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HOM > Digestion > Flashcards

Digestion Flashcards

1
Q

What are the key layers of the gut tube

A

Mucosa
Submucosa
Muscularis externa
Serosa

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2
Q

Describe the muscosa

A

Innermost layer of gut tube

Consisting of epithelium, lamina propria and muscularis mucosae

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3
Q

What is the lamina propria

A

Loose connective tissue containing glands, lymph nodes and capillaries

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4
Q

What is the muscularis mucosae

A

A thin layer of smooth muscle which throws the muscosa into folds

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5
Q

Where is Meissner’s plexus found

A

In the submucosa hence it is also called the submucosal plexus

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6
Q

What does the submucosa contain (3)

A

Blood vessels
Nerves
Glands

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7
Q

What is the muscularis externa

A

Consists of 2 muscular layers : inner (circular muscle) and outer (longitudinal muscle)

The myenteric plexus is located between these layers

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8
Q

What is the serosa

What kind of epithelium does it have

A

The outermost layer of connective tissue

Covered by simple squamous epithelium

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9
Q

What is the name of the intestinal blood supplY

What does it also supply (supplies 5 structures in total)

A

The splanchnic circulation

Stomach, intestines, spleen, liver and pancreas

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10
Q

How much blood passes through the splanchnic bed

How much passes through the hepatic portal vein

A

1200ml per min

75% passes via the intestines to the liver in the HPV

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11
Q

How does oxygenated blood reach the liver

A

The hepatic artery

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12
Q

How does functional anaemia affect the gut

A

Splanchnic blood flow increases to 2500ml/min after a meal

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13
Q

What is the role of the parasympathetic NS in functional anaemia after a meal

A

Increases blood flow only locally (eg in salivary gland)

Elsewhere increased flow following parasympathetic stimulation may largely be a secondary effect, following increases metabolic rate which occurs with increased activity

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14
Q

Does the SNS have a big effect on splanchnic blood flow

A

Yes

Maximum sympathetic vasoconstriction can reduce blood flow to 300ml/min

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15
Q

Name 2 hormones that cause splanchnic vasoconstriction

A

Angiotensin II

ADH

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16
Q

What is the primary role of the gut’s great veins

A

As capacitance vessels, holding 20% of blood volume at rest

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17
Q

How much can venoconstriction affect the gut’s blood circulation

A

Venoconstriction can add ~400ml from the mesenteric veins and 200ml from the liver to the general circulation

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18
Q

What is the blood supply of a villus like

A

The arterial blood supply to each villus ascends from the base while the venous supply descends

This is called a counter current arrangement

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19
Q

How do water soluble substances leave the gut and enter the blood

Give 2 examples of water soluble substances

A

They enter the descending veins to ultimately enter the hepatic portal vein

Monosaccharides and amino acids

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20
Q

Where do the products of fat digestion enter the villi

A

They enter the lacteals

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21
Q

How are lacteals emptied

A

By irregular contraction of the smooth muscle in. The lamina propria, squeezing the products of fat digestion into the lymphatic system

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22
Q

What causes the smooth muscle to contact to empty the lacteals

A

An increase in interstitial fluid pressure

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23
Q

What prevents back flow in the submucosal lymphatics

A

Valves

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24
Q

What is the epithelium of the gut comprises of

A

A single layer of columnar cells

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25
Q

Why do gut epithelium have a v high turnover rate

A

They are vital for preventing microbial disease but are vulnerable to mechanical damage so must be constantly renewed

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26
Q

How often is the entire gut replaced

A

Every 2-6 days

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27
Q

Where do new gut epithelium come from

A

Stem cells from the crypts of Lieberkühn

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28
Q

What are the crypts of Leiberkühn

A

Blind ended tubules projecting into the gut lining between villi

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29
Q

If the epithelial cells are constantly renewed, what stops the barrier function of the gut being comprised

A

Before older cells are shed from the villus tip, a new tight junction is formed beneath them, between the neighbours

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30
Q

What is the ENS and what does it consist of

A

Enteric nervous system

Consists of the submucosal and myenteric plexuses which extend from the middle of the oesophagus to the colon

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31
Q

What do the submucosal and myenteric plexuses coordinate respectively

A

Submucosal: secretion
Myenteric: motility

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32
Q

Where is autonomic nervous system input particularly important in the gut

A

In the proximal gut and rectum

The intrinsic ENS and hormonal control is more important between these

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33
Q

Where do sympathetic fibres synapse

A

There is a cholinergic synapse in the prevertebral ganglia in the sympathetic chain OR in a separate pre-vertebral ganglion within the abdominal cavity (this second option is more common with fibres to the gut)

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34
Q

Post ganglionic fibres are typically cholinergic. True or false?

A

False

They are noradrenergic

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35
Q

What is usually the effect of the SNS on the gut

What is the exception

A

Inhibitory

It stimulates sphincter contraction

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36
Q

What is the PNS carried to the gut in

A

The vagus nerve

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37
Q

What kind of synapse is the PNS pre ganglionic fibres to the ENS

A

Cholinergic

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38
Q

What is the general effect PNS stimulation on the gut

What is the exception

A

Excitatory

Sphincter relaxation (inhibitory post ganglionic fibres release VIP)

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39
Q

Which nerves supply the distal colon, rectum and anus

From which region do they arise

Are they PNS or SNS

A

The pelvic nerves

sacral

Used to be thought they were PNS but actually SNS

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40
Q

What are IPANS

A

Intrinsic Primary Afferent Neurons

These are located entirely within the ENS

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41
Q

What do IPANs form

A

The afferent limbs of local reflexes eg response to peristalsis

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42
Q

Where are the cell bodies of general visceral afferent fibres to the gut

A

In the dorsal root ganglia or a homologous ganglion in the vagus

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43
Q

What are the 3 types of sensory fibres to the gut

A

IPANs
General visceral afferent fibres
Sensory fibres with cell bodies in the ENS (IFANs)

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44
Q

What do the general visceral afferent fibres do

What reflex are they involved in

A

Their axons transmit signals from the gut to the spinal cord or brainstem

Stomach reflexes, pain and defaecation reflexes

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45
Q

How many fibres in sympathetic nerves are afferent?

What about parasympathetic?

A

Sympathetic: 50%
Parasympathetic: 75%

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46
Q

What are vagovagal reflexes?

A

Reflexes in which both afferent and efferent arms are carried by the vagus nerve

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47
Q

Which nerves carry pain signals ?

A

Sympathetic

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48
Q

What are IFANs

A

Intestinofugal afferent neurons

Sensory fibres with cell bodies in the ENS, which send axons with sympathetic fibres to synapse at the pre vertebral sympathetic ganglia

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49
Q

What do IFAN fibres do

A

They form afferent limbs of long range inhibitory reflexes used to coordinate different parts of the gut

IFANs and pre vertebral ganglionic connections provide short cut around the multi synaptic pathway through the ENS

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50
Q

Why are feedback and feed forward mechanisms used in the gut

A

Feedback: to reduce mortality in proximal sections of the gut if it looks like contents are moving too quickly

Feed forward: to enhance motility in distal parts of the gut in order to make room

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51
Q

Give examples of 2 GI reflexes

A

Ileal brake

Gastrocolic reflex

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52
Q

What is the ileal brake

What communication is utilised

A

The effect of nutrients which have reached the ileum without being absorbed reducing motility and secretion in the more proximal parts of the digestive tract.

PYY and GLP-1
Nerve fibres

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53
Q

What is the gastrocolic reflex

A

Where food entering the stomach promotes motility in the colon

This may result in the need to defaecate

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54
Q

What chemical is involved in the signalling of the gastrocolic reflex

A

CCK

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55
Q

What kind of nutrient being present in the ileum is most likely to cause the ileal brake

A

Fat

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56
Q

Where is voluntary control exerted on the gut

Why is this possible

What else may affect bowel movements

A

Swallowing and defaecation

There is striated muscle here

Emotions, especially anxiety

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57
Q

What is neurocrine transmission

A

When nerve terminals release a transmitter to a target cell or into the blood

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58
Q

Name 4 neurocrine transmitters in the gut

A

ACh
Nitric Oxide
Vasoactive Intestinal Peptide
Noradrenaline

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59
Q

Discuss briefly ACh in the gut

A

Released onto muscarinic receptors

Excites gut smooth muscle and stimulates secretion

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60
Q

Discuss the effects of VIP and NO on the gut

A

Relax smooth muscle

VIP stimulates secretion

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61
Q

What is the effect of noradrenaline in the gut

A

Typically inhibitory but promotes sphincter contraction and vascular smooth muscle

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62
Q

What releases noradrenaline in the gut

A

Sympathetic neurons rather than neurons of the ENS

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63
Q

What is paracrine transmission

A

Locally produced substances diffusing through the ECF to work on neighbouring cells of a different type

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64
Q

How do endocrine transmitters travel

A

Via the blood

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65
Q

What kind of molecule are all gastrointestinal hormones

What secretes them

A

Peptides

Enteroendocrine cells

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66
Q

Where are enteroendocrine cells found

A

Scattered throughout gut endothelium

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67
Q

What secretes secretin

When does it happen

A

S cells

In response to acid secretion

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68
Q

Give the key roles of secretin

A 
Stimulates pancreatic growth
Stimulates bicarbonate and water secretion 
Inhibits gastric acid secretion 
Inhibits motility
Promotes sphincter contraction
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69
Q

