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Y1 Body system lecture notes year 1 > GI > Flashcards

GI Flashcards

1
Q

What are the major functions of the GI tract

A

Ingestion: occurs when materials enter digestive tract via the mouth

Mechanical processing: crushing, shearing, wetting, softening; makes materials easier to propel along digestive tract

Digestion: the chemical breakdown of food into small organic fragments for absorption by digestive epithelium

Secretion: the release of water, acids, enzymes, buffers and salts by epithelium of digestive tract or by glandular organs

Absorption: movement across digestive epithelium into interstitial fluid of digestive tract

Excretion: removal of indigestible material and waste products from bodily fluids

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2
Q

What is peristalsis

A

Smooth muscle contraction
Co-ordinated to move bolus forwards
Need relaxation of sphincters

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3
Q

What does the stomach do

A

Storage vessel
Churns food
Produces acid to start breakdown of food

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4
Q

What are the functions of the pancreas

A

Exocrine secretions aid digestion: discharged into intestine via pancreatic duct; Amylase, Lipase and trypsin; need alkaline medium for efficiency; produces bicarbonate

Endocrine secretion regulate carbohydrate metabolism: glucagon, insulin, gastrin, somatostatin

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5
Q

What is the function of the liver

A

Synthesis of bile
Helps to digest fats
Detoxification of blood from the GI tract
Metabolism of carbohydrates, proteins, fats
Manufacture proteins (clotting factors)
Storage of carbohydrates and fat-soluble vitamins

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6
Q

What are the functions of the small and large intestine

A

Large: water absorption (can survive without
Small: Major role in absorption (cannot survive without)

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7
Q

What are the stages of liver disease

A

Fatty liver -> liver fibrosis -> cirrhosis

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8
Q

What are the EAR, LRNI, RNI and safe intake in the guidelines for nutritional requirements

A

EAR: estimated average requirement, half the population usually need more and half less

LRNI: lower reference nutrient intake, sufficient for the few people who have low needs but not meeting the needs of 97.5% of population

RNI: reference nutrient intake, sufficient for about 97.5% of the population

Safe: Sufficient for almost everyone but not so large as to cause undesirable effects

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9
Q

What does energy expenditure depend on

A

Basic metabolic rate

Amount and intensity of physical activity

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10
Q

What are the essential amino acids

A

9 amino acids that cannot be synthesised by humans and must be obtained from diet

Methionine
Valine
Histidine
Leucine
Phenylalanine
Tryptophan
Isoleucine
Lysine
Threonine

Many Very Happy Little Pigs Try Iced Lemon Tea

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11
Q

What are the different types of fats and where are they found

A

Saturated: no double bond, found in meat and dairy
Monounsaturated: one double bond, found in olive and peanut oil
Polyunsaturated: more than 1 double bond, corn and sunflower oil
Trans: trans double bonds, cakes, biscuits and pastry

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12
Q

What are the different types of carbohydrates and where are they found

A

Polysaccharides: mainly starch
Disaccharides: mainly sucrose
Monosaccharide: mainly glucose and fructose
Non-starch polysaccharide: dietary fibre

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13
Q

What is a vitamin

A

Organic compounds required for normal metabolic function, which cannot be synthesised by the body

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14
Q

What are minerals

A

A naturally occurring inorganic compound

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15
Q

What are the key minerals needed by the body

A 
Iron
Zinc
Calcium
Magnesium
Iodine
Fluoride
Phosphate
Sodium
Potassium
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16
Q

Why may nutritional deficiencies arise

A

Inadequate intake:
Food availability
Food choices
Problems with eating

Inadequate absorption:
Problems with fat absorption affects fat soluble vitamins
Pernicious anaemia

Excess loss/increased requirements:
Iron deficiency anaemia
Folic acid deficiency

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17
Q

What is malnutrition

A

Inadequate or excess intake of protein, energy, and micronutrients scubas vitamins and minerals

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18
Q

What are current nutritional guidelines

A 
Starchy foods ~40% of energy intake
At least 5 portions of fruit and veg per day
Moderate amounts of protein-rich foods
Moderate amounts of milk and dairy
Less saturated fat, salt and sugar
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19
Q

What are current vitamin guidelines

A

Children should take vitamin A, D and C supplements

Pregnant women should take folic acid daily until week 12

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20
Q

What is the GI tract

A

Also called digestive tract or alimentary canal
Muscular tube lined by epithelium
Extends from oral cavity to anus, passing through pharynx, oesophagus, stomach, small and large intestines
About 8-9 meters long: Pharynx, oesophagus and stomach ~1m
Small bowel ~6m
Large bowel ~1.5m

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21
Q

What is the peritoneum

A

Parietal: Lines the abdominal cavity
Visceral: covers organs
Forms mesenteries, which suspend the organs, support them and keep them from tangling
Secretes peritoneal fluid, which provides lubrication and permits organs to move against each other without friction

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22
Q

What parts of the GI tract are supplied by each of the 3 unpaired arteries of the Aorta

A

Coeliac trunk: Foregut
Superior mesenteric artery: mid gut
Inferior mesenteric artery: hind gut

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23
Q

What is epithelia

A

Layers of polarised cells covering internal or external surfaces

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24
Q

What are glands

A

Structures the produce secretions

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25
Q

What is the Net flux

A 
Net flux (Jnet) = absorptive flux (Jabs)- secretory flux (Jsec)
Difference between the absorption and sectarian of molecules into and from the blood stream
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26
Q

What are the layers of the abdominal wall

A

Skin
Subcutaneous tissue (fat)
Muscle layers
Peritoneum

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27
Q

What are the three pairs of the muscles of the abdominal wall

A

External oblique
Internal oblique
Transversus abdominus

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28
Q

What is the line alba

A

A thick cartilaginous tendon which connects the abdominal wall muscles in the midline

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29
Q

What is an aponeurosis

A

A flat tendons sheet

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30
Q

What is the rectus abdominis

A

Long strap muscles which are divided into six muscle bays with small tendon interfaces between
Form the six pack

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31
Q

What are the function the abdominal muscles

A

Support for vertebrae
Protection
Aids with deification

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32
Q

What is the rectus sheeth

A

Aponeurosis formed from the layers of abdominal wall muscle

Fibrous compartment containing rectus abdominis, epigastric arteries and tips of thoracoabdominal nerves

