GI physiology Flashcards

1
Q

What are the four layers of the alimentary canal?

A

Mucosa
Submucosa
Muscularis externa
Serosa/adventitia

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2
Q

What is the parietal membrane of the peritoneal cavity attached to?

A

The muscle wall

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3
Q

What is the visceral membrane of the peritoneal cavity attached to?

A

The organs

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4
Q

How can organs be arranged in the peritoneal cavity?

A

Reteroperitoneal – Encased on only the anterior side, no movement

Intraperitoneal (peritonised) – Encased on all sides, little movement

Mesentery – attached to a mesentery, free movement

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5
Q

How does the blood supply the organs in the peritoneal cavity?

A

Through the mesentry and omenta

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6
Q

Which organs are retroperitoneal?

A
SAD PUCKER:
SVC/Aorta 
Adrenal glands 
Duodenum (2nd/3rd parts) 
Pancreas (other than tail) 
Ureters 
Colon (asc/desc) 
Kidneys 
Oesophagus 
Rectum
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7
Q

Which organs are intraperitoneal

A

SALTD SPRSS

Stomach 
Appendix 
Liver 
Transverse colon 
Duodenum 
Small intestines (jejunum, ileum and cecum) 
Pancreas (only the tail) 
Rectum (only upper third) 
Sigmoid 
Spleen
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8
Q

What forms the boundaries of the peritoneum?

A

Abdominal wall
Diaphragm
Pelvic floor
Lumber vertical column

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9
Q

What are the three parts of the embryonic development?

A

First phase – growth – cell division
2nd phase – morphogenesis – development of size and shape of organs
3rd phase – differentiation

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10
Q

What is gastulation?

A

Where bilaminar disc turns into trilaminar disc

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11
Q

When does the priomordial gut form?

A

4th week of human development

From endoderm lining yolk sca

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12
Q

What does the foregut become?

A
Pharynx + oesophagus (cranial end) 
Lungs 
Stomach 
Duodenum – proximal to opening of bile duct 
Liver + billary apparatus (distal end) 
Spleen 
Pancreas 
Celiac trunk
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13
Q

What does the midgut become?

A
distal part of duodenum 
jejunum 
ileum 
casecum 
appendix 
asc colon 
proximal 2/3rds of transverse colon
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14
Q

What does the hind gut become?

A
Distal 1/3rd transverse colon, 
desc colon, 
sigmoid colon, 
rectum 
upper part of anal canal 
Epithelium of urinary bladder + most of urethra 
Inferior mesenteric artery
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15
Q

How does the stomach develop?

A

The dorsal and venteral sides of the tubes expand rapidly, dorsal expanding faster so that when it rotates 90 degree (anterioposterly) one side is more curved than the other.
These are the Greater (from the dorsal) and Lesser ( ventral) curvatures.

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16
Q

How is the omental bursa formed?

A

Its rotation alters its position creating the omental bursa (smaller sac).
Small vacuoles break down part of the dorsal mesogastrium making it narrower

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17
Q

How does the duodenum develop?

A

Formed from caudal part of foregut and cranial part of midgut, it rotates with the stomach.
All sections bar the duodenum cap become retroperitoneal as the dorsal mesentery fuses with the peritoneum of the posterior abdominal wall.

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18
Q

What blood vessels supply the duodenum?

A

Coeliac trunk

Superior mesenteric arteries

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19
Q

How does the liver develop?

A
Liver primordium appears middle of 3rd week as an outgrowth in the distal end of the foregut 
Liver bud (hepatic diverticulum) grows into the septum transversum (mesodermal plate between pericardial cavity and yolk stalk)
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20
Q

How does the billary apparatus develop?

A

Connection between liver bud and foregut narrows to form bileduct.
Ventral outgrowth from bile duct forms gall bladder and cystic duct

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21
Q

How does the spleen develop?

A

End of 4th week mesenchymal condensation develops in the dorsal mesogastrium near body wall
During 5th week this mesenchyme differentiates to form spleen (a mesodermal derivative not endodermal dervivitive of gut tube)

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22
Q

What phases does the spleen go through?