When was secretin discovered

What was the experiment

A

1902

HCl added to duodenum of a dog; pancreatic secretion increases
HCl added to denervated loop of jejunum (blood vessels intact) and pancreatic secretion increases
Extract of mucosa of jejunum into jugular vein: pancreatic secretion increases

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70
Q

What secretes gastrin

A

G cells in the gastric antrum and duodenum

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71
Q

What stimulates gastrin secretion

A

Nervous stimulation and the presence of peptides and amino acids

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72
Q

What are the roles of gastrin

A

Stimulate gastric acid secretion by parietal cells

Promote growth of oxyntic mucosa

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73
Q

What is CCK

Where is it secreted

A

Cholecystokinin

I cells in the duodenum and jejunum

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74
Q

What stimulates secretion of CCK

A

Long chain FFAs and monoglycerides

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75
Q

What is the role of CCK

A

Stimulates gall bladder contraction, pancreatic secretion and growth
Inhibits gastric emptying and appetite

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76
Q

Name the incretins

A

GIP (glucose dependant insulinotropic polypeptide)

GLP-1 (glucagon-like peptide 1)

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77
Q

What secretes GIP

What secretes GLP-1

A

K cells in the upper small intestine

L cells in both small and large intestine

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78
Q

When are incretins released

A

After a meal and augment insulin release from pancreas

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79
Q

How is knowledge of incretins used to combat type 2 diabetes

A

GLP-1 agonists are used to treat type 2 diabetes and are used to treat obesity

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80
Q

Discuss motilin

A

Secreted cyclically during fasting by M cells in the upper small intestine
Release is under neural control
Initiates the migrating myoelectrical complex

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81
Q

Which is the only GI hormone to stimulate appetite

Where and when is it secreted and where does it act

A

Ghrelin

Secreted by endocrine cells of the stomach in response to fasting

Acts on the hypothalamus
Also promotes growth hormone release from the pituitary

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82
Q

What is the Roux en Y surgery

A

A gastric bypass surgery where the lower small intestine is attached to the upper stomach
The duodenum is still attached in the bypass to allow bile secretion

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83
Q

What is potentiation

A

When the response of a cell with receptors for more than one type of chemical messenger, or different subtypes for the same messenger, to a combination of messages exceeds the sum of the responses to each individual message

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84
Q

How does the incretin effect act as potentiation

A

Plasma glucose alone stimulates insulin release

However if β cells are simultaneously exposed to the incretins, insulin production is greatly augmented

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85
Q

Why does glucose taken orally lead to higher insulin secretion than glucose injected intravenously

A

Oral glucose intake leads to incretin release

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86
Q

Give evidence of the potentiation in the incretin effect

A

Glucose taken orally leads to insulin secretion rates 2-3x higher than glucose injected intravenously because oral glucose leads to incretin release

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87
Q

How long can the smooth muscle in sphincters be tonically contracted

A

From minutes to hours

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88
Q

What kind of contraction is usually going on in the stomach and intestines

A

Phasic contractions

They contract slowly and rhythmically

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89
Q

Describe the electrical activity for phasic contraction in the smooth muscle of the stomach and intestine

A

A wave of depolarisation spreads through gap junctions and the cells are mechanically coupled, allowing coordinated contraction

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90
Q

What is single unit smooth muscle

A

Smooth muscle in which the cells are electrically coupled

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91
Q

How many nuclei in a smooth muscle cell

A

1

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92
Q

What are caveolae

A

Indentations in the plasma membrane of a smooth muscle cell

These increase surface area and act as calcium stores

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93
Q

What is the ratio of thin (actin) to thick (myosin) fibres in

a) smooth muscle
b) skeletal muscle

A

a) 10:1

b) 2:1

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94
Q

Describe the excitation contraction coupling in gut smooth muscle

A

Intracellular calcium binds to calmodulin
This complex activates myosin light chain kinase
This phosphorylates a light chain on myosin, allowing it to bind to actin

When calcium levels fall, myosin is dephosphorylated by myosin light chain phosphotase, which prevents further cycling

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95
Q

What is peristalsis

A

The general term referring to gut motility patterns which propel food in the anal direction

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96
Q

What is the peristaltic reflex

A

When stretching of the gut Wall elicits contraction of the longitudinal and circular muscle behind a bolus but relaxation of the muscle in front, propelling the food onwards

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97
Q

What is the propulsion of the peristaltic reflex know as

A

The law of the intestine

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98
Q

Which messengers mediate the peristaltic reflex

What about nervous stimulation

A

ACh mediates contraction
Nitric oxide mediates relaxation

But it is entirely mediated by the ENS

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99
Q

How may the bolus be detected in the gut

A

Maybe via mechanical stretch receptors in the myenteric plexus
Or
Mechanical/ chemical stimuli to the mucosa promoting serotonin release

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100
Q

What is 5-HT

Where is it released in the gut

A

Serotonin

Enterochromaffin cells

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101
Q

What modulates the smooth muscle of the muscularis external

A

Both stretch and chemo sensitive neurons indirectly, via the myenteric plexus

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102
Q

Can you get peristalsis in the striated parts of the gut

A

Yes it is controlled by somatic motor neurons

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103
Q

What special kind of peristalsis exists in parts of the gut like the colon

A

Reverse peristalsis/ retroperistalsis

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104
Q

What is the resting potential of the smooth muscle cells of the gut

A

Range from -70 to -40mV

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105
Q

Describe slow wave electrical activity

A

Slow waves of electrical activity are slow, undulating depolarisations of amplitude between 10 and 50mV

These slow waves represent the basal electrical rhythm intrinsic to the gut
They are responsible for phasic contractions

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106
Q

What happens to the smooth muscle between slow waves

A

It retains a basal level of tension referred to as tone

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107
Q

What is the range of the rate of slow wave occurrence

A

3-12 cycles per minute depending on the part of the gut

The shape of the wave also vary with location

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108
Q

What are ICCS

A

Interstitial cells of Cajal

The pacemakers of the gut: initiating and propagating slow waves

The ENS mainly innervates the ICCs rather than the smooth muscle directly

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109
Q

What is the structure of ICCs

Where are they

A

They are specialised smooth muscle cells containing few contractile elements

They are located mainly between the longitudinal and circular muscle layers

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110
Q

What is the pacemaker activity of ICCs based on

A

Calcium being take up/ released from intracellular stores, resulting in the activity of nearby plasma membrane channels

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111
Q

What do the fine processes of the ICCs form

A

Gap junctions with each other and nearby smooth muscle cells

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112
Q

What does depolarisation of smooth muscle by slow waves result in

When will contraction occur

A

The opening of L type voltage gated calcium channels in their membrane

If the amount of calcium entered exceeds the contraction threshold

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113
Q

When are action potentials generated in the gut

What are these called

A

If the calcium entered after slow wave depolarisation exceeds the electrical threshold

Spike potentials

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114
Q

How long are spike potentials

A

20msec

Longer than a sodium based AP

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115
Q

All smooth muscle requires APs to contract. True or false

A

False

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116
Q

What effect does ACh have on slow waves

What is the effect on contraction

A

Increases amplitude

Eg by opening action channels which contribute to depolarisation

More depolarisation results in more spikes, more calcium entry and a stronger contraction

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117
Q

What is the effect of NA on slow waves

What is the effect on contraction and why

A

Decrease amplitude by opening K channels for hyperpolarisation

Weaker contraction or no contraction as amplitude may be below threshold

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118
Q

Do sphincters depend on slow waves

A

No tonic contraction does not
It may be caused by a continuous sequence of APs, partial depolarisation of smooth muscle without APs or other mechanisms resulting in sustained levels of intracellular calcium

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119
Q

What is segmentation

A

Where different regions of circular muscle of the gut tube wall contract to aid mixing

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120
Q

What drives segmental contractions

A

Slow waves

But it is modulated by nerves and hormones (eg gastrin)

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121
Q

How does the PNS affect segmentation

A

PNS is excitatory, SNS is inhibitory

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122
Q

What is segmentation like without myenteric stimulation

A

Segmentation contractions become very weak in the absence of appropriate myenteric stimulation

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123
Q

What are the 3 major salivary glands

What do each produce

A

Submandibular - mucus serous mix
Sublingual - mucus/ serous mix
Parotid - serous

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124
Q

What are the major functions of saliva

A

Lubrication
Defence
Buffering
Digestion

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125
Q

How does saliva provide lubrication

A

Glycoproteins called mucins are produced by mucus secreting glands

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126
Q

What does salivary lubrication facilitate

A

The solution of food products facilitates taste, speech and swallowing

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127
Q

How does saliva provide defence

A

Lysozyme, lactoferrin and antibodies (IgA) are found in saliva

Proline rich proteins bind to and neutralise the effects of plant tannins

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128
Q

How does saliva act as a buffer

A

HCO3- ions raise the pH from slightly acidic (at basal severe thin levels) to ~pH 8 (during active secretion

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129
Q

How does saliva aid digestion

A

Contains salivary amylase you break down starch

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130
Q

What does amylase break starch down into

A

Oligosaccharides

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131
Q

Salivary amylase is inhibited by the low pH of the stomach. How can it continue to work despite this?