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33
Q

How does the rectus sheeth above the umbilicus compare to that below

A

Above:
Anterior: external oblique aponeurosis, anterior layer of internal oblique aponeurosis
Posterior: Posterior layer of internal oblique aponeurosis, transversus abdominis and peritoneum

Below:
Anterior: external oblique aponeurosis, internal oblique aponeurosis, transversus abdominis
Posterior: peritoneum

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34
Q

What is the inguinal region

A

An area of the abdominal call that extends from the anterior superior ilia spine (ASIS) to the pubic tubercle
The inguinal can is found here

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35
Q

What is in the inguinal canal

A

Spermatic cord in the male and the round ligament in the female

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36
Q

What teeth are in our mouths

A 
Central incisors
Lateral incisors
Cuspid
1st Premolar
2nd Premolar
1st molar 
2nd molar 
3rd molar
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37
Q

What are the functions of the muscles of mastication (chewing)

A 
Close the jaw
Slide or rock lower jaw from side to side
Chewing involves mandibular: 
Elevation and depression
Protraction and retraction
Medial and lateral movement
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38
Q

What do the tongue and cheeks do

A

Move food across teeth

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39
Q

What are the functions of saliva

A 
Lubrication of mouth and food and cleaning:
serous fluid
mucus
Facilitation of taste
Protection against acid and bacteria:
antibacterial enzymes
bicarbonate 
calciumions
Digestion:
salivary amylase
lingual lipase
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40
Q

How is saliva production regulated

A 
Almost entirely due to neural control
Both parasympathetic (watery) and sympathetic (mucoid) activity increase secretion
Parasympathetic controlled by salivary centre in the brain stem, driven by: 
local stimuli (test and touch in mouth)
Central stimuli (smell and sight of food)
Learned reflex (think of Pavlov's dogs
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41
Q

What are the major salivary glands

A

Parotid gland
Tongue
Sublingual gland
Submandibular gland

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42
Q

What are the characteristics of the parotid gland

A

Largest salivary gland
Predominantly serous secretion
About 25% of salivary volume
Main source of salivary amylase and proline-rich proteins
Parasympathetic supply via CN IX
Sympathetic supply from superior cervical ganglion

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43
Q

What are the characteristics of the submandibular gland

A

Mixed serous and mucous secretion
About 70% of salivary volume
Main source of lysozyme and lactoperoxidase
Parasympathetic supply via CN VII
Sympathetic supply from superior cervical ganglion

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44
Q

What are the characteristics of the sublingual gland

A 
Predominantly mucous secretion
About 5 % of salivary volume
Main source of lingual lipase
Parasympathetic supply via CN VII
Sympathetic supply from superior cervical ganglion
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45
Q

What problems will patients with Sjogren’s syndrome present with, what is this syndrome and how is it treated

A

An autoimmune condition in which salivary and lacrimal glands are damaged

Dry eyes
Dry mouth
Difficulty speaking and swallowing
Sever dental disease
Other autoimmune issues
Artificial tears 
Acid sweets
Drink water
Careful dental care
May need steroids or immunosuppressants
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46
Q

What is Ptyalin

A

An a- Amylase
Can cut at a-1,4 sites of carbohydrates
pH optimum is about 7 and denatured at pH 4

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47
Q

What is lingual lipase

A

initial digestion of triglycerides
Cleave the outer fatty acids off triglycerides, leaving diacyl glycerol
pH optimum is ~4 so stable in the stomach but denatured by pancreatic proteases
Works together with gastric lipase

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48
Q

What are the different types of papillae on the tongue

A

Foliate
Circumvaliate
Fungiform

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49
Q

What are the two types of taste sensors and what are the sensing

A

Specialised epithelial cells
Ion-channel based sensor: salty and sour
GPCR-based sensor: sweet and bitter

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50
Q

What are odour receptors

A

Nerve cells

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51
Q

What is the cephalic phase

A

A combination of stimuli
Mediated by parasympathetic nervous system:
Salivary secretion via facial and glossopharyngeal nerves
Control of GI motility and secretion via vagus
Vagus also carries afferent fibres which contribute- feedback system

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52
Q

What are the roles and secretions of the LES and cardia region of the stomach

A 
Mucos
HCO3-
Prevention of reflux
Entry of food
Regulation of belching
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53
Q

What are the roles and secretions of the fundus and body region of the stomach

A 
H+
Intrinsic factor
Mucus
HCO3-
Pepsinogens
Lipase

Reservoir
Tonic force during emptying

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54
Q

What are the roles and secretions of the Antrum and pylorus region of the stomach

A

Mucus
HCO3-

Mixing
Grinding
Sieving
Regulation of emptying

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55
Q

How is gastric emptying controlled

A

Particles larger than 1-2 mm cannot pass pyloric sphincter

Duodenum senses delivery of acid, amino acids and lipids, and so secretes hormone which decrease gastric motility and emptying

Enteric nervous system

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56
Q

What is gastrin

A

Peptide hormone release from G cells of stomach and duodenum into the bloodstream

Two forms:
G17: main form secreted from Antrum
G34: main form secreted from duodenum

Main actions on the stomach are to stimulate acid secretion and promote mucosal growth

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57
Q

What is gastrin release stimulated by

A

Lumenal proteins/amino acids

Parasympathetic input, mediated by gastrin releasing peptide from interneurons

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58
Q

What is gastrin release inhibited by

A

Lumenal (H+) negative feedback

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59
Q

What is pepsin

A

Family of proteases, secreted from the chief and mucus cells in response to ACh, [H+]
Secreted as pro hormones (pepsinogens)
Cleave spontaneously at low pH (

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60
Q

What is gastric lipase

A

Initial digestion of triglycerides
Cleave the outer fatty acids off triglycerides, leaving diacyl glycerol
pH optimum is ~4
Stable in the stomach but denatured by pancreatic proteases
Works together with lingual lipase

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61
Q

What causes vomiting

A

Centrally controlled: area postrema = chemoreceptor trigger zone
Vagal afferents in response to irritants in or around the bowel
Psychogenic: pain, revulsion
Motion sickness
Drugs or toxins with a direct effect
Pregnancy