A

Up to week 14 acts as haematopoietic organ
Week 15-17 spleen aquires its lobular shape and colonised by t lymphocytes
Week 23 B cell precursors arrive and spleen can start lymphoid function

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23
Q

How does the pancreas develop?

A

forms from two buds from the endodermal lining in the duodenum week 5
Dorsal pancreatic duct in dorsal mesentery, venteral near bile duct
As duodenum rotates, ventral bud moves to lie close to the dorsal bud
Ventral bud comes to lie behind and below the dorsal and then fuse
Main pancreatic duct from ventral duct plus distal part of dorsal duct
Proximal part of dorsal duct may form an accessory duct

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24
Q

What are the possible complications in the development of the pancreas?

A

Annular pancreas – If ventral bud fails to migrate around the duodenum correctly, it may cause duodenal stenosis
Pancreatic tissue may also form in other parts of foregut (accessory pancreatic tissue)

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25
Q

What is the early development of the gut tube?

A

There is a rapid elongation of gut tube/associated mesentery (primary intestinal loop)
Cephalic part becomes: distal duodenum, jejunum + proximal ileum
Caudal part becomes: distal ileum, caecum, appendix, asc colon, proximal 2/3rds of transverse colon
Both parts undergo rotation and physiological herniation

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26
Q

What is the initial rotation?

A

In the 6th week, the primary intestinal loop rotates 90 degrees anticlockwise around the axis of the superior mesenteric artery.
This results in the cranial part of the midgut being carried to the right.

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27
Q

What is physiological herniation, why is it necessary?

A

As it rotates, the gut tube herniates extraembryonic cavity in umbilical cord
It allows for the growth of the gut tube as liver growing quickly and liver taking up space

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28
Q

What allows for the retraction of the gut tube back into the peritoneal cavity?

A

During the 10th week abdominal cavity becomes relatively more spacious (due to growth, regression of kidneys and slower growth of liver)

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29
Q

How does the gut tube retract back into the peritoneal cavity?

A

Intestinal loops begin to move back in to the cavity.
Proximal part of the jejunum enters first towards the left side.
As the rest enter they are further to the right with the caecum being the last to re-enter
As it returns, a further rotation of 180 degrees anti-clockwise, moving the transverse colon in front of the duodenum.
It then continues to elongate

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30
Q

What abnormalities can occur wih the retraction of the gut tube?

A

Can either have abnormal rotation, leading the colon to the left, and all the small intestine to the right
Or, can be reversed

Can fail to retract – omphaloclele (Viscera covered by a layer of amnion)

Gastroschisis – herniation of abdominal contents directly through the body wall into amniotic cavity. Not covered by peritoneum of amnion
>Through weak area right of umbilicus (1/10000 births)

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31
Q

What are teh complications of an incomplete disintegration of the vitelline duct, how common is it?

A

2-4% of the population a small duct persists.
It leads to the formation of the Meckel’s diverticulum.
May form a fistula, vitelline cyst or a ligament.

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32
Q

What forms the lining of the bladder and urethra?

A

The endoderm of hindgut

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33
Q

How does the anal canal develop?

A

Terminal portion of hind gut joins with posterior part of cloaca (primitive anal canal)
Allantois (endoderm lined cavity with surface ectoderm at its ventral boundary) enters into anterior part of cloaca
Endoderm/ectoderm boundary is the cloacal membrane. Mesoderm (urorectal septum) separates the allantois and hindgut
These septa merge to cover yolksac and to surround the allantois

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34
Q

How do the anal canal and urethra separate?

A

The tip of urorectal septum lies close to the cloacal membrane
At the end of week 7 this ruptures, leaving an opening for the hindgut
Ectoderm of the anal canal proliferates closing at the caudal end
Week 9 it then reopens

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35
Q

What are the abnormalities associated with the hindgut/anal canal?

A

Urorectal fistula – anus to bladder system
Rectovaginal fistula – anal to vagina
Rectoanal atresia – thin tube to anus
Imperforate anus- (failure of anal membrane to break down - surgery)

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36
Q

What are the three layers of the mucosa?

A

Epithelium
Lamina propria
Muscularis mucosae

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37
Q

What type of epithelium lines the mouth, oesophagus and anal canal?