How long can it continue to work?
How much starch can it break down?

A

It is protected inside a bolus of food

For up to half an hour and has time to digest 75% of the starch in a meal

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132
Q

What is the primary secretion and what produces it

A

A fluid which is isotonic to plasma and high in NaCl

Produced by acinar cells

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133
Q

Why does primary secretion have high NaCl

A

The accumulation of NaCl in the acinar lumen draws water into the lumen by osmosis

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134
Q

Acinar cells only produce the primary secretion. True or false?

A

False

They also secrete salivary enzymes and other proteins via exocytosis
Some specialised acinar cells secrete mucus

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135
Q

How is saliva emptied from the lumen of the acinar cells to the ducts

A

Contraction of the myoepithelial cells

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136
Q

How do the duct cells modify the primary secretion

A

They make saliva more hypotonic

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137
Q

Which hormone acts on the salivary duct cells to promote ion exchange

What is this similar to

A

Aldosterone

Aldosterone acts here in the same way as in the kidney

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138
Q

What almost entirely controls salivation

A

The ANS

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139
Q

What phase of digestion involves the anticipatory response to food

A

The cephalic phase

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140
Q

How do the PNS and SNS act on salivation? (3 points each)

A

PNS: secrete ACh and VIP to promote vasodilation and increase blood supply, metabolism and growth.
Also contracts myoepithelial cells.
ACh opens more acinar cell channels increasing volume of saliva

SNS: promotes vasoconstriction but not during salivary reflex
Promotes myoepithelial contraction
NA acts on β1 receptors, increasing cAMP and thus increasing exocytosis, thereby increasing protein content

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141
Q

How does the PNS increase secretory volume

A

Releases ACh which acts on M1 and M3 receptors to increase [Ca2+] thus increasing channel activity

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142
Q

How is potentiation found in acinar cells

A

The cAMP (SNS) and Ca2+ pathways cross over within the acinar cells, potentiating the secretion of amylase

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143
Q

What is deglutition

A

Swallowing

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144
Q

What initiates the deglutition reflex

What coordinates this reflex

A

When a bolus of food is pushed to the back of the throat by the tongue, touch receptors in the pharynx start the reflex

The swallowing centre of the medulla and lower pons

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145
Q

How is the respiratory centre of the medulla affected by the swallowing centre?

What is this called

A

Respiratory centre is directly inhibited by the swallowing centre during the time it takes to swallow

Deglutition apnoea

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146
Q

Which muscles are involved in swallowing

What is the aim

A

It is v complicated involving the fine control of many striated muscles in the pharyngeal region

To swallow food without inhaling it

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147
Q

What does the upper oesophageal sphincter (UOS) consist of

A

Striated cricopharyngeus muscle

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148
Q

Describe the muscle of the upper third of the human oesophagus

A

Both longitudinal and circular layers are striated and innervated by the vagus

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149
Q

What is the muscle like in the middle third of the oesophagus

What about the last third

A

A mixture of smooth and striated

Entirely smooth

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150
Q

Where does a primary peristaltic wave begin

What does it do

A

Just below the UOS

Sweeps the bolus downwards at a rate of 3-5cm/sec

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151
Q

When is the secondary peristaltic wave initiated

What initiates it

What kind of reflex is it

A

If the bolus fails to move all the way to the stomach

Initiated by the persistent stretch of the oesophagus

Partly a local reflex, partly a vagovagal reflex

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152
Q

What is the lower oesophageal sphincter

What controls it

A

A region of specialised circular smooth muscle at the bottom of the oesophagus

ENS fibres which receive input from the ANS

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153
Q

Describe the action of the lower oesophageal sphincter

A

Normally tonically contracted

Sphincter relaxes even before food arrives as part of the feed forward Vagal reflex

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154
Q

What promotes the relaxation of the lower oesophageal sphincter as part of the Vagal feed forward reflex?

A

NO is the key ENS transmitter

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155
Q

Which structures are important in preventing acid entering the oesophagus

A

Lower oesophageal sphincter and surrounding crural diaphragm

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156
Q

Which reflex can lead to heart burn

What other condition can this lead to

A

The gastro oesophageal reflux

Barrett’s oesophagus

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157
Q

What is Barrett’s oesophagus

A

A condition of meta plastic change in mucosal cells in the lower oesophagus

The normal stratified squamous epithelium change to simple columnar epithelium with interspersed goblet cells that are normally only present in the intestines

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158
Q

When may the relaxation of the lower oesophageal sphincter be compromised

What can this lead to

A

Achalasia

Difficulty swallowing

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159
Q

What does the oesophagus secrete

What is used for

A

A small amount of mucus

Lubrication of food during swallowing and to protect mucosa against acid reflux

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160
Q

What is emesis

Where is it controlled

A

Vomiting

The vomiting centre in the medulla oblongata

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161
Q

What is stimulated to cause vomiting

A

A chemoreceptor trigger zone on the floor of the fourth ventricle of the brain

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162
Q

Why can the chemoreceptor trigger zone be triggered by blood borne drugs (emetics)

A

It lies outside the blood brain barrier

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163
Q

What are emetics and can they work within the gut

A

Drugs which induce vomiting

Yes they can send stimuli to the brain vie the vagus

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164
Q

Name an emetic

A

Ipecac

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165
Q

What does vomiting entail

A

Increased salivation
Retro peristalsis
Pressure changes
Relaxation of the lower oesophageal sphincter and eventually the upper oesophageal sphincter

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166
Q

Where does retro peristalsis begin in emesis

What must be relaxed to allow food to return to the stomach from the small intestine

A

From the middle of the small intestine and sweeps the contents up the digestion tract into the stomach

The pyloric sphincter

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167
Q

How does pressure change during emesis

What does this allow

A

Intrathoracic pressure decreases and abdominal pressure increases

Stomach contents to enter the oesophagus without retro peristalsis

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168
Q

Other than pressure changes, what is needed for the stomach contents to enter the oesophagus

A

Relaxation of the lower oesophageal sphincter

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169
Q

How are the pressure changes in emesis achieved

A

intrathoracic pressure is lowered by inspiring against a closed glottis

Abdominal pressure is increased by contracting abdominal muscles

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170
Q

Why does retching occur

After retching a few times what happens

A

If most of the mechanisms of emesis occur without the upper oesophageal sphincter relaxing

The sphincter relaxes and vomitus is expelled

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171
Q

When does bile enter the vomit

A

Due to duodenal contraction in severe vomiting

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172
Q

Name 3 animals that cannot vomit

A

Rats
Mice
Rabbits

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173
Q

Give 4 functions of the stomach

A

A good reservoir so good can be eaten quickly and released at a controlled rate

To facilitate digestion

To destroy ingested microbes through acidity

To regulate appetite through feed back effects to the brain and regulate late gut activity through feed forward mechanisms

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174
Q

How does oesophageal stretch affect the stomach

What does this allow

Which part of the stomach is not affected

What is this whole effect called

A

A vagovagal reflex causes the fundus and body of the stomach to relax

Up to 1500ml of food can be accommodated with little increase in pressure

The antrum

Receptive relaxation

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175
Q

How is the antrum different to the rest of the stomach

A

It has thicker muscular walls so can perform more powerful contractions than the proximal stomach

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176
Q

Discuss the plyoric sphincter

A

It is a functional sphincter but is not anatomically discrete
It is formed from the circular muscle of the plyorus

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177
Q

How open is the pyloric sphincter usually

What happens at the on set of feeding
Why is this

A

V narrow usually, limiting rate of stomach emptying

A small amount of liquid drains rapidly into the duodenum at the onset of feeding
The nutrients are sampled, which affects the rate of stomach emptying via a feedback mechanism

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178
Q

Where are ICCs found in the stomach

What do these do

A

In the body

Generate slow waves at a frequency of 3 per min

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179
Q

What happens to the slow wave generated by the ICCs in the stomach

A

Propagate down toward the pylorus and stop there

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180
Q

Why do stomach slow waves stop at the pylorus

Can APs propagate here

A

The pyloric sphincter lacks ICCs

Yes

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181
Q

What is the characteristic structure of gastric slow waves

How does this change towards the antrum

A

Spike and plateau

APs May be superimposed on the plateau

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182
Q

Which substances increase the duration and amplitude of the plateau in gastric slow waves in the fed state

Why do they do this

A

ACh and gastrin

To increase the chance of APs and contractions occurring

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183
Q

How do contractions spread through the stomach

What happens as the contractions approach the pyloric sphincter

A

They sweep down the body and antrum becoming increasingly powerful

The sphincter contracts to prevent passage of ingesta

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184
Q

Why does the pyloric sphincter close immediately following a meal

What is this process called

A

So the stomach contents are forced backwards towards the middle of the stomach

Retropulsion

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185
Q

Why does retropulsion occur in the stomach

A

To produce the “Antral mill” which breaks up larger particles and mix food with gastric secretion forming chyme