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62
Q

What are the three parts of the primitive gut tube

A

Foregut: mouth to 1st half of duodenum
Midgut: 2nd half of duodenum to 2/3 along transverse colon
Hindgut: distal 1/3 transverse colon to superior 2/3 rectum

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63
Q

What are intraperitoneal organs vs retroperitoneal organs

A

Organs enclosed in a mesentery are intraperitoneal

Organs that are not surrounded by peritoneum are retroperitoneal

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64
Q

Where are the dorsal and ventral mesenteries

A

Dorsal: from lower oesophagus to cloaca
Ventral: from lower oesophagus to 1st part of duodenum

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65
Q

What is formed by the ventral mesentery

A

Lesser momentum and falciform ligament (umbilical vein)

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66
Q

What happens to the vitelline arteries

A

Give rise to the 3 arteries which supply the GI tract by undergoing remodelling, losing their connection to the yolk sac in order to supply the GI tract

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67
Q

How is the definitive gut lumen formed

A

In week 6, proliferation of the endoderm derived epithelial lining occludes the gut tube
Apoptosis occurs over the following 2 weeks to create vacuoles (racanlisation)
During the process the epithelial lining further differentiates

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68
Q

What can happen as a result of abnormal recanalization

A

Can cause duplication of the GI tract

Incomplete recanalosation can cause stenosis (narrowing) or atresia (blockage) of the gut tube

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69
Q

What happens with the oesophagus in embryological terms

A

Forms in week 4
Caudal to the lung bud
Has endodermal epithelial lining and smooth muscle layer from visceral mesoderm
Some skeletal muscle derived from the paraxial mesoderm
Initially very shirt with the stomach located in the future thorax
Extens rapidly in weeks 4-7 as stomach descend to abdomen

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70
Q

How does the stomach develop

A

Appears in week 4 as a dilation of the foregut
Is suspended in the abdomen by the dorsal and ventral mesenteries
Differential growth in week 5 forms the greater curvature
In weeks 7-8 the stomach rotates around 2 axes

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71
Q

How does the stomach rotate

A

90* clockwise rotation around the craniocaudal axis causes the lesser curvature to move from ventral position to right while greater curvature moves from dorsal to left
Vagus nerves are initially on left and right sides but rotate also such that the left vagus nerve becomes anterior and right vagus nerve becomes dorsal
Also some rotation around the ventrodorsal axis so that the GC faces slightly caudally and the LC slightly cranially

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72
Q

How are the lesser and greater peritoneal sacs formed

A

Lesser: As the stomach rotates around the craniocaudal axis, it creates a space behind it

Greater: the remaining peritoneal cavity

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73
Q

What is the epiploic foramen

A

the narrow opening that connects the greater and lesser sacs

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74
Q

What is congenital pyloric stenosis

A

Narrowing of the pyloric sphincter caused by hypertrophy of smooth muscle

Restricts gastric emptying and so can lead to dilation of the stomach

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75
Q

How is the duodenum formed

A

Has to origins, 0.5 foregut, 0.5 midgut
Boundary is distal to the entrance of the common bile duct
It elongated in week 4 resulting in a ventrally projecting C-shape
This is dragged to the right by the rotating stomach
Dorsal mesentery attached to the duodenum degenerates so that the majority of it lies against the posterior abdominal wall

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76
Q

What are the characteristics of the small intestine

A

Villi and microvilli amplify the surface area available for interaction with food
Crypts secrete bicarbonate-rich fluid
Brush border enzymes

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77
Q

What are brush border enzymes

A

Integral membrane proteins
On surfaces of intestinal microvilli
Break down materials in contact with the brush border

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78
Q

How are carbohydrates digested

A

Soluble amylases only break internal a1,4 bonds

Remaining short chain carbs are broken down by specific enzymes on the brush border

Glucose and galactose actively absorbed by SGLT1

Fructose passively absorbed by GLUT5 transporter

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79
Q

What are endopeptidases vs exopeptidase and what are some examples

A

Endopeptidases cut within protein chain: trypsin, chymotrypsin, elastase
Cut at the last peptide bond: carboxypeptidases

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80
Q

How is fat digested

A

Bile salts break up lipid droplets increasing surface area
Pancreatic lipase cleaves off outer fatty acids
Once broken down, form a complex with bile salts, solubilising them allowing to diffuse close to brush border delivering contents to the membrane

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81
Q

How are vitamins absorbed

A

Fat-soluble (ADEK): absorbed with lipids
Water-soluble: require special transport proteins, usually Na+ linked
Vitamin B12: absorbed when bound to intrinsic factor

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82
Q

Where does most digestion and absorption happen

A

In the small bowel

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83
Q

What is the colon important for

A

Electrolyte balance and final water reabsorption

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84
Q

What does the small bowel secrete and where does it receive secretions from

A

Alkaline fluid into the lumen and hormones into the blood

Liver and pancreas

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85
Q

What is the ampulla of Vater

A

The little prominence where the common duct enters the duodenum

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86
Q

Where is bile stored and where does it secrete to and what stops this secretion

A

The bile produced by the liver and the secretions from the pancreas enter the duodenum via a common duct
The sphincter of Oddi can close this of and relaxes in response to CCK-PZ
When the sphincter is closed the bile is stored in the gall bladder

87
Q

What is secretin

A

Peptide hormone secreted by S cells of the small intestine
Stimulated mainly by acid in the small intestine
Main effect is to stimulate bicarbonate secretion by ductal cells in the pancreas and liver
Trophic effect on the pancreas
Modest inhibition of gastric acid production

88
Q

What is CCK

A

Peptide hormone secreted by I cells of of the small intestine
Release stimulated mainly by lipids and peptides in the small intestine
CCK-A receptors for CCK
CCK-B receptors for gastrin
Two effects: stimulate pancreatic secretion
stimulate gallbladder emptying

89
Q

What does bile contain

A

A complex mixture of components
Phospholipids and cholesterol
Pigments from the breakdown of haemoglobin
Inorganic ions: cations> antions, due to negative charge of bile acids
Bicarbonate
Salt
Water

