of glucose transporters?

A

GLUT and SGLT

484
Q

What is the difference between GLUT and SLGT transport?

A
  • SLGT transport is an Na+ symport

- GLUT transport is a passive process with no role for Na+

485
Q

Describe GLUT-1

A
  • Km: 20mM
  • found in tissues, red cells, endothelium and b cells
  • constitutive
486
Q

Descrive GLUT-2

A
  • Km: 42mM
  • mobile
  • found in kidney, ileum, liver and pancreatic beta cells
  • high kM means low affinity
  • insulin insensitive
487
Q

Describe GLUT-4

A
  • Km: 2-10mM
  • mobile (vesicles)
  • found in skeletal muscle, heart and adipocytes
  • low kM means high affinity
  • insulin responsive
488
Q

Describe GLUT-3

A
  • Km: 10mM
  • apical
  • found in neurons and placenta
  • high-affinity
489
Q

Describe GLUT-5

A
  • are both apical and mobile
  • wide distributed throughout tissues
  • fructose sensitive
490
Q

Describe SGLT-1

A
  • high affinity
  • apical
  • found in small intestine and kidney tubules
491
Q

Describe SGLT-2

A
  • low affinity
  • brush-border
  • found in kidney proximal tubule
  • have a high capacity
492
Q

Describe beta cells of the pancreas

A
  • mainly central
  • most abundant
  • secrete insulin
493
Q

Describe alpha cells of the pancreas

A
  • at the periphery

- secrete glucagon

494
Q

Describe gamma cells of the pancreas

A
  • few in number

- secrete somostatin

495
Q

How is insulin secreted?

A
  • GLUT 2 picks up glucose as it increases in the blood flowing through the pancreas
  • Glucose is metabolised through glycolysis and oxidative phosphorylation to generate ATP
  • ATP closes KATP channels, depolarising the membrane
  • Ca2+ influx then induces exocytosis of preformed insulin from granules
  • Other secretagons act to increase exocytosis
496
Q

How is insulin processed?

A
  • metabolism from a preprohormone occurs in the endoplasmic reticulum
  • disulphide bonds are inserted in the ER to stabilise
  • cleaved to give A and B chains which are linked and a C peptide in the golgi apparatus
497
Q

What is the function of the C peptide of insulin?

A

Acts as a biomarker for insulin production

498
Q

How does insulin work?

A

binds to a receptor kinase stimulating a signalling cascade which increases cycling of GLUT4 transporters to cell membrane and translation and expression of proteins required for glycolysis and anabolism

499
Q

What are the effects of insulin on the liver?

A
  • promotes glycolysis
  • promotes lipogenesis
  • promotes glycogenesis
  • inhibits gluconeogenesis
500
Q

How does insulin promote glycolysis in the liver?

A

Increased activity of PFK increases the conversion of glucose to glucose-6-phosphate

501
Q

How does insulin promote lipogenesis in the liver?

A
  • conversion of fatty acids through glucose metabolism (excess acetyl Co-A from glycolysis)
  • synthesis and release of VLDL
502
Q

How does insulin promote glycogenesis in the liver?

A

Increased activity of glycogen synthase

503
Q

How does insulin inhibits gluconeogenesis in the liver?

A

inhibition of key glucagon reponsive enzymes such as fructose-1,6-bisphosphate

504
Q

What are the effects of insulin on skeletal muscle?

A
  • promotion of glycolysis
  • promotion of lipogenesis
  • promotion of glycogenesis
  • promotion of protein synthesis
505
Q

What are the effects of insulin on adipose glucose metabolism?

A
  • promotion of lipogenesis

- inhibition of lipolysis

506
Q

How does insulin promote lipogenesis in the adipose tissue?