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186
Q

What happens to the pylorus between contractions

A

It relaxes and contents pass into the duodenum

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187
Q

What forces chyme through the pylorus

A

Tonic gastric pressure

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188
Q

What size do solids need to be to pass through the pylorus

A

<2mm in diameter

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189
Q

What did Hinder and Kelly show

When did they show this

A

The tougher and larger the food, the longer it stays in the stomach

1977

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190
Q

Describe the activity of the stomach in the fast state

A

Rests quietly for 90mins then 10 mins of intense activity

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191
Q

How do contractions in the stomach differ in the fasted state from the fed state

What does this mean

A

Contractions in the fasted state sweep food towards the pylorus rather than performing the antral mill

This helps larger particles to enter the duodenum

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192
Q

In the fasted state how does the wave of contractile activity move

What is this called

What initiates it

A

Continues down to the terminal ileum

This process is the migrating myoelectric complex

Motilin

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193
Q

What is the daily volume of secretion into the stomach lumen

A

2 litres

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194
Q

What are the 3 glands of the stomach mucosa

A

Cardiac
Oxyntic
Pyloric

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195
Q

What do the cardiac glands secrete and where are they located

A

Mucus

Near the entrance of the oesophagus

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196
Q

Where are the oxyntic glands

What do they contain

A

The oxyntic glands in the fundus and body contain parietal cells

Mucus secreting cells line

Chief cells also exist

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197
Q

What is another name for parietal cells in the oxyntic glands

What do they do

A

Oxyntic cells

Secrete HCl and intrinsic factor

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198
Q

What is another name for chief cells

What do they do

A

Peptic cells

Secrete pepsinogens and prochymosin

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199
Q

Where are the pyloric glands

What do they contain

A

In the antrum

Mucus secreting cells 
G cells (secrete gastrin)
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200
Q

Where is gastrin secreted into

A

The blood

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201
Q

What promotes pepsinogen secretion

A

Vagal ACh and a cholinergic response to acidity

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202
Q

How does acidity increase the amount of pepsins

A

Acidity catalyses the cleavage of inactive pepsinogens into pepsins

HCl also provides the low pH ideal for pepsin activity

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203
Q

What do pepsins do

A

Digest proteins and peptides

Cleave pepsinogens

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204
Q

How does acidity affect prochymosin

A

Acidity catalyses cleavage of prochymosin to form chymosin (AKA rennin)

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205
Q

What does chymosin do

A

Curdles milk in neonatal mammals, converting caseinogen (soluble) into casein (insoluble)

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206
Q

Why is caseinogen converted to casein in neonatal mammals

A

It allows milk proteins to remain in the stomach long enough to be acted upon by pepsins

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207
Q

How is milk curdled in human neonates

A

Pepsins curdle milk as the prochymosin gene is inactive in humans

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208
Q

Where is gastric lipase secreted

A

Stomach

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209
Q

What protects Vit B12 from stomach acidity

A

It binds to haptocorrin in saliva

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210
Q

What stops B12 being digested by proteases

A

Binds to intrinsic factor and this complex resists such digestion

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211
Q

What ultimately happens to B12

A

The B12-intrinsic factor complex is taken up into epithelial cells of the ileum by receptor mediates endocytosis

212
Q

What is the only gastric function that is essential to human life

A

Secretion of intrinsic factor

213
Q

Where is intrinsic factor secretes in dogs and cats

A

Pancreas

214
Q

Give 4 functions of gastric acid

A

Delays gastric emptying
Solubilises and thus improves calcium and iron absorption, also helps to release B12 from food
Activates pepsinogens
Destroys many ingested microbes

215
Q

What happens to the NaCl and HCl in gastric juice between meals

A

Juice contains more NaCl

HCl is secreted at a low basal rate

216
Q

What happens within minutes of stimulation to parietal cells

A

Many tubules and vesicles, whose membranes contain transport proteins, fuse with the luminal membrane of the parietal cell

217
Q

What happens to gastric juice wither the parietal cells are maximally stimulated

What happens to the intracellular pH

A

It becomes an isotonic solution of
HCl

Intracellular pH= 7

218
Q

What is the pH of the parietal cell’s gastric gland during maximal secretion

What does this require of the pumps in the luminal membrane of the cells

A

0.8

They must pump against a million fold concentration gradient

219
Q

What is the proton pump

A

The H+/K+ ATPase pumps

220
Q

What generates the protons for the proton pumps on the luminal membranes of parietal cells

A

They’re generated from the intracellular reaction of CO2 with water (carbonic anhydrase is the catalyst)

This reaction forms H+ and HCO3-

221
Q

How is HCO3- removed from parietal cells after it is generated as a byproduct of forming H+

A

Chloride shift

222
Q

What kind of transporter is the chloride shift

A

Secondary active transporter

It’s energy comes from the electrochemical gradient for HCO3-

223
Q

What is the alkaline tide

How is it detected

A

As acid secretion proceeds, CO2 is removed from the plasma and bicarbonate is added, making gastric venous blood more alkaline

A rise in urinary pH

224
Q

3 things which act on parietal cells to increase acid secretion

A

Gastrin (endocrine)
Histamine (paracrine)
ACh (neurocrine)

225
Q

How does gastrin reach the parietal cells

A

Travels in the blood from G cells in the antrum and duodenum

226
Q

What prompts gastrin release

A

Local stretch reflexes (via ACh)
Vagal stimulation
Peptides, amino acids, and Ca2+ in the stomach lumen

227
Q

Via which action does Vagal stimulation prompt gastrin secretion

A

Via gastrin releasing peptide (GRP)

228
Q

What is gastrin‘a most important role

A

To prompt histamine production and release from ECL cells

229
Q

What is the strongest agonist of HCl secretion

A

Histamine

230
Q

Where is histamine released

A

From enterochromaffin - like cells (ECL cells)

231
Q

What makes histamine a paracrine transmitter

A

It is secreted from ECL cells which are found in the gastric glands themselves to increase gastric acid secretion from parietal cells

232
Q

What is the effect of ACh on acidity in the stomach

What else does it do, having a similar effect?

A

ACh is released from nerve terminals to promote acid release

Also increases release of histamine and gastrin
Inhibits release of somatostatin

233
Q

What is the effect of ACh on somatostatin

A

Inhibits its release

234
Q

How do ACh, gastrin and histamine increase acid secretion from parietal cells

A

ACh and gastrin increase free Ca2+
Histamine acts on H2 receptors to increase cAMP
Maximum acid secretion requires both Ca2+ and cAMP pathways to be activated, resulting in potentiation

235
Q

3 things which mediate inhibition of acid secretion

A

Somatostatin (paracrine)
Secretin
Prostaglandins (paracrine)

236
Q

How to remember 3 things which enhance gastric acid secretion

A

1 paracrine, 1 endocrine, 1 neurocrine

237
Q

What secretes somatostatin

In response to?

What’s its effect

What kind of feedback is this

A

D cells

Luminal acidity

Inhibits parietal cells

Negative feedback- prevents excessive acid secretion

238
Q

What releases secretin

In response to

A

S cells

Acid in duodenum

239
Q

How does secretin inhibit acid secretion

A

Indirectly: stimulates Vagal afferent fibres, which reduce gastrin release fromm G cells

240
Q

What do prostaglandins do

A

They are paracrines which promote bicarbonate and mucus production

241
Q

What are the 3 phases of acid secretion

A

Cephalic
Gastric
Intestinal

242
Q

What mediates the cephalic phase of acid secretion

How is the pH affected here? Why?

How much of total acid secretion does this account for

A

Feedforward ACh

No pH change as somatostatin release increases in response to increased acid secretion

30%

243
Q

What stimulates gastric phase of acid secretion

What happens to the pH

What further happens in this phase (3)

A

Presence of food in the stomach

Initially protons are buffered by proteins in the food and luminal pH rises to 6. This rise releases secretory cells from inhibition

Stretch of stomach wall results in vagovagal and local reflexes which increase both gastrin and acid release
Peptides and amino acids stimulate G cells to further increase gastrin release

244
Q

When does the intestinal phase of acid secretion occur

What happens initially

A

When chyme enters the duodenum

Duodenal Stretch triggers vagovagal reflexes, increasing acid secretion in the stomach and the products of protein digestion result in gastrin release from duodenal G cells

245
Q

What happens in the intestinal phase of acid secretion after the initial reflexes

A

As duodenal contents become increasingly acidic, different vagovagal reflexes, local enteric reflexes, and secretin production all decrease acid secretion by the stomach

246
Q

What protects the stomach mucosa

Where is this present

What is this lining called

What does it protect from

A

Secretion of mucus and HCO3- by the mucous cells forming the stomach’s epithelial lining and in the necks of gastric glands

Gastric mucosal barrier

Protection from mechanical and chemical damage

247
Q

What pH is the luminal surface of the stomach

A

6-7

248
Q

What replaces the epithelial mucous cells that are continually lost from the stomach surface

A

They are replaced by mucous cells from the necks of the gastric glands which migrate up and over the surface

249
Q

What replaces the neck mucous cells if they replace epithelial mucous cells of the stomach

A

Stem cells which have divided and differentiated

250
Q

What happens if the gastric mucosal barrier is compromised

A

Stomach’s surface can be attacked by acid and peptides, giving rise to a gastric ulcer

251
Q

How are gastric ulcers treated

A

With drugs that decrease acid secretion, including H2 receptor antagonists and proton pump inhibitors

252
Q

Name 2 H2 receptor antagonists and give an example of proton pump inhibitors

A

Ranitidine, cimetidine

PPIs eg omeprazole

253
Q

What is are 2 predisposing factors to gastric ulcers

A

Overuse of NSAID drugs (eg aspirin)

Helicobacter pylori (a Gram negative bacterium that inflames the stomach Wall)

254
Q

How are stomach ulcers, caused by helicobacter pylori, treated

A

Antibiotics as well as acid suppressors

255
Q

What relaxes the pyloric sphincter

A

Inhibitory fibres in the ENS, which release NO

256
Q

How do neural and hormonal reflexes slow stomach emptying

A

Inhibiting gastric motility

Tightening pyloric sphincter

257
Q

What do enterogastric reflexes do

A

Slow gastric emptying when the distal gut is stretched

258
Q

Name 3 things which appear in the duodenum, suggesting stomach emptying is too fast

A

Excess acid (if duodenal pH drops below 4)
Fat digestion products
Peptides and amino acids

259
Q

What is absorbed by the stomach

Give 3 examples

A

Lipid soluble substances

Alcohol
Ketamine
Aspirin

260
Q

The pancreas is purely exocrine. True or false?