90
Q

What are the different types of pancreatic enzymes secreted in an alkaline fluid

A 
Proteases (trypsinogen)
Pancreatic a-amylase
Pancreatic lipases (nonspecific esterase)
Nucleases (DNA, RNA)
Monitor peptides
91
Q

What are the boundaries of the abdominal cavity

A

Superior: thoracic diaphragm
Inferior: continuous witch pelvic cavity
Anterior and lateral: abdominal muscles
Posterior: lumbar vertebrae

92
Q

What is parietal peritoneum

A

Layer of peritoneum lining the abdominal wall, pelvic and inferior surface diaphragm

93
Q

What is the visceral peritoneum

A

Layer of peritoneum the specifically covers a viscus organ , the parietal and visceral layers of peritoneum are continuous just like the pleura

94
Q

What are the greater and lesser sac

A

Greater: main peritoneal cavity which is subdivided into supracolic and infracolic
compartments

Lesser: Recezz of peritoneal cavity between stomach and posterior abdominal wall

The two are linked by the epiglottic foramen

95
Q

How is the midgut formed

A

Week 5 midgut and associated dorsal mesentery undergo rapid elongation form the primary intestinal loop, containing cranial and caudal limbs, which communicates with the yolk sac through the vitelline duct

96
Q

What do the cranial and caudal limbs form

A

Cranial: distal duodenum, jejunum and proximal ileum
Caudal: distal ileum, caecum, appendix, ascending colon and proximal 2/3 transverse colon

97
Q

Why does the primary intestinal loop herniate into the umbilical cord in week 6 and what happens while herniation is happening

A

There is not enough room in the abdomen due to elongation of the midgut and growth of the liver

The midgut rotates 90* anti-clockwise bringing the cranial limb to the right and the caudal limb to the left

Jejunal loops form

98
Q

What happens to the midgut in week 10

A

The midgut returns to the abdomen and rotates a further 180* anti-clockwise, bringing the proximal jejunal loops to the left and the caecum lies inferior to the liver, forming a wormlike diverticulum called the vermiform appendix

The vitilline duct is obliterated during this

99
Q

What has happened to the midgut by week 11

A

It has returned to the abdomen and undergone 270* anti-clockwise rotation in total

100
Q

What is the result of the descent of the caecum

A

Caecum descends from below the liver to right iliac fossa pilling the ascending and transverse colon into place resulting in the final arrangement of the midgut

101
Q

What is Meckel’s diverticulum and what is the role of 2s in relation to it

A

A remnant of the vitilline duct that created an out pocketing of the ideal wall
Usually asymptomatic but may contain ectopic pancreatic or gastric tissue causing inflammation, ulceration and bleeding

Affects 2% population
2 times more common in males
2 feet from ileocaecal junction
2 inches long
Symptomatic in 2% of cases
102
Q

What is omphalocele

A

Failure of midgut to return to abdomen in week 10
Associated with an increased risk of mortality and other malformations
Diagnosed prenatally by ultrasound
Varies in size depending on contents

103
Q

What is the result of non-rotation of the midgut

A

Gut undergoes initial 90* anti-clockwise rotation but fails to rotate a further 180* when gut is retracted
Results in small intestine on the right side and large intestine on the left
Usually asymptomatic

104
Q

What is reversed rotation of the midgut

A

Initial 90* anti-clockwise rotation occurs normally but the gut rotates 180* clockwise upon retraction, thereby entering abdomen in correct order but duodenum lies ventral to transverse colon

105
Q

What is volvulus of the midgut

A

Twisting due to abnormal rotation causing parts that would normally be retroperitoneal to remain suspended by the dorsal mesentery and can cause acute obstruction of the bowel and bilious vomiting and may constrict arterial supply to the gut causing schema and infarction

106
Q

How is the hindgut formed

A

The distal end of the handout enters the dorsal part of the cloaca- anorectal canal.

Ventral part of the cloaca (urogenital sinus) will form the bladder, pelvic urethra, penile urethra (males) and caudal part of vagina (females)

During weeks 4-6 a layer of mesoderm extends caudally to separate the urogenital sinus and anorectal canal (urorectal septum)

107
Q

What happens in week 7 th the cloacal membrane and the urorectal septum

A

It ruptures to create the anal opening and ventral opening for the urogenital sinus

Urorectal septum lies between them and forms the perineal body

108
Q

How is the anal canal formed

A

The upper 2/3 is derived from endoderm (hind gut) and the lower 1/3 is derived from ectoderm (proctodeum) which become continuous when the cloacal membrane degenerates

The pectinate line in adults marks the junction between endoderm and ectoderm derivatives

Each area has different epithelial linings, lymphatic drainage and blood supply

109
Q

What are congenital recourethral and rectovaginal fistulas

A

Uncommon
Caused by abnormal cloaca, e.g. too small or failure of urorectal septum to extend caudally
Opening of handgun is shifted ventrally to the urethra in males and the vagina in females

110
Q

what is an imperforate anus

A

Failure od anal membrane to degenerate

Usually requires immediate surgery to allow defection of faeces

111
Q

What are the 2 enteric plexi

A

Myenteric plexus: between the circular and longitudinal muscle layers co-ordinated muscle contraction

Submucosal plexus between circular muscle and mucosa and regulates secretion

112
Q

What is Hirschprung disease

A

Failure of neural crest cells to migrate to migrate to bowel
Absence of enteric ganglia leads to bowel obstruction due to lack of peristalsis causing dilation of the aganglionic part of the bowel
Genetic condition commonly associated with trisomy 21
Treated by removing the affected bowel

113
Q

What are the parts of the large intestine

A

Cecum -> ascending colon -> transverse colon -> descending colon -> sigmoid colon -> rectum

114
Q

How does the ileoceacal valve work

A

Flutter valve acts one way
Periodic relaxation allows flow to pass through
Opens due to ideal distention and closes due to cecal distention

115
Q

How is the motility in the colon

A

Designed not to move contents along
Slow contractions of circular muscle squeeze contents back and forth
Occasional organised into peristaltic wave- mass movement

116
Q

How is motility coordinated and regulated

A

Controlled mostly intrinsically by enteric nervous system and some parasympathetic control
Enteroendocrine and neurocrine influences from cells releasing 5-HT and peptide YY
Gastocolic and orthocolic reflexes can trigger mass movements