A

Stratified squamous (for protection)

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38
Q

What type of epithelium lines the stomach and intestines?

A

Simple columnar

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39
Q

What is the lamina propria?

A

Loose connective tissue

Comprised of glands, blood and lymph vessels

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40
Q

What is the muscularis mucosae?

A

A thin layer of smooth muscle

41
Q

What is the function of the epithelium?

A

Barrier separating lumen of alimentary canal from body
Synthesis and secretion of digestive enzymes, hormones, mucus
Absorbs products of digestion
Epithelium differs along length of gut tube  adaptation for function

42
Q

What is the function and makeup of the submucosa?

A

Thick, irregular connective tissue – supports the mucosa
Contians neurones, lymphatic vessels and blood vessels (for mucosa, muscularis externa, serosa)
Neurones form extensive networks – sub mucosal plexus (parasympathetic)
Submucosal glands in oesophagus and duodenum

43
Q

Describe the function of the serosa/adventitia, both inside and outside the peritoneal cavity.

A

The connective tissue outer layer of the alimentary canal
Outside – adventitia attaches oesophagus and rectum to surround structures
Inside – serosa surrounds stomach, small + large intestines

44
Q

What is the action of the different nervous systems on the GI tract?

A

Autonomic control – long (parasympathetic) and short (ENS) reflexes
Parasympathetic (vagus nerve) everything bar salivation (facial + glossopharyngeal cranial nerves)
>Stimulates the gut, increasing secretion and motility
Sympathetic (splenic nerve) is inhibitory of the gut (except salivation)
>So decreases secretion and motility

45
Q

What is the function of the muscularis externa?

A

Produces motility through peristalsis and segmentation

46
Q

How is the muscularis externa made up?

A

Two thick layers of smooth muscle
Inner circular muscle (constricts lumen), outer longitudinal (shortens tube)
Myenteric plexus between the two layers
Submucosal + myenteric plexus = enteric nervous system (independent control of gut function)

47
Q

What arteries supply the gut?

A

The descending abdominal aorta splits into:
Celiac trunk (splits into splenic, common hepatic and left gastric arteries)
Superior mesenteric artery
Inferior mesenteric artery

48
Q

What does the coeliac trunk supply?

A

Stomach
Small intestine
Pancreas
Liver

49
Q

What does the superior mesenteric artery/vein supply?

A

Small intestine
Caecum
Ascending colon
Transverse colon

50
Q

What does the inferior mesenteric artery/vein supply?

A

Descending colon
Sigmoid colon
Rectum

51
Q

What veins supply the gut?

A

IVC supplied by hepatic vein (form hepatic portal vein)

Four distributes – Gastric veins, splenic vein, superior/inferior mesenteric

52
Q

What does the splenic vein supply?

A

Spleen

Pancreas

53
Q

What are the three types of transport from the gut?

A

Transcellular
Vectoral transport
Paracellular

54
Q

What is transcellular transportation?

A

goes straight through the membrane passively both sides

55
Q

What is vectoral transportation?

A

Needs a carrier protein on at least once side of the cell

56
Q

What is paracellular transportation?

A

goes between the cells, like water

57
Q

How is glucose absorbed?

A

Glucose and sodium ions enter into the SGLT1 transporter
By active transport they enter the cell
The glucose then passively leaves the cell through the glut-2 transporter
Sodium then leaves via a na/K transporter into the blood
Remember SGLT1 with sodium glucose transporter 1

58
Q

How is fructose absorbed?

A

Passively through glut-5 into the cell

Passively through glut 2 into blood

59
Q

How are simple amino acids absorbed?

A

Like glucose, a NA + amino acid bind in a carrier protein (SAAT1)
Enters cell through active transport
The amino acid then passively leaves the cell through transporter
Sodium then leaves via a na/K transporter into the blood
Remember SAAT1 by sodium amino acid transporter1

60
Q

How are dipeptides absorbed?

A

Sodium enters through a receptor (NHE3) and is exchanged for H+
Hydrogen outside increases pH
The hydrogen, on leaving the cell, binds to a pepT1 transporter with the dipeptide
The dipeptide then passively leaves the cell via a transporter
Sodium then leaves via a na/K transporter into the blood

61
Q

What does emulsification require?