A

False

It also produces endocrine secretion of insulin and glucagon

261
Q

Describe the exocrine of the pancreas

A

Bicarbonate rich

Includes enzymes eg amylase, lipase, proteases, ribonuclease, deoxyribonuclease

Enters the duodenum

262
Q

How do pancreatic acinar cells secret enzymes

How are proteases released

A

Exocytosis

As zymogens

263
Q

What molecule helps protect acinar cells from inappropriate activation of trypsin

A

PSTI (pancreatic secretory trypsin inhibitor) is packaged in the same zymogen granules are trypsinogen

264
Q

What secretes the bulk of pancreatic juice

In what form

A

Pancreatic duct cells in the form of bicarbonate rich solution

265
Q

How do the PNS and SNS affect pancreatic secretion

A

PNS: stimulate
SNS: reduce, via vasoconstriction

266
Q

How is each digestive phase controlled in relation to the pancreas

A

Cephalic: feed forward control
Gastric: vagovagal and local neural reflexes
Intestinal: pH <4.5 in duodenum and jejunum

267
Q

Discuss the intestinal phase of digestion in relation to pancreatic secretion

A

Much high levels of secretion compared to other phases, mainly due to secretin
Secretin is a potent stimulator of bicarbonate and wager secretion from pancreatic duct cells

268
Q

What is the main stimulus for CCK release in the duodenum

What does CCK do here

A

The presence of fat digestion products

Stimulates enzyme secretion from acinar cells and potentiates the effect of secretin (some effects may be indirect via vagovagal reflexes)

269
Q

How do ACh, CCK, secretin, and VIP affect pancreatic cells

A

ACh and CCK: increase intracellular [Ca2+]
Secretin and VIP: increase cAMP

Potentiation is possible

270
Q

What does cAMP do in both acinar and duct cells?

What channels is specifically affected?

A

Open luminal chloride channels, increasing secretion

CFTR

271
Q

What is the CFTR

A

Cystic fibrosis transmembrane conductance regulator

272
Q

What is the most common form of cystic fibrosis

A

Impaired electrolyte and water secretion into duct system
Clogged guts lead to severe maldigestion and nutrient deficiency
Pancreatic damage results from the blockage combined with premature activation of proteolytic enzymes

273
Q

What secretes NaCl in the intestines

What is the mechanism of this secretion

A

Crypts of Lieberkühn

CFTR on apical membrane is enhanced by cAMP, increasing Cl- secretion

274
Q

What causes cholera

What does cholera toxin result in

What does this ultimately lead to

A

The bacterium Vibrio cholerae

Results in permanently high [cAMP] leading to excessive Cl- secretion, with Na+ and water following.

Potentially life threatening diarrhoea

275
Q

How long is the human small intestine in vivo

How long does it take chyme to pass through it

A

3-5m

2-5 hours

276
Q

What controls small intestine motility

A

Slow wave activity

277
Q

How does the rate of slow wave activity change from the duodenum to the ileum

A

12 per min in the duodenum

8 per min in the terminal ileum

278
Q

What is required of the slow wave for contraction

A

The slow waves are large enough to generate action potentials

279
Q

What is the most common form of motility in the small intestine

Describe the propulsion of this movement

A

Segmentation

Weakly propulsive

280
Q

Peristalsis usually involves the entire small intestine at once. True or false?

A

False

Peristalsis usually involves only a short segment at a time

281
Q

What increases peristaltic activity in the small intestine

A

Stretch of the gut wall

282
Q

Where does the terminal ileum empty into and at what point

A

Into the large intestine at the junction of the caecum and colon - the ileocaecal valve

283
Q

What is the ileocaecal valve

A

The projecting lips of the terminal ileum at the junction of the caecum and the colon

284
Q

What reduces movement through the ileocaecal valve

What is the smooth muscle here called

A

High pressure in the colon and the colonoileal reflex

The ileocaecal sphincter

285
Q

What happens at the junction of the small and large intestine when the terminal ileum is distended

A

A peristaltic reflex coordinated by the ENA pushes the contents through the ileocaecal valve

286
Q

What is the gastroileal reflex

A

When a full stomach signals for ileal motility to be enhanced

287
Q

What does the colonoileal reflex do

A

Inhibits movement through the ileocaecal sphincter when the colon is full

288
Q

What are the nutrients absorbed everyday on an average diet

A 
300g carbohydrate 
100g fat
75g amino acids
75g ions
9L water
289
Q

How is the surface area of the small intestine increased

What is the total increase

A

Folds of Kerckring: 3x increase
Villi: 10x increase
Microvilli: 20x increase

600x increase

290
Q

What is the total surface area of the small intestine

A

250-400m^2

291
Q

What forms the brush border in the small intestine

A

The microvilli in the epithelial cells

292
Q

What do the crypts of Lieberkühn in the small intestine do

A

They are between villi and secrete fluid as well as containing stem cells for the replacement of desquamated epithelial cells

293
Q

How often is the entire epithelium of the small intestine replaced

A

Every 3-6 days

294
Q

How much fluid does the small intestine secrete everyday

How does the volume pancreatic and biliary secretions compare

A

Up to 2 litre

Small intestine secretion is matched in volume by pancreatic and biliary secretions

295
Q

What does acid in the stomach do to protein

A

Helps denature it, rendering it vulnerable to attack

296
Q

How much of protein digestion is contributed to by pepsins

What do they digest in particular

A

15%

Collagen

297
Q

What primarily converts trypsinogen to trypsin

Where is this converter found

What else can do this conversion

A

Enteropeptidase

On the brush border of the upper small intestine

Trypsin itself can activate trypsinogen

298
Q

What pancreatic proteases can trypsin activate

What do this molecules do

A

Trypsinogen
Chymotrypsin
Elastase
Carboxypeptidases

Digest proteins to peptides

299
Q

How are peptides digested

A

By brush border peptidases

300
Q

Where are brush border peptidases found

A

On the apical membranes of epithelial cells in the upper small intestine

301
Q

How are the products of protein digestion taken up

A

Facilitated diffusion or secondary active transport into the cells

302
Q

What happens to peptides once they are taken up by the small intestine cells

A

Peptides are further digested into amino acids which are then released from the cell by facilitated diffusion or secondary active transport

303
Q

What happens to the protein digestion product glutamine after the protein is fully digested?

A

Glutamine is oxidised for energy within the rapidly dividing intestinal cells themselves

304
Q

What is percentage of carbohydrates in the human diet is starch

A

50%

305
Q

What does amylase do to starch

What does this produce

A

Cleaves the internal α-1,4 bonds but cannot cleave the α-1,6 branching links

Smaller chains of glucose: oligosaccharides (mostly 2 or 3 units long) and α-limit dextrins

306
Q

What are α limit dextrins

A

Smaller chains of glucose, severed from starch, which contain the branch points that amylase cannot cleave

307
Q

What do you call a chain of 2 glucose molecules

A

Maltose

308
Q

Where is carbohydrate digestion completed

A

The brush border of the duodenum and jejunum

309
Q

What breaks down α-1,4 bonds in oligosaccharides?

What about the α-1,6 bonds

A

Glucoamylase

α-dextrinase

310
Q

What does lactase do

A

Digests lactose, forming glucose and galactose

311
Q

What does sucrase do in the small intestine

A

Digests sucrose, forming glucose and fructose

312
Q

What does trehalase do in digestion

A

Trehalose

313
Q

How is galactose taken up in the small intestine

What else is absorbed here

Where is this found exactly

A

SGLT-1

Glucose

The apical membrane of the epithelial cells in the duodenum and jejunum villi

314
Q

What is fructose taken up by in digestion

What can happen to it when it enters the cell

A

GLUT5

Some can be converted to glucose

315
Q

How is fructose exported from the small intestine cells

A

Via GLUT2 on the basolateral membrane

316
Q

Where is sodium absorption highest

Why here?

A

In the small intestine

The movement down its electrochemical gradient can be coupled to the movement of monosaccharides and amino acids

317
Q

In which transporter is the movement of sodium down its electrochemical gradient is coupled to the movement of monosaccharides ?