117
Q

What causes a release of peptide YY and what happens as a result

A

Ileal break which is the presence of undigested lipid in distal ileum and proximal colon releases peptide YY, slowing gastric emptying and small bowel peristalsis

118
Q

How does digestion work in the colon

A

Done by bacteria digesting:
Fibre -> short chain fatty acids
Urea and amino acids -> ammonia
Bilirubin -> urobilinogen and stercobilins
Cystein and methionine -> hydrogen suphide
Primary bile acids ->secondary bile acids
Conjugated bile acids -> unconcjugated bile acids

Fermentation releases about 1l of nitrogen, hydrogen and CO2

119
Q

What types of muscle make up the anal sphincter

A

Intern anal sphincter: smooth muscle

External anal sphincter: skeletal muscle

120
Q

What happens in the rectum and anus

A

As faeces enter the rectum, pressure rises triggering reflex relaxation of internal anal sphincter and urge to defaecate
A small amount enters the anus to allow anal sampling
External anal sphincter contracts

121
Q

How does defection happen

A

Sitting to squatting increases the rectosigmoid angle facilitating passage of faeces
relaxation of puborectalis muscle also increase the angle
Relaxation of EAS and pelvic floor muscles open the way
Rectal peristalsis, sometime triggering colonic mass movement, provides the motive force

122
Q

What does the colon secrete and absorb

A

Secretes: Potassium and bicarbonate
Absorbs: salt and water

123
Q

What are the general principles of immune response

A 
Multilayer defense
Network of pathogen recognition
Effective inter-cellular communication
Multiple mechanisms of pathogen clearance
Adaptive réponses to changing pathogen
Self-regulation
Limitation of host damage
124
Q

What are pattern recognition receptors

A

Inclusive term for antigen recognition receptors in innate system
2 groups
Cell surface, transmembrane and intracellular receptors
Fluid-phase soluble molecules

125
Q

What are the roles of the GI tract mucosal surface

A

Separates the external environment from the internal sterile environment and therefore represent the first line of defence

Encounters:
Harmless antigens (food)
Commensal bacterial flora
Pathogenic organisms which have developed effective methods for colonisation and invasion

This requires:
Ignorance/ tolerance (harmless encounters)
Robust protective immune response (potentially harmful encounters)

126
Q

What does the gut immune system comprise of

A

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

Specific:
Lymphoid tissue associated with mucosal surfaces

127
Q

What are the benefits of commensal bacterial flora

A 
Resistance to colonisation by pathogens
Stimulate local immunity\Oral tolerance
Nutrition
Epithelial cell turnover
Intestinal motility
128
Q

What are some hazards of gut microflora

A

It is a reservoir of pathogens so can cause:
Disease of GI tract: IBS, Ulcers (H.pylori)
Extraintestinal disease: septicaemia
Autoimmunity: reactive arthritis
Allergy

129
Q

What is the epithelial barrier of the gut immune system

A

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

130
Q

What can the stem cells in the epithelial barrier differentiate into and what do these cells do

A

Enterocytes: mechanical action creates current to remove microbes that are poorly adhered and produces antimicrobial peptides and proteins
Goblet cells: produce mucins to provis mucus layers that resist microbial access
Enteroendocrine cells
Paneth cells

131
Q

What happens at Peyer’s patches in a specific immune response

A

Initiation of immune responses
M-cells: specialised enterocytes adapted to antigen uptake
Pass antigens to professional APCs (dendritic cells)
Dendritic cells present antigens to t and B cells which then become activated
B-cells migrate to mesenteric lymph nodes
Differentiated plasma cells migrate to tissues
Plasma cells secrete IgA

132
Q

What are intraepithelial lymphocytes

A 
Found between intestinal epithelial cells
Large granular lymphocytes
Mostly CD8+ (cytotoxic T-cells)
Produce IL-2, IFN-y, CCL5 
Function:
epithelial homeostasis
mucosal barrier function
reactivity with stress-induced epithelial cell antigens
133
Q

What are Lamina Propria Lymphocytes

A

Found in loose connective tissue, the lamina propria, the lies under the epithelium

Mostly CD4+ (helper T-cells)

134
Q

What are the helper T-cells

A

Th1: cell-mediated responses (intracellular pathogens)
Th2: antibody-mediated responses (allergens, parasites
Th17: cell-mediated responses (mucosal pathogens, IBS)

135
Q

What are B-cells

A

Synthesised by plasma cells in lamina propria
Transported across epithelium
Secreted in colostrum, maternal milk, saliva and tears
Prevents attachment of bacteria or toxins to epithelia
Protects against infectious agent

136
Q

Wha does IgA do in the gut and how does it exist

A

Binds to mucus layer on top of epithelial cells to form a barrier that neutralises pathogens before they reach the underlying cells

Exists as two isotopes:
IgA1: found inserumand made by bone marrow B-cells
IgA2: made by B-cells in the mucosa
IgA2: IgA1 ratio in the gut is 3:2

137
Q

What are the properties of secretory IgA

A 
Relatively resistant to proteolysis
Neutralises viruses and toxins
Enhances non-specific defence mechanisms
Inhibits:
Bacterial adhesion
Macromolecule absorption
Inflammatory effect of other immunoglobins
138
Q

What is metabolism

A

All the chemical reactions in the body

139
Q

What is anabolism

A

The reactions the synthesise new (larger) molecules from smaller precursors
These need energy

140
Q

What is catabolism

A

The reactions the break down larger molecules into smaller ones
These release energy

141
Q

What are the phases of metabolism

A

Absorptive: dealing with a meal
Post-absorptive: maintaining homeostasis between meals
Fasting: dealing with the challenge of longer periods without food
Intense exercise: responding to dramatic increases in demand

142
Q

What are the time scales of matabolism

A

Acute: minute to minute regulation of plasma glucose

Longer term: maintenance of adequate stores, turnover of proteins and cells, growth, reproduction

143
Q

What is AMP

A

A marker od low-energy state and regulates a number of metabolic enzymes allosterically

144
Q

How is excess glucose stored and then released

A

As polymers, mainly glycogen, in liver and muscle which provides a rapid but relatively short-lived store