A
  • increased expression of GLUT 4
  • increased glucose uptake and glycolysis
    – Glycolysis provides key substrates for lipogenesis
    Phosphoenolpyruvate as a precursor of glycerol Acetyl CoA ( malonyl CoA) for FA synthesis
  • increased expression of lipoprotein lipase
507
Q

Glucagon release is translated as a …

A

preprohormone

508
Q

Glucagon release is driven by …

A

alpha cells

509
Q

Glucagon release is antagonised by …

A

glucose

510
Q

What is the difference between processing of insulin and glucagon?

A

processing of glucagon results in the generation of multiple incretins depending on whether the processing occurs in the intestine or pancreas. Insulin produces the same, wherever it is processed

511
Q

What drives secretion of glucagon? How?

A

Low glucose keeps ATP level in a-cells low and keeps the K+ channel open
Causes opening of Ca2+ channel
This drives exocytosis

512
Q

What inhibits release of glucagon? How?

A

High glucose keeps ATP level in a-cells elevated and closes the K+ channel
Membrane depolarization and Ca2+ channel closes
Exocytosis is inhibited

513
Q

The key driver of metabolism in exercise is …

A

adrenaline

514
Q

What is the effect of adrenaline on metabolism in the liver?

A

Promotes glucose production by the Cori-Cori cycle

515
Q

What is the effect of adrenaline on metabolism in the muscle?

A

glycogenolysis, and glucose uptake through increased GLUT4 expression

516
Q

What is the effect of adrenaline on metabolism in the adipose tissue?

A

Lipolysis and FFA release into the blood

517
Q

What is the Cori-Cori cycle/

A

A metabolic pathway in which lactate produced by anaerobic glycolysis in muscles is transported to the liver and converted to glucose, which then returns to the muscles

518
Q

What are the symptoms of diabetes mellitus?

A 
Polyuria 
Polydipsia 
Weight loss 
Blurred vision 
Ketoacidosis (in type 1)
519
Q

What is type 1 diabetes?

A

Primary defect is an inability to produce (enough) insulin

Autoimmune disease, in which β cells are destroyed

520
Q

What happens in type 1 diabetes?

A

Excess glucagon (or insulin:glucagon imbalance) leads to lipolysis and proteolysis, and gluconeogenesis and ketogenesis in the liver

521
Q

What is type 2 diabetes?

A

Primary defect is an impaired cellular response to insulin (insulin resistance)

522
Q

What may insulin resistance in type 2 diabetes be as a result of?

A
  • receptor downgrading

- reduced signalling

523
Q

how can the marginal artery assist if there is a blockage in the IMA

A

if the IMA becomes blacked the marginal artery can provide a functional anastomosis between the midgut and hindgut

524
Q

why is the sigmoid colon mobile

A

due to its mesentery - sigmoid mesocolon

525
Q

what is a sigmoid Volvulus ? what can it lead to

A

where the sigmoid twists around itself

can lead to constipation, ischemia, necrosis, infarction, rupture

526
Q

what is the physical connection between the foregut and the hindgut? does this serve any other purpose

A

connection between superior pancreaticoduodenal and inferior pancreaticoduodenal - they anastomose

this is not a functional anastomosis however beaucse the arteries are so narrow

527
Q

what is the sympathetic nerve supply of the abdomen.

A
  • greater, lesser, least splanchnic nerves

- lumbar splanchnic nerves

528
Q

what is the parasympathetic nerve supply of the abdomen and which part of the abdomen do they supply?

A
  • vagus : all the way to distal transverse colon

- pelvic splanchnic nerves (S2-S4)- to hindgut and pelvic organs

529
Q

name the only splanchnic nerve which is of parasympathetic supply

A

pelvic splanchnic nerves

530
Q

what takes the nerve innervation for the abdomen directly to target vessels and organs

A

autonomic plexuses(nerve networks) around the coeliac trunk, SMA, IMA

531
Q

describe the sympathetic pathway from the spinal chord to the target organ in the thorax

A

pre ganglionic fibre —> white ramus —> grey ramus –> post ganglionic fibres : cardiac plexus