A

SGLT-1

318
Q

What are the 3 sodium transporters in the intestines

A

Na+/H+ antiporter

ENaC

SGLT1

319
Q

Where is ENaC found in the gut

A

In the colon

320
Q

Describe potassium digestion in the small intestine

A

K+ becomes concentrated as water is absorbed, providing a driving force for para cellular uptake by the small intestine

321
Q

K+ movement in the colon is into the cells. True or false?

A

False

There is a net secretion of K+ from the colon via apical potassium channels

322
Q

How is chloride absorbed in the gut

Where

A

Via para cellular pathways and by exchange with bicarbonate

Throughout the digestive tract

323
Q

How does water enter the digestive tract

A

Through ingesta (2L/day) and gastrointestinal secretions (7L/day)

324
Q

How does water enter the digestive tract through gastrointestinal secretions

A

From saliva, stomach, pancreas, bile and crypts

325
Q

How much of the water that enters the digestive tract is absorbed where

A

7.5L by the small intestine

1400ml by the colon

326
Q

What is the key place of water absorption in the small intestine

A

Ileum

327
Q

How much of the water that enters the digestive tract is lost in faeces

A

100ml

328
Q

What is reserve capacity

A

The gut’s ability to contain 2-3x the amount of water it usually does

329
Q

What is the standing gradient model

A

Sodium is pumped into the intracellular clefts by the Na pumps, which are concentrated around the edges of the basolateral membrane.
Anions follow, creating a solute concentration gradient, which is highest near the tight junctions.
This concentration gradient decreases towards the open end where it becomes equal to the concentration in the bulk phase
The high concentration at the top draw water in from the cells and from the lumen via leaky tight junctions, putting pressure on the clefts.
The water and salts flow into the capillaries a

330
Q

Why is absorption in the small intestine isosmotic

A

The small intestine epithelium is leaky

331
Q

Why is there a larger osmotic gradient in the colon

A

The tight junctions between cells are tighter which limits back diffusion of ions

332
Q

How is calcium and iron availability reduce in digestion

How is availability improved

A

They bind to other dietary constituents to yield insoluble salts

Gastric acid increases solubility while Vit C in the stomach helps reduce insoluble Fe 3+ to Fe2+

333
Q

When is paracellular calcium uptake important

A

If calcium intake is high

334
Q

Why may paracellular uptake of calcium not be important even if calcium uptake is high

A

If the active form of Vit D3 can up regulate the expression of proteins for trans cellular uptake (eg calbindin)

335
Q

How is Fe3+ reduced in the duodenum

How is the Fe2+ produced taken up

A

Iron reductase on the duodenal brush border

Via the DMT1 or by haem

336
Q

How does iron leave the duodenal cell

A

Ferroportin

337
Q

How does iron travel in the blood (not in haem)

A

Bound it transferrin

338
Q

What does hepicidin do to iron

Where is hepicidin produced

A

Reduces efflux of iron and excess iron is trapped in the cell, bound to ferritin

The liver

339
Q

What happens to excess iron when it is trapped in the duodenal cell under the action of hepicidin

A

Binds to ferritin and is lost when the epithelial cell is shed

340
Q

Why might we want to reduce iron availability

How do we do this

A

Bacteria need iron to grow so this mechanism is used to fight infection

Hepicidin production is increased in response to inflammation, reducing circulating iron levels

341
Q

What are the fat soluble vitamins

A

A
D3
E
K

342
Q

How are fat soluble vitamins absorbed

A

In a similar way to fat and transported mainly in lymph

343
Q

How are water soluble vitamins taken up

A

Mostly in the small intestine via active transport or diffusion

344
Q

How is B12 absorbed

How does it travel round the body

A

Bound to intrinsic factor it is absorbed via Receptor mediated endocytosis in the ileum

In the blood, bound to transcobalamin II

345
Q

What is the liver divided into

A

Lobules

346
Q

How big are lobules

A

Several mm long and 2 mm in diameter

347
Q

Where are the portal triads

What are the portal triads composed of

A

Between hepatic lobules

A branch of the hepatic portal vein, a branch of the hepatic artery and a branch of the bile duct

348
Q

What happens to mixed blood from the hepatic artery and portal vein

A

It drains through hepatic sinusoids towards the central vein, which empties into the hepatic vein

349
Q

What like the hepatic sinusoids

A

Rows of hepatocytes

350
Q

What are bile canaliculi

A

Tiny channels which drain bile produced by the hepatocytes towards the branches of the bile duct in the portal triads

351
Q

How does blood flow in the liver’s lobules in relation to blood

A

Bile flows countercurrent to blood

352
Q

Give 6 functions of the liver

A
  1. Metabolism (carbohydrate, protein, lipid)
  2. Bile formation
  3. Storage of vitamins and iron
  4. Destruction and detoxification of hormones, drugs and toxins
  5. Filtration of blood
  6. Blood reservoir
353
Q

What kind of metabolism in the liver includes cholesterol synthesis and excretion in bile

A

Lipid metabolism

354
Q

True or false: the liver only stores fat soluble vitamins

A

False

Also stores B12 (water soluble)

355
Q

What does the first pass metabolism of toxins ensure

A

Ensures they do not reach the rest of the circulation

356
Q

How does the liver help excrete fat soluble compounds

A

They are made more water soluble and are thus more readily excreted by the kidney by conjugation

357
Q

Name a substance the liver might conjugate a fat soluble molecule with to make it more water soluble

A

Glucuronic acid

358
Q

What is the key role of the lover’s filtration of the blood?

A

Removal of effete RBCs and any gut bacteria which have entered the hepatic portal vein

359
Q

How can the liver supply blood to the circulation

A

The liver is a blood reservoir and venoconstriction can empty more blood into the circulation

360
Q

How does the liver take up monosaccharides

What happens to them

A

Facilitated diffusion via GLUT2

They can be metabolised directly or inter converted

361
Q

What can the liver converted glucose to for storage

Where is it stored? How much?

How long can this supply the body for?

A

Glycogen

Stored in liver (100g) and muscle cells (400g)

24 hours

362
Q

Can all glycogen be exported?

A

No - the glucose from liver glycogen can be released into the blood but muscle cannot directly export glucose

363
Q

What happens to excess glucose

A

It is converted to triglycerides by the liver, exported as lipoproteins and stored as fat in adipocytes

364
Q

If carbohydrate stores are low, how can new glucose be made?

A

From lactate, amino acids (eg alanine and glycerol) vis gluconeogenesis in the liver

365
Q

Can long chain fatty acids in triglycerides be made into glucose

What about propionate (a short chain fatty acid)

A

No

Yes - ruminants rely on this

366
Q

How can intracellular proteins be decomposed

What then happens to them

A

Via lysosomal enzymes

Returned as amino acids to the blood

367
Q

How are extracellular proteins digested

A

By macrophages

368
Q

Most amino acids are recycled. What happens to the rest?

A

30-50g per day are broken down to provide energy

369
Q

What does transamination allow

A

The liver to interconvert amino acids, pyruvate, and TCA cycle intermediates

370
Q

Which amino acids must be synthesised and which must enter in our diet

A

Non essential - can be synthesised

Essential- must be included in the diet

371
Q

What does it mean if an amino acid is conditionally essential

A

We may not be able to make them fast enough at certain times eg as we are growing as a child

372
Q

What happens to excess amino acids

A

Either oxidised directly for energy or converted to glucose or ketone bodies

Urea and glutamine are produced and exported

373
Q

What does bile contain and in what proportions

A

Bile acid: 65% dry mass of bile
Phospholipids: 20%
Cholesterol: 4%
Bile pigment: 0.3%

374
Q

What are the 3 roles of bile

A

Promote fat absorption
Excrete waste
Protect

375
Q

What products in bile promote fat absorption

A

Bile acids are surfactants and they are used with phospholipids

These normally conjugate with glycine or taurine to increase solubility and are found as salts of cations (bile salts)

376
Q

How are primary bile acids made

What about secondary bile acids

A

From cholesterol in the liver

Primary acid salts can be converted to secondary bile acids by gut bacteria

377
Q

How does bile aid excretion

A

Bile is the primary means of cholesterol excretion (directly or I the form of bile acids) when synthesis exceeds requirements

Excess heavy metals (including copper and cadmium) are also secreted in bile

378
Q

3 things in bile that help it act as a protector

A

IgA
Mucus
Tocopherol

379
Q

What is the role of the gall bladder

A

To collect and concentrate bile before expulsion in to the digestive tract during a meal

380
Q

Where is the sphincter of Oddi

What happens to it between meals

A

At the entrance of the duodenum from the bile duct

It is contracted and bile is diverted to build in the gall bladder

381
Q

What happens to the gall bladder during a meal

A

CCK promotes gall bladder contraction and relaxation of the sphincter of Oddi emptying bile into the duodenum

382
Q

Where and how are bile acids taken up

How many are lost each day in faeces

A

In the terminal ileum by secondary active transport in the epithelium

Or

Absorbed passively by the colon

5% lost each day

383
Q

How do bile acids return to the liver

A

HPV

384
Q

Where can secondary bile acids be converted back into primary

What then happens to both primary and secondary bile acids

A

In the hepatocytes

Re-secreted into the bile canaliculi

385
Q

The bile acid pool circles once during a meal. True or false?