Liver can release glucose derived from glycogen into the circulation

145
Q

What happens to excess fats

A

Provide a dense energy store
Takes longer to re-release the energy
Many tissues use fatty acids as their main source of energy
The liver can convert fatty acids into ketone bodies during starvation

146
Q

What happens to excess protein

A

Not ideal as a source of energy ad mainly stored a s functional proteins
Liver can convert amino acid to glucose by gluconeogenesis
Muscle cells contain a lot of protein, and can be converted to alanine and glutamic which can be exported for gluconeogenesis

147
Q

How do erythrocytes use metabolism

A

Lack mitochondria so unable to carry out aerobic metabolism but has low metabolic demand
Positive: job is to carry oxygen not use it up
Negative: must get all energy from anaerobic metabolism which is inefficient

148
Q

How does the brain use metabolism

A

Has mitochondria and has high metabolic demand
Blood-brain barrier limits what foodstuffs can cross
Brain depends on a fairly steady plasma glucose concentration which if lower than 3mM can be fatal
During fasting ketone bodies are used

149
Q

How do Adipocytes use metabolism

A

Insulin-sensitive uptake of glucose and glucagon-sensitive release of FFA and glycerol
During periods of high glucose, convert glucose to triglyceride
As glucose levels fall, metabolise triglyceride to release FFA and glycerol

150
Q

How does the liver use metabolism

A

First place for food stuffs absorbed from the gut
Insulin sensitive uptake, and glucagon-sensitive release of glucose
During high glucose, converts to glycogen
During low glucose, metabolises glycogen to release glucose

151
Q

What is used in gluconeogenesis

A

Lactate
Glycerol
Amino acids

152
Q

How do cardiac muscles use metabolism

A

Highly aerobic: up to 40% mitochondria and abundant in myoglobin
Main energy source is fatty acids but can also use lactate or ketone bodies
Glucose uptake is insulin-sensitive

153
Q

How do skeletal muscle types use metabolism

A

Type 1:
Highly aerobic
Adapted to prolonged, relatively modest, activity
Main energy source is fatty acids

Type 2a:
Intermediate between 1 and 2b
contain some mitochondria and myoglobin
Maintain aerobic as much as possible
Phosphocreatine and glycogen are good energy stores
Adrenaline or insulin allow glucose uptake
At low exercise levels, fatty acids are main energy source
Release amino acids for gluconeogenesis during fastin

Type 2b
Fast-teitch muscle: explosive performance but quickly fatigued
Few mitochondria and little or no myoglobin
Phosphocreatine provides rapid replenishment of ATP, but only for a few seconds
Rely mainly on anaerobic glycolysis, with glucose from glycogen store
Adrenalin or insulin allow glucose uptake

154
Q

Why is plasma glucose not just kept high

A

Osmotic effects
Glucose lost in urine, wasting energy and causing polyuria
Glycation of proteins and later cross-linking:
microvascular and microvascular disease
peripheral neuropathy
low grade inflammatory effects

155
Q

What are the possible fates of sugars after absorption

A

Metabolism to produce energy
Conversion to glycogen for storage
Synthesis of other cellular components
Conversion to fat for storage

156
Q

How is glucose metabolised anaerobically

A

Glycolysis in absence of oxygen
Takes place incytosol of all cells
2 phases:
Preparative phase: Glucose
-> fructose 1,6 bisphosphate (requires ATP)
Generating phase: fructose 1,6 bisphosphate -> (2) pyruvate (generates ATP and NADH)
Pyruvate -> lactate
2 molecules of ATP are generated per molecule of glucose
NAD+ is regenerated from NADH

157
Q

How is glucose metabolised aerobically

A

NADH is used to generate further 3-5 molecules of ATP via oxidative phosphorylation
Aerobic glycolysis generated 5-7 molecules of ATP per glucose molecule
Complete oxidation of glucose via the Krebs cycle yields 30-32 ATP

158
Q

How is excess glucose stored

A

As glycogen mainly found in the liver and skeletal muscle

Glycogen has a branched structure with a-1,4 linkages and a-1,6 branch points

159
Q

How is glucose converted to fatty acids and triacylglycerol for energy storage

A

Glucose -> fatty acids -> triacylglycerols

Fatty acid synthesis occurs in the cell cytosol of:
mainly the liver
adipose tissue
breast tissue during lactation

Triacylglycerol synthesis:
Addition of 3 fatty acids to a molecule of glycerol-3-phosphate
Occurs in endoplasmic reticulum

In adipose tissue: stored in cytosol
In liver: packaged to form VLDL -> secreted into blood and transported to:
adipose tissue for storage
other peripheral tissues for use as energy store

160
Q

What is the importance of metabolic control

A

At least 1/3 of all serious health problems are consequences of metabolic disorders
Maintaining blood glucose at ~5mM is crucial for survival
Brain relies on glucose for ATP synthesis:
Below 3mM: confusion, coma, death
Above 8mM long term vascular damage occurs through protein glycation

161
Q

How is glycogen synthesised

A 
Conversion of glucose-6-phosphate to glucose-1-phosphate
Synthesis of UDP-glucose
Needs a primer
Chain elongation
Insertion of branch points

Key control enzyme:
glycogen synthase

162
Q

How is glycogen broken-down by glycogenolysis

A

Glycogen phosphorylase removes glucose units
Additional enzymes required to remove branches
Glucose-1-phosphate converted to glucose-6-phosphate enters glycolysis

163
Q

How does insulin influence glycolysis

A

Increases expression of genes which code for enzymes of glycolysis
Decrease expression of genes which code for enzymes of gluconeogenesis

164
Q

How does glucagon influence glycolysis

A

Regulates the level of fructose 2,6 bsphosphate which activates glycolysis and inhibits gluconeogenesis
This occurs via phosphorylation of a protein which catalyses synthesis and degradation of fructose 2,6 bisphosphate

When phosphorylated:
Glucagon high
Enzyme degrades F 2,6 BP
Glycolysis decreases

When dephosphorylated:
Glucagon low
Enzyme synthesises F 2,6 BP
Glycolysis increases