532
Q

describe the sympathetic pathway from the spinal chord to the target organ in the abdomen

A

pre ganglionic —> white ramus —> splanchnic nerves –> prevertebral ganglion (post-ganglionic neurons)—> Target organ

533
Q

where do pre ganglionic nerve originate from for the empathetic supply

A

from T1-L2

534
Q

where are pre-vertebral sympathetic ganglia located

A

Coeliac trunk
SMA
LMA
(these are also the arteries they are associated with)

535
Q

what does the prevertebral sympathetic ganglia contain

A
  • presynaptic parasympathetic (vagal) fibres
  • visceral affront fibres
  • pre synaptic sympathetic (splanchnc) fibers
536
Q

are all the autonomic plexus interconnected

A

yes all 3 around the coeliac artery, SMA and the IMA are

537
Q

what are the 3 ways the ganglions travel through the SNS

A
  • synapse at entry level- paravertebral ganglia
  • pass through sympathetic trunk without synapsing - prevertebral ganglia
  • ascend and descend and synapse anywhere from the spinal chord
538
Q

which route do the sympathetic ganglions take to get to the digestive system

A

pass through the sympathetic trunk without synapsing - synapse at the prevertebral ganglia

539
Q

which route do the sympathetic ganglions take to get to the cardio-pulmonary system

A

synapse at the entry level- the paravertebral ganglia

540
Q

what is the prevertebral ganglia also known as and why

A

pre aortic ganglia as its close to the aorta

541
Q

what are the relative lengths for the pre ganglionic and post ganglionic fibres in the SNS

A

pre ganglionic is short and post ganglionic is long

542
Q

where do pre-ganglionic neutrons for the parasympathetic supple of the abdomen come from

A

brainstem or sacral spinal chord

543
Q

what are the relative lengths for the pre ganglionic and post ganglionic fibres in the paraNS

A

long pre ganglionic and short post ganglionic fibres

544
Q

what do they autonomic plexus join with when they extend inferiorly

A
  • superior hypogastric plexus (at the level of aortic bifurcation)
  • inferior hypogastric plexus via the hypogastric nerves
545
Q

at what level do we get aortic bifurcation in the abdomen

A

L4

546
Q

what nerves do the inferior hypogastric plexus receive

A

pelvic splanchnic nerves : S2-S4

547
Q

At what vertebral level do we get the innervation of referred pain for the foregut

A

T6-T9

548
Q

At what vertebral level do we get the innervation of referred pain for the midgut

A

T8-T12

549
Q

At what vertebral level do we get the innervation of referred pain for the hindgut

A

T12-L2

550
Q

what ‘centres’ in the hypothalamus control eating

A

hunger and satiety (feeling of fullness after a meal)

551
Q

what is ghrelin

A

28 AA peptide

552
Q

what cells is ghrelin produced by

A

neuroendocrine cells of stomach

also present as neuropeptide in the brain

553
Q

when is ghrelin released

A

when the stomach is empty

554
Q

what is the action of ghrelin

A

orexigenic agent - stimulates appetite

555
Q

contrast orexigenics to anorexigens

A

orexigenics stimulate appetite whilst anorexigens suppress hunger

556
Q

name hormones which are anorexigens

A 
CCK
insulin 
GLP-1
Peptide YY
somatostatin 
oxyntomodulin
557
Q

what cells produce leptin

A

adipocytes / adipokine

558
Q

what are the effects of leptin

A

central effects - potentiate insulin

559
Q

what cells produce adiponectin

A

adipocytes

560
Q

what are the effects of adiponectin

A

potentiate insulin

561
Q

what certain things can inhibit leptin and insulin

A

inflammatory cytokines: TNF-a and IL-6

562
Q

where are central and peripheral the signals of anorexigens sent

A

nucleas of solitary tract in the medulla

563
Q

where do the anorexigen signals travel to after going to the nucleas of solitary tract in the medulla