A

False

Thanks to the enterohepatic circulation, the bile acid pool recirculates several times during a meal

386
Q

Why is inhibition of bile acid uptake used to lower cholesterol levels

A

Bile acids are originally made from cholesterol so more is lost bile (and therefore more cholesterol) is excreted

387
Q

What colour is bilirubin

Where is it made

A

Yellow

Spleen
Bone marrow
Liver

388
Q

What happens to bilirubin when it is made

A

Travels in the blood, bound to albumin, and is taken up by the liver

389
Q

What happens to bilirubin when it reaches the liver

A

It is rendered soluble by conjugation with glucuronic acid before excretion into bile

390
Q

What happens to bilirubin in the bile

A

It is broken down to urobilinogen by bacteria in the ileum and colon

391
Q

What happens to urobilinogen

A

Some is reabsorbed into blood and re-secreted in bile or secreted in urine

The rest is lost in faeces

392
Q

What happens to urobilinogen in urine

A

It is oxidised slowly to urobilin when exposed to air

393
Q

What colour is urobilin

A

Yellow

394
Q

What happens to urobilinogen in the gut e

A

Some converted to urobilin

And some converted to stercobilin

395
Q

What is the colour of stercobilin

A

Brown

396
Q

True or false:

Bile salts are amphipatic

A

True

The hydrophobic domain binds to surface of a fat globule While hydrophilic domains face outward, stabilising the complex

397
Q

What aids the detergent action of bile salts

A

Phospholipids and cholesterol

398
Q

What does the detergent action of bile acids do to dietary triglycerides and lipids in the duodenum

Why do they do this

A

Emulsifies them into tiny emulsion droplets

Increase surface area for lipase attack

399
Q

How big a lipid emulsion droplets

A

1μm in diameter

400
Q

What is the helper protein of pancreatic lipase

A

Collapse

401
Q

What do pancreatic lipase and colipase do

A

Hydrolyse triglycerides within an emulsion droplet to form 2 free fatty acids and one 2-monoglyceride

402
Q

What do pancreatic enzymes other than pancreatic lipase do to the fatty acids from cholesterol esters and phospholipids

A

Remove them

403
Q

What does the action of lipases eventually result in

What is usually mixed with this

A

Mixed micelles

More bile salts

404
Q

What are mixed micelles

A

Tiny aggregates (5nm in diameter) of long chain fatty acids, monoglycerides, phospholipids and cholesterol

405
Q

What do mixed micelles do

A

Ferry the products of fat digestion to the brush border, keeping the solution there saturated with lipid digestion products

406
Q

What happened to the lipid digestion products at the brush border

A

They enter the epithelial cells either by diffusion or active transport

407
Q

Where is dietary fat mostly absorbed

A

The end of the ileum

408
Q

How does cholesterol enter the enterocytes

How can this absorption be reduced

A

Via special transporters

By plant sterols

409
Q

How do plant sterols reduce cholesterol absorption

A

They displace cholesterol from mixed micelles but the sterols are then pumped out of enterocytes

410
Q

Do fat soluble vitamins enter mixed micelles

A

Yes and then are absorbed by diffusion

411
Q

How are fat digestion products and cholesterol delivered to the endoplasmic reticulum

What happens to them inside the ER

A

They bind to fatty acid binding proteins (FABP) within epithelial cells of the small intestine

Converted back to triglycerides

412
Q

How are chylomicrons made

A

Triglycerides combined apolipoproteins, phospholipids and cholesterol

413
Q

What type of particle is a chylomicron

A

A lipoprotein

414
Q

Once the chylomicrons are created, where do they go?

A

To the Golgi apparatus and are released via exocytosis to enter the lacteals of the villi

415
Q

How do the chylomicrons within the lymph enter the venous circulation

A

Via the thoracic duct

416
Q

What catalyses the hydrolysis of the triglycerides within the chylomicrons

Where is it found

What happens to the FFAs produced

What happens to the rest of the chylomicron?

A

Lipoprotein lipase

Bound to capillary walls in tissues eg muscle, fat and lactating mammary glands

Transported across the endothelium and into cells where they can be resynthesised into triglycerides

Taken up by the liver

417
Q

Where do most dietary triglycerides end up

What happens when blood sugar is low

A

In adipocytes

Some Triglycerides are hydrolysed and FFAs are released

418
Q

What process allows FFAs to be used in most cells for energy

Which cells can they not be used for energy in

A

β-oxidation

The brain

419
Q

What are LVDLs

When are they released
From where
Why

A

Very Low Density Lipoproteins

Secreted by the liver when fasting as a means of if exporting triglycerides and hepatic cholesterol to tissues

420
Q

Like other lipoproteins and chylomicrons, What do VLDLs contain other than triglycerides and cholesterol?

A

Phospholipids and apolipoproteins

421
Q

Name the ketoacids that are siphoned off from products of oxidation of lipids in the liver

What else can be produced

What are these 3 products known as

A

Acetoacetate
β-hydroxybutyrate

Acetone

Ketone bodies

422
Q

How much of the brain’s energy can be derived from ketone bodies?

How long would it take for it to rach this percentage?

A

75% of its energy

Over the course of several weeks

423
Q

If we have enough ketone bodies, the brain has no requirement for glucose. True or false?

A

False

Ketone bodies can only account for 75% of the brain’s energy

424
Q

How might you recognise someone with ketosis?

A

Bad breath as the acetone is blown off from the lungs

425
Q

How long is the large intestine

A

1.5m

426
Q

How is the longitudinal muscle of the large intestine arranged

A

Into 3 bands (the taeniae coli) running through length of the colon up to the rectum

427
Q

What are the non-permanent division in the large intestine calls

A

The haustra

428
Q

How do the haustra arise

A

From the contractions of circular smooth muscle

429
Q

What type of villi exist in the large intestine?

A

NONE

THERE ARE NO VILLI IN THE LARGE INTESTINE

430
Q

How does the large intestine increase surface area?

A

It is internally folded

431
Q

What is the key role of the proximal large intestine

A

Water and ion absorption

432
Q

What does the transverse colon do

A

Stores faeces

433
Q

3 key roles of the large intestine

A

To store, mix and process contents
To expose contents to microbes and absorb nutrients from microbial fermentation
To expel waste as faeces in a controlled manner

434
Q

How are slow waves generated in the large intestine and at what rate?

A

ICCs within circular muscle generate slow waves at 3-6 per min

435
Q

How can large intestine slow wave duration be extended

Why

A

ACh

ACh allows slow waves to elicit contractions of circular muscle in the absence action potentials

436
Q

The longitudinal muscle of the large intestine requires action potentials to contraction. True or false?

A

True

437
Q

What is transmit time usually through the stomach and small intestine

What about the large intestine

A

Under 12 hours

May be 1-2 days
The large intestine accounts for 90% of total transit time

438
Q

Why is colonic transit time so long

What is the purpose

A

Colonic movements are low amplitude contractions which propel contents in a retrograde direction

To allow time for fluid absorption

439
Q

What are the retrograde movements of the colon driven and modulated by?

A

Driven by slow waves

Modulated by autonomic input

440
Q

How is the contents of the colon moved onward?

A

By High Amplitude Propagating Contractions (HAPCs) which occur periodically

441
Q

What are HAPCs also called

A

Mass movements

442
Q

What are HAPCs

How far do they move contents

What occurs to the haustra

A

Periodic waves of prolonged contractions

30cm

HAPCs are associated with the relaxation of te haustra

443
Q

When do mass movements occur and which reflex is associated?

A

After a meal, promoted by the gastrocolic reflex

444
Q

What is the internal anal sphincter

A

A thickening of the circular smooth muscle just inside the anus

445
Q

How is the internal anal sphincter controlled

A

It has its own myogenic tone which is modulated by the ANS

446
Q

What kind of muscle is the external anal sphincter

What controls it

A

Striated

Pudendal nerves

447
Q

What is usual about the external anal sphincter muscle

A

Despite being skeletal muscle it is tonically contracted

448
Q

What causes the resting tone of the external anal sphincter to rise

A

Any increase in intra-abdominal pressure other than when defaecating

449
Q

True or false: the rectum is usually empty.

A

Yes but it can be filled by mass movement from the sigmoid colon

450
Q

What happens when to rectum is filled with contents from the sigmoid colon? (5 steps)

A

Rectal sensory nerves signal to the sacral spine, which responds via the ANS in the pelvic nerves. This results in highly propulsive movements

The internal anal sphincter relaxes

The external anal sphincter may be voluntarily relaxed

Relaxation of pelvic floor muscles lowers the anus, straightening the rectal angle

Defaecation is aided by the Valsalva movement

451
Q

What causes Hirschsprung’s disease?

A

It is a congenital disease whereby the ENS ganglion cells are absent in the descending colon And internal anal sphincter

452
Q

What does Hirschsprung’s disease cause

What is the symptom called

A

Reflex relaxation of rectum and internal anal sphincter cannot occur as the rectum fills during mass movements.

This dilates the colon to a large size and may be perforated (congenital megacolon)

453
Q

How much alkaline fluid and mucus is secreted each day

A

200ml

454
Q

What does the consistency of stool reflect ?