165
Q

Describe some roles of lipids other than their role in energy production

A

Incorporation into cell membranes: particularly phospholipids and cholesterol
Essential fatty acids are precursors for prostaglandins, leukotrienes and thromboxanes

166
Q

Describe how lipids are transported in the blood

A

Chulomicrons are formed in the intestinal epithelial cells, released into the lymph, enter circulation via thoracic duct into subclavian vein

167
Q

Describe the oxidation of fatty acids to acetyl CoA and the control of this pathway

A

fatty acid activated to fatty acetyl CoA in cytosol

B oxidation takes place in mitochondria:
spiral process
each turn releases 1 acetyl CoA and produces NADH and FADH2 which are oxidised by the electron transport chain
acetyl CoA then enters the Krebs cycle
Overall reaction produces 108 tap from each molecule of fatty acetyl CoA

Long chain fatty acids require carnitine for transport which is inhibited by malonyl CoA, which prevents the synthesis and degradation fatty acids and is formed by acetyl CoA carboxylase

168
Q

Explain what ketone bodies are and how they are formed

A

Ketone bodies are formed from excess acetyl CoA
Synthesis occurs in the mitochondria of liver cells under conditions where the body relies on fatty acid oxidation for energy: fasting and uncontrolled diabetes
Ketone are released into the blood and are oxidised to produce energy in peripheral tissues including brain tissue

But ketoacidosis is a life-threatening condition

169
Q

Outline the synthesis of cholesterol and the control of this pathway

A

Acetyl CoA to melvalonate (C6) -> melvalonate to phosphorylated isoprene units (C5) (activation) -> polymerise 6 isoprene units to form a C30 chain (squalene) -> cyclisation to form ring structure (lanosterol) then cholesterol

First stage controls rate of synthesis by adjusting the activity or amount of HMG CoA reductase
High cholesterol levels inhibit further synthesis
Insulin increases synthesis by signalling energy availability
Occurs in the cytosol and smooth endoplasmic reticulum

170
Q

What common diseases are the result of excess lipids

A

Coronary heart disease: elevated cholesterol levels
Alzheimer’s disease: raised cholesterol
Steatohepatitis: can lead to cirrhosis and hepatic carcinoma

171
Q

What is cholesterol needed for

A 
Bile salts
Membranes
Vitamin D
Steroid hormones:
androgens (testosterone)
oestrogen
progestogens (progesterone)
mineralocorticoids (aldosterone)
glucocorticoids (cortisol)
172
Q

How does fat arrive at peripheral tissue

A

In chylomicrons or VLDL: released by lipoprotein lipase
or
From adipose tissue:
triacylglycerols broken down by hormone sensitive lipase
fatty acids release into blood
transported to tissues bound to albumin

173
Q

What results form high LDL and HDL levels

A

High LDL: increased risk of atherosclerosis

High HDL: decreased risk of atherosclerosis

174
Q

What is atherosclerosis

A

Damage to endothelial cells allows LDL access to suboptimal space
LDL become oxidised and are internalised by macrophages to make foam cells
Accumulation of foam cells create bulge in vessel wall called an atherosclerotic plaque
Fibrous collagen cap is formed
Plaque may restrict blood flow, in coronary arteries this causes angina
Strokes and heart attack occur when plaques rupture and thrombosis follows

175
Q

What are the different parts of the liver and the structures associated with it

A 
Liver body
Hepatic vein
Hepatic artery
Hepatic portal vein
Common bile duct
Stomach 
Cystic duct
Gallbladder
176
Q

What are the input and output blood supply of the liver

A 
Input:
Portal vein (75%)
Hepatic artery (25%)

Output:
Hepatic vein into inferior vena cava

177
Q

What are the cell types of the liver and what do they do

A

Hepatocytes: 60% of live cells, carry out most of metabolic functions

Endothelial cells: lining of sinusoids, contain fenestrations so don’t form a barrier against small molecules

Kupffer cells: located within sinusoidal lining, macrophages, phagocytose bacteria, old erythrocytes, protect liver from gut derived bacteria

Pit cells: natural killer cells, help protect liver from viruses/ tumour cells

Hepatic stellate cells: lipid-filled cells, primary state of vitamin A storage, also control turnover of connective tissue, synthesise collagen and regulate contractility of sinusoids

178
Q

What are the functions of the liver

A

The factory:
receive raw materials, manufacture new goods, recycle, deliver and store

Waste management:
treat hazardous material, dispose of internal waste

179
Q

What is a prodrug

A

An inactive or less active compound which is metabolised by the liver to produce the therapeutically active form into the body

180
Q

What happens to amino acids

A 
Protein synthesis
Synthesis of nitrogen containing metabolites 
Energy (ATP)
Fatty acids, ketone bodies
Glucose, glycogen
181
Q

How is ammonia disposed of

A

It is converted to urea for excretion by the kidneys

3 steps:
transamination: transfer of amino group from amino acid to a-ketoglutarate forming glutamate (all tissues)
deamination: release of ammonia from glutamate (in liver)
urea synthesis: urea cycle (in liver)

182
Q

What is the urea cycle

A

Inside mitochondria:
Carbamoyl phosphate formed from ammonia and bicarbonate (control step)
Carbamoyl group transferred to ornithine to form citrulline

In the cytosol:
Second Amin group added from aspartate
Arginine formed
Urea released

183
Q

What do glycogenic and ketogenic mean

A

Glucogenic: can be degraded to glucose precursors
Ketogenic: can be degraded to precursors of fatty acids and ketone bodies

184
Q

What is the turnover of of ATP

A

~ 75 kg/day

185
Q

What is the structure of mitochondria

A

Outer:
smooth and freely permeable to molecules under 5000 Da
no ionic or electrical gradients

Inner:
folded into christae
permeable to a small number of molecule only via specific transporters
a very good electrical insulator, capable of maintaining large ionic and electrical gradients
contains more protein than lipid- respiratory enzymes, transporter proteins

186
Q

What is the matrix of the mitochondria

A

contains wide range of enzymes for: Krebs cycle, fatty acid oxidation, urea cycle
High concentrations of substrates, cofactors and ions
Contains mitochondrial DNA, RNA and ribosomes though few mitochondrial protein are coded on mitochondrial DNA