A

Mechanical disruption of large lipid droplets to small droplets
Smooth muscle contraction grinds/mixes luminal contents
Emulfication agent prevents droplets reforming in to large ones
>Bile salts +phosopholipids secreted in bile

62
Q

What are micelles made up of?

A

Bile salt
Monoglycerides
Fatty acids
Phospholipids

63
Q

How are fattya cids absorbed?

A

Diffusion across cells after the micelle has been broken down by the acidic conditions outside the epithelial cells
After entering the epithelial cells, monoglycerides enter sER, and reformed into triglycerides
Coated in amphipathic proteins (emulsified)
Transported out via vesicles into extracellular fluid
Chylomicrons pass into lacteals between endothelial cells

64
Q

How are vitamins absorbed?

A
Fat soluble (A,D,E,K) -  same path as fat
Water soluble (B groups, C, folic acid) – either passive or carrier proteins
Vitamin B12 – binds to intrinsic factor in stomach, absorbed by specific transport mechanism in distal ileum
>Deficiency leads to pernicious anaemia – failure for RBCs to mature
65
Q

How is iron absorbed?

A

Transported across membrane (via DMT1) into duodenal enterocytes
Unbound iron transported across serosal membrane into the blood
When the body has the iron it needs, the rest is stored with ferritin
Iron in the blood binds to transferrin
Ferritin expression regulated depending on the body’s iron status

66
Q

How is the voluntary phase of chewing controlled?

A

Through somatic nerves of mouth/jaw

67
Q

What is the chewing reflex?

A

Contraction of jaw muscle leads to food being pressed against gums, hard palate and tongue
This innervates mechanoreceptors which inhibit contraction og jaw muscles
Leads to reduced pressure, allowing for reflex to start

68
Q

What makes up saliva?

A

Water (99%)
Mucins
Electrolytes
Lysozyme

69
Q

What is the function of mucins?

A

They are a large protein component of saliva which act as lubricant
A-amylase also catalyses the breakdown of polysaccarides

70
Q

What is the function of lysozome?

A

It is bacterialcidal

>Acts by cleaving polysaccaride component of bacterial wall

71
Q

How is salivary secretion controlled?

A

Both parasympathetic and sympathetic both stimulatory
Parasympathetic – cranial nerves facial and glossopharyngeal
Reflex control – presence of food in mouth –> chemoreceptors/pressure receptors (walls of mouth/tongue)

72
Q

What does parasympathetic innervation of saliva lead to?

A

profuse watery salivary secretion

73
Q

What does sympathetic innervation of saliva lead to?

A

Small volume, viscous salivary secretion
High mucus content (a1 adrenoceptors)
High amylase content (b2 adrenoceptors)

74
Q

What are the phases of swallowing?

A

Oral
Pharyngeal
Oesophageal

75
Q

What is the pharyngeal phase of swallowing?

A

presence of bolus activates reflex contractions
Co-ordinated by swallowing centre (medulla)
Soft palate reflected backward and upwards to close of nasopharynx
As the bolus approaches the oesophagus, the upper oesophageal sphincter relaxes and epiglottis covers opening to larynx
UOS then contracts to prevent reflux

76
Q

What is the oesophageal phase of swallowing?

A

propulsion of bolus to stomach
Peristaltic wave sweeps along entire oesophagus, propelled ~10 secs
As it nears stomach, lower oesophageal sphincter relaxes and bolus enters
Vagal reflexes causes relaxation of the muscle around the gastric fundus and body so that volume can increase with no change in pressure.

77
Q

What are the functions of the stomach?

A

Temporary storage of digested material
Dissolve food particles and initiate digestive process
Control delivery of contents to small intestine
Sterilise ingested material
Produce intrinsic factor

78
Q

What are thehistological layers of the stomach?

A

Serosa = connective tissue outer layer
Muscularis externae = three layers: longitudinal (outer), circular (middle), oblique (inner)
Submucosa and mucosa folded (= rugae) when empty, relax as stomach fills
Lumenal surface = surface mucus cells –> gastric pits –> gastric glands –> mucus neck, parietal and chief cells

79
Q

What are the functional parts of the stomach, what do they do?