A

project to the arcuate nucleas - ARC

564
Q

what 2 areas does the ARC have

A
  • satiety centers in the ventromedial nucleas :VMN

- hunger centers in the lateral hypothalamic area -LHA

565
Q

what 2 types of neurons are present in the arcuate nucleas

A
  • anorexigenic neurons

- orexigenic neurons

566
Q

what do anorexigenic neurons secrete

A
  • proopiomelanocortin (POMC)

- and ‘cocaine-amphetamine- related transcript’ - CART

567
Q

what do orexigenic neurones

A

secrete agouti-related peptide -AGRP and neuropeptide Y - NPY

568
Q

what fuels are used in starvation

A

glucose
fatty acids
ketone bodies
amino acids

569
Q

what do muscles use for fuel

A

glucose
fatty acids
ketone bodies

570
Q

what does the kidney convert glutamine to

A

glucose

571
Q

what happens in extreme starvation

A
  • wasting of muscle
  • muscle fatigue and reduced exercise capacity
  • diminished respiratory capacity
  • slow HR and decreased contractility
  • loss of heat generating capacity
  • apathy (lack of motivation)
  • death from respiratory or cardiac failure or infection
572
Q

how are eating disorders defined

A

voluntary/ deliberate maintenance of low dietary intake which may lead to low body weight - or ‘binging and purging’

573
Q

is there a genetic concordance to eating disorders

A

yes there may be some

574
Q

what are the associated psychological and psychiatric characteristics of eating disorders

A
  • low self esteem
  • perfectionism
  • desire to control their environment
  • depression
  • distorted body image
575
Q

what are the hallmark signs of anorexia

A
  • body weight more than 15% below standard
  • weight load due to voluntary abstinence
  • distorted body image
  • morbid fear of fatness
  • amenorrhoea in women
576
Q

do people suffering from bulimia have a better look than those suffering from anorexia

A

yes - usually not have the drastic low body weight

577
Q

why do mouths of bulimic patients have rotten teeth

A

due to purging - gastric acid can damage the teeth

578
Q

a BMI of under what is underweight?

A

<18.5

579
Q

a BMI of under what is overweight?

A

> 30

580
Q

can obesity be due to genetic defects

A

yes - a small fraction are affected this way

581
Q

what are the effects of obesity on the musculoskeletal system

A
  • osteoarthritis

- lower back pain

582
Q

what are the effects of obesity on the circulatory system

A
  • hypertension (CHD, stroke, renal failure)
  • DVT
  • pulmonary embolism
583
Q

what are the effects of obesity on the metobolic and endocrine system

A
  • type 2 diabetes
  • dyslipidaemia
  • metabolic syndrime
584
Q

what are the effects of obesity and cancer

A

-endometrial, breast, colon cancers

585
Q

what are the effects of obesity on the reproductive and urological system

A
  • stress incontinece
  • men stroll abnormaliities
  • PCOS
  • infertility
  • ED
586
Q

what are the effects of obesity on respiratory system

A

sleep apnoea

587
Q

what are the effects of obesity on the gl system and liver

A

NAFLD
gasto-oesphageal reflux
gall stones

588
Q

what symptoms contribute to metabolic syndrome

A
  • obesity
  • type 2 diabetes
  • hypertension
  • high plasma triglycerides
  • low HDL cholesterol
589
Q

in obesity which organs does fat accumulate in

A

muscle
heart
liver

590
Q

what are the 2 types of fat

A

ectopic and visceral fat

591
Q

is visceral fat responsive to insulin

A

no

592
Q

what does visceral fat daily produce

A
  • non-esterified fatty acids
  • pro infamtory cytokines (IL-1/6, TNF-a)
  • less adiponectin
593
Q

how do non esterfied fatty acids affect the liver

A

makes the liver less sensitive to insulin - impress B cell insulin release

594
Q

how do cytokines released affect cells

A

produce reactive oxygen species - which can increase risk of anthroma and CVS disease

year 1 flash cards (23 decks)

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