187
Q

What is the inter membrane space of the mitochondria

A

Has metabolite and ion concentrations similar to cytosol

contains cytochrome C

188
Q

What is the turnover of of ATP

A

~ 75 kg/day

189
Q

What is the structure of mitochondria

A

Outer:
smooth and freely permeable to molecules under 5000 Da
no ionic or electrical gradients

Inner:
folded into christae
permeable to a small number of molecule only via specific transporters
a very good electrical insulator, capable of maintaining large ionic and electrical gradients
contains more protein than lipid- respiratory enzymes, transporter proteins

190
Q

What is the matrix of the mitochondria

A

contains wide range of enzymes for: Krebs cycle, fatty acid oxidation, urea cycle
High concentrations of substrates, cofactors and ions
Contains mitochondrial DNA, RNA and ribosomes though few mitochondrial protein are coded on mitochondrial DNA

191
Q

What is the inter membrane space of the mitochondria

A

Has metabolite and ion concentrations similar to cytosol

contains cytochrome C

192
Q

What is the function of antiporters

A

Antiporter in the inner mitochondrial membrane allows transport of ADP into the mitochondria and ATP out to other areas of the cell
This is aided by phosphate

193
Q

How is the Krebs cycle controlled

A

Entry of pyruvate is controlled by need for energy and availability of Acetyl CoA from fat oxidation

Control of cycle by need for energy as monitored mainly by ATP:ADP and NADH:NAD+ ratios

194
Q

How is the Krebs cycle used in other metabolic pathways

A

Amino acid carbon skeletons feed into the Krebs cycle

A number of anabolic pathways use Krebs cycle intermediates as binding blocks

195
Q

What is the ATP synthesis step

A

Oxidative phosphorylation is made up of two tightly coupled processes

Electron transport: the energy of the electrons in NADH/FADH2 is used to create a proton gradient across the inner mitochondrial membrane- OXIDATION

ATP synthesis: the energy from the proton gradient is used to phosphorylate ADP to synthesise ATP- PHOSPHORYLATION

196
Q

What is the function of antiporters

A

Antiporter in the inner mitochondrial membrane allows transport of ADP into the mitochondria and ATP out to other areas of the cell
This is aided by phosphate

197
Q

What do the out pocketings of the foregut give rise to

A

Liver
Gallbladder
Pancreas

198
Q

How do the liver and gallbladder develop

A

In week 3, the liver appears as an out pocketing of the future duodenum- hepatic diverticulum

This contains rapidly proliferating cells that penetrate the septum transversum

The connections between the hepatic diverticulum and duodenum narrows to form the bile duct

A ventral outgrowth of the bile duct forms the gallbladder and cystic duct

Endodermal cells differentiate into hepatocytes of liver

Haemotopoietic, Kupffer cells and connective tissue are derived from mesoderm of the septum transversum

Liver continues to rapidly expand and becomes too large to be contained within the septum transversum so protrudes into the ventral mesentery, dividing the mesentery into 2 parts:
Falciform ligament
Lesser omentum

199
Q

Why is the liver so large in utero and why does this change after birth

A

In utero liver is important in haematopoiesis

After birth haematopoiesis shifts to the bone marrow

200
Q

How does the spleen develop

A

Derived from the mesoderm and appears in week 5 as a mesenchymal condensation in the dorsal mesentery

Rotation of stomach brings the spleen to left side

The dorsal mesentery between the stomach and the spleen is the gastosplenic ligament and the dorsal mesentery between the spleen and kidney is the spleorenal ligament

201
Q

What do the ventral and dorsal buds of the developing pancreas form

A

Dorsal: head, body and tail of pancreas
Ventral: uncinate process

202
Q

How are the ducts of the pancreas formed an

A

Main pancreatic duct: distal portion of dorsal pancreatic duct and all of the ventral pancreatic duct

Accessory pancreatic duct: proximal portion of the dorsal pancreatic duct

203
Q

What is an annular pancreas

A

The ventral pancreatic duct is bilobed and one lobe migrates ventral to the duodenum and the other dorsally to surround the duodenum, resulting in compression of the duodenum causing gastrointestinal obstruction

204
Q

What do Beta cells secrete and why

A

Insulin in response to glucose

205
Q

What is secreted by alpha cells and what does it do

A

Glucagon and antagonises the effects of insulin

206
Q

What are the effects of insulin and glucagon on muscle

A

Insulin:
Glycogen, triglyceride and protein synthesis increase

Glucagon:
Proteolysis: releasing AA for gluconeogenesis

207
Q

What are the functions of glucocorticoids

A

Inhibit insulin responses and enhance SNS responses (sending glucose to brain and other organs to use fat)
In liver, promotes gluconeogenesis and glucose release
In fat, lipolysis
In muscle, protein breakdown for gluconeogensis

208
Q

What is secreted by alpha cells and what does it do

A

Glucagon and antagonises the effects of insulin

209
Q

What are the results of excess and deficient growth hormone levels in children and adults

A

Children:
Excess: leads to gigantism
Deficiency: leads to dwarfism

Adults:
Excess: leads to acromegaly where bones are excessively thick and other tissues overgrow
Deficiency: no obvious disease but replacement increases body mass, decreases fat and increases vigour

210
Q

What are the functions of glucocorticoids

A

Inhibit insulin responses and enhance SNS responses (sending glucose to brain and other organs to use fat)
In liver, promotes gluconeogenesis and glucose release
In fat, lipolysis
In muscle, protein breakdown for gluconeogensis

211
Q

What is ghrelin

A

28 amino acid peptide produced from neuroendocrine cells in the stomach
Released when stomach is empty
Appetite inducing agent
Present as neuropeptide in the brain

212
Q

What are anorexigens

A 
suppress hunger
Examples:
CCK
Insulin
FLP-1
Peptide YY
Oxyntomodulin
Somatostatin
213
Q

What are the results of extreme starvation

A

Wasting of muscle
Muscle fatigue and reduced exercise capacity
Diminished respiratory capacity
Slowed heart rate and decreased contractility
Loss of heat-generating capacity
Apathy
Death from respiratory or cardiac failure or infection

214
Q

How is BMI calculated

A

BMI = (weight in kg) / (Height in meters)squared

Y1 Body system lecture notes year 1 (5 decks)

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