A

Fundus – storage
Body – storage, + production of: mucus, HCL, pepsinogen, intrinsic factor
Antrum – mixing/grinding, produces gastrin

80
Q

What do mucous neck cells produce?

A

Mucus

81
Q

What do chief cells produce?

A

pepsinogens

82
Q

What do parietal cells produce?

A

HCL

Intrinisc factors

83
Q

How do parietal cells produce HCl?

A

CO2 enters the cell, and combines with water to create carbonic acid – catalysed by carbonic anhydrase
Carbonic acid, splits into Hydrogen ions and bicarbonate
H+ exchanged for potassium with stomach lumen
Bicarbonate exchanged for Cl- from blood
The chloride ion passes through the cell, and creates acid in the lumen with water next to cell
The bicarbonate in the blood decreases the pH (more alkaline) for a while after a meal.

84
Q

What are the mechanisms that control HCl secretion?

A

Neurocrine (vagus/local reflex)
Paracrine (Histamine)
Endocrine (gastrin)

85
Q

What substance inhibits HCL secretion?

A

Prostaglandins

86
Q

What is the cephalic phase of gastric acid secretion?

A

Sight, smell, + taste of food innervates vagus nerve.
Through following mechanisms Parietal cells are stimulated:
Directly from ACh (released from vagus nerve)
From G cells’s gastrin
>Which are stimulated by ACh as well
By histamine produced by ECL cells
>Gastrin and ACh stimulate these to form histamine

87
Q

What is the gastric phase of gastric acid secretion?

A

Distention of stomach causes Vagus/enteric reflexes to release ACh
Peptides in lumen stimulates G cells to form gastrin
Gastrin/ACh causes ECL cells to release histamine
All three act on parietal cells

88
Q

What mechanisms in the cephalic phase inhibit gastric acid secretion?

A

stop eating,

>Leads to decrease in vagal activity

89
Q

What causes a decrease in gastric acid secretion in the gastric phase?

A

decrease in pH (HCl increase) causes decrease in gastrin

90
Q

What causes a decrease in gastric acid in the intestinal phase?

A

Acid in duodenum causes enterogastric (sphlanic reflex) and secretin release
Fat in duodenum causes GIP release
>Both cause decrease in gastrin secretion (therefore parietal stimulation of HCl)

91
Q

What are enterogastrones?

A

Hormones released from glands in duodenal mucosa – secretin, cholecystokinin (CCK), GIP
>Released in response to acid, hypertonic solutions, fatty acids or monoglycerides in duodenum
>Act collectively to prevent further acid build up
>Either inhibit gastric acid secretion, or reduce gastric emptying (inhibit motility of pyloric sphincter)

92
Q

How is pepsinogen secreted?

A

Pepsinogen secreted by chief cells
>(zymogen is the inactive precursor)
Low pH (<3) causes pepsinogen to turn to pepsin, and then pepsin acts as a catalyst leading to more pepsin
Zymogen storage prevents cellular digestion
Pepsins inactivated at neutral pH
Pepsin controls of secretion mirror HCl secretion

93
Q

What is the role of gastric mucosa?

A
Produced by surface epithelial and mucus neck cells
Has a cytoprotective role, here it protects mucosal surface from mechanical injury
Neutral pH (HCO3) protects against gastric acid corrosion and pepsin digestion
94
Q

What is intrinsic factor?

A

Only essential function of stomach, produced by parietal cells
Is required for vitamin B12 absorption
Intrinsic factor/ B12 complex absorped from ileum
Defect leads to pernicious anaemia (due to B12 deficiency)

95
Q

What is a probiotic?

A

A live organism which confers a health benefit

96
Q

What is a prebiotic?

A

A substrate used to host microorganisms giving a health benefit

97
Q

What is faecal microbial transplantation?

A

Faecal sample taken from healthy donor into recipient
Repopulates large intestine
Displaces C. Dff

98
Q

What is dysbiosis?

A

Where normal flora of gut is disrupted

99
Q

What protects the gut from pathogens?

A

Barrier effect (microbiota prevent colonisation of ingested pathogens)
Active competitive eclusion
Gut’s immune system