A

The balance between overall GI secretion, tendency for the gut to hold water osmotically, and absorption

455
Q

What may increases overall GI secretion be prompted by

A

Irritation

456
Q

What can compact faeces be caused by

Why does this cause compact faeces

A

Decreases motility

It extends time for absorption

457
Q

How what are the effects of stimulation of opioid receptors in the gut?

Name an exogenous drug that stimulates these receptors

A

When stimulated by endogenous transmitters, propulsion is decreased, secretion is decreased, and sphincter tone is increased

Loperamide

458
Q

Name an endogenous transmitter that stimulates opioid receptors in the GI tract

A

β-endorphins

459
Q

How much bacteria is there in the small and large intestine respectively

When is this mixture established

A

Small: 10^4 per gram of digesta
Large: 10^11-12 per gram of digesta

After birth gradually

460
Q

Name 3 examples of colonic organism species

A

Bacteroides
Bifidobacterium
Eubacteria

461
Q

Most colonic organisms are aerobic. True or false?

A

False

They are strictly anaerobic

462
Q

How much of colonic organisms are escherichia coli

Are these aerobic

A

1%

No they are anaerobic

463
Q

Name 3 organisms that are found in the gut that are not bacterium

A

Yeasts
Non pathogenic protozoa
Archaea

464
Q

What do bacteria do to carbohydrates that reach the colon?

A

Metabolise it to produces volatile fatty acids

465
Q

What do VFAs represent for colonic cells

A

An energy source

This is the colonic salvage of energy which would otherwise be lost

466
Q

What vitamins do intestinal flora produce

A

K and B group

467
Q

What is dietary fibre made of

A

Cellulose and other plant cell wall components that resist hydrolysis

468
Q

4 things that a high fibre diet is good for

A

Provide a substrate for te metabolism of beneficial gut bacteria

Relieve constipation; prevent/ relieve haemorrhoids

Promote satiety

Protect against bowel cancer

469
Q

How can the human digestive system break down cellulose

Therefore is cellulose digestion very important

A

Colonic bacteria are efficient at it

No cellulose digestion is of negligible importance

470
Q

Where may VFAs account for up to 10% of caloric intake

A

In societies which eat poor quality, high fibre diets

471
Q

How much urea passes through the colon

What happens to it here

A

About 20% of the urea synthesised everyday

It is metabolised by bacteria

472
Q

Why do lactose intolerant people get gas and diarrhoea if they ingest lactose?

A

No lactase present so lactose is not digested
When it reaches the colon, bacteria thrive on it, producing metabolites which contribute to osmotic water retention, diarrhoea and excess gas

473
Q

What is the test for lactose intolerance

What is the basis for this

A

The breath hydrogen test

The excess gas produced from bacteria who have metabolised lactose in the colon contains hydrogen. Some hydrogen enters the blood and eventually the alveoli to be exhaled

474
Q

When might we lose gut bacteria

A

After diarrhoea or a course of antibiotics

475
Q

What sprouts from the small caecum of humans

A

Vermiform appendix

476
Q

What is in the mucosal walls of the appendix

What is the point of this

A

Gut associated lymphoid tissue (GALT)

Local defence against infection and might assist with maturation of B lymphocytes and production of of IgA antibodies

477
Q

What might appendices be used for?

A

A store of beneficial microbes, used to re-inoculate the rest of the gut following diarrhoea

478
Q

What are Helminths

A

Roundworms, flukes, and tapeworms

479
Q

Where do Helminths live

A

In human intestines in 1/3 of the population especially poorer, warmer countries

480
Q

What is flatus

What does it contribute to

A

Gas in the digestive tract

Borborygmi

481
Q

What is the gas composition of flatus

A 
N2=50%
Small amount of swallow O2
H2=25%
CO2=15%
Methane=10%
482
Q

Which gases In flatus come from colonic microbes

A

Methane
H2
CO2

483
Q

What do archeon produce

A

Methane

484
Q

How do methanobrevibacter smithii contribute to gases in flatus

A

They reduce CO2 to CH4 using H2

485
Q

What decreases flatulence

But what else do they do

A

Sulphate reducing bacteria as they inhibit methane production

Produce hydrogen sulphide

486
Q

What contributes to the odour of flatulence

A 
Hydrogen sulphide
Methyl sulphides 
Ammonia
Indole
Skatole
Volatile amines
VFAs
487
Q

How much faeces are produced everyday

How much is water

A

120g

75%

488
Q

What constitutes faeces

A 
75% water
40% bacteria
15% fat
2.5% protein
15% inorganic matter 
And the rest is indigestible fibre
489
Q

What colours faeces and gives it its smell?

A

Bile pigment - sterocobilin

Methyl sulphides

490
Q

What causes Chagas’ disease

Where is this common

A

Trypanosoma cruzi

Rural Latin America

491
Q

How many nephrons in the ENS

A

500 million

492
Q

What part of the ANS to the ENS was considered to be parasympathetic but is not any more

A

Sacral outflow to the gut

493
Q

Give examples of paracrine transmission(3)

Where are they produced and what is their action?

A

Histamine (from ECL cells within gastric glands to increase HCl secretion from gastric glands )

Somatostatin (released from D cells and inhibits parietal cells)

Prostaglandins (promote bicarbonate and mucus production )

494
Q

Who discovered secretin

A

Ernest Starling

495
Q

What is the etymology of cholecystokinin

A

Chole = bile

Cysto = sac

Kinin = move

(Greek)

496
Q

Who discovered the ICCs

A

Santiago Ramón y Cajal

497
Q

What is xerostomia

A

Dry mouth often caused by hypo function of the salivary glands

498
Q

What does lysozyme do

A

Prevents bacterial infection by attacking the cell wall

499
Q

What does lactoferrin do

A

Apart from its main biological function, namely binding and transport of iron ions, lactoferrin also has antibacterial, antiviral, antiparasitic, catalytic, anti-cancer, and anti-allergic functions and properties.

It reduces iron availability in the mouth to combat bacterial growth

500
Q

Etymology of acinus

A

Latin for kernel

501
Q

What is the purpose of the upper oesophageal sphincter

A

To prevent air entering the oesophagus when breathing

To prevent reflux of oesophageal contents into the pharynx, guarding airway aspiration

502
Q

Why do we produce extra Saliva when vomiting

A

Vomit is highly acidic - saliva dilutes it and rinses the mouth

Saliva is also slightly alkaline so can help to raise the pH in the mouth

503
Q

What is rennet used to do

A

Coagulate milk into curds and whey this helping in the cheese making process

504
Q

What does a lack of intrinsic factor lead to

A

Pernicious anaemia and B12 deficiency

505
Q

Where are H1 factors found

A

In the brain (eg hippocampus, thalamus, posterior hypothalamus)

506
Q

What is Zollinger Ellison syndrome

A

A rare condition where tumours (gastrinomas) form in the pancreas or duodenum
These secrete large amounts of gastrin, increasing stomach acid secretion

507
Q

Which hormones regulate gastric emptying

A 
CCK
GIP
Glucagon
GLP-1 
PYY
508
Q

What is the nick name for secretin

A

Nature’s antacid

509
Q

What does the ileocaecal valve do

A

Controls passage of digested food from the small intestine into the large

510
Q

What part of the gut is destroyed by coeliac disease

A

Small intestine

511
Q

What class of drug disrupts hepatic cholesterol synthesis

A

Statins

512
Q

What are Kupffer cells

A

Stellate macrophages in the liver

They remove senescent cells and particulates including bacteria

513
Q

Where does gluconeogenesis occur

A

In the liver and the cortex of the kidneys

514
Q

What is the main bile pigment

A

Bilirubin

515
Q

What can bile obstruction lead to

A

Jaundice
Light brown urine
Bilirubin build up

516
Q

What causes the makes on side of the bile salt hydrophilic

A

OH groups
Peptide bonds
Ionised acidic groups

517
Q

What is the etymology of haustra

A

Latin for bucket

518
Q

What is the etymology of taenia

A

Greek: “band”

519
Q

Describe the Valsalva manoeuvre

A

A forceful attempted exhalation against a closed airway

520
Q

What is the brand name of loperamide

When would you take it

A

Imodium

To decrease frequency of diarrhoea

521
Q

Name 3 VFAs

A

Acetate
Propionate
Butyrate

522
Q

How might you restore gut flora

A

Probiotics

Faecal transplant

523
Q

What does vermiform mean

A

Resembling a worm

524
Q

The duct cells reabsorb Na+ and secrete HCO3 - . Why?

A

HCO3- raises the pH of saliva

Reabsorption of Na+ allows regulation of volume as water follows salt

525
Q

Where does aldosterone act in the gut

A

Aldosterone promotes ion exchange in the salivary ducts as in the kidney

526
Q

Where would you find lipoprotein lipase

A

Capillary wall

527
Q

Describe protein absorption

A

Partially broken down by peptin and gastric acid

Trypsin is activated by enteropepsidase

Pancreatic enzymes (trypsin, chymotrypsin, elastase and carboxypeptidase) break it down to peptides

Peptides are further digested by brush border peptidases and products are absorbed by cell

Most amino acids are released to blood, glutamine remains in the cell to be broken down for energy

HOM (11 decks)

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