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Lectures Flashcards

1
Q

What are macro and micro nutrients?

A

Macro nutrients - fats, carbs & protein

Micro nutrients - vitamins, minerals & trace elements

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2
Q

Which are the fat soluble vitamins?
Where are they absorbed?
Where are they stored?

A

A, D, E & K
Absorbed in SI in presence of fat
Stored in body tissues.

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3
Q

Which are water-soluble vitamins? Where are they absorbed?

A

C, B1, B2 & Folate - absorbed SI - generally not stored in the body.

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4
Q

What is the function of Vitamin A? Where is it found?

A

Function - immunity, night vision, dec risk of bone fractures in older Ps

Found - liver, offal, oily fish, eggs, dairy & fortified foods.

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5
Q

What is the function of Vitamin D? Where is it found?

A

Used in Ca absorption & bone mineralisation. Deficiency –> rickets.

Found - cod liver oil, oily fish, eggs, liver, fortified food (not UK milk)

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6
Q

What is the function of Vitamin E? Where is it found?

A

Eyes, skin, immune system, protection of CSM from free radicals & lipoproteins, prostaglandin synthesis & DNA synthesis.

Found - plant oils, nuts, seeds & wheatgerm (cereals)

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7
Q

What is the function of Vitamin K? Where is it found?

A

Used for blood clotting, healing & poss bone health

Found - green leafy veg, veg oils, cereal grains, eggs, small amt in meat & dairy

FYI - DO NOT TAKE IF ON ANTI COAGS

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8
Q

What is the function of Vitamin C?

Where is it found?

A
  • Antioxidants
  • Collagen synthesis
  • Peptide hormone activation
  • Bile
  • Metabolism of drugs & carcinogens
  • Inc absorption of iron if in same meal.

Found: citrus, peppers, strawberries, blackcurrants, broccoli, brussel sprouts, sweet & normal potatoes.

CANT BE STORED IN THE BODY

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9
Q

What is the function of Vitamin B1?

Where is it found?

A

Release of energy from food + nervous system.

Found: Peas, pulses, nuts, some fruits (banana, orange), wholegrain bread, cereals, liver, yeast, milk

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10
Q

What is the function of B12?

Where is it found?

A

Erythropoiesis, NS, releases energy from food, in use of folate

Found: Meat, fish, milk, cheese, eggs & fortified cereals

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11
Q

What is the function of folate?

Where is its found?

A

Folate = folic acid (man made version)

Used in maintaining health RBCs, prevents neural defects in pregnancy

Found - broccoli, Brussels sprouts, peas, green leafy veg, chickpeas, kidney beans, liver, fortified cereals

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12
Q

What Is the function of calcium?

Where is it found?

A

Used to make rigid bones & teeth, muscle contractions, heart beat, blood clotting

Found - dairy, leafy green veg, bread & fortified flour, fish with bones

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13
Q

What is sodium used for?

A

Balance of fluid levels - adults need <6g/day. Too much = hypertension, heart attacks

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14
Q

Where is iron found?

A

Liver, red meat, beans, nuts, dried fruit, fortified cereals, soy bean flour.

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15
Q

What is K used for?

Where is it found?

A

Used for fluid balance & heart muscle contraction

Found - bananas, oranges, some veg, beans & pulses, nuts & seeds, coffee, dark choc, you, potatoes, LO salt.

Older Ps - kidneys may remove less K.

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16
Q

What additional requirements are there for diet in pregnancy?

A

Additional energy & thiamine needed in 3rd trimester
FA - take for first 12 weeks
Take daily Vitamin D throughout
Avoid cod liver oil / Vitamin A supplements
Vegans - need a DHA supplement (Omega3)

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17
Q

What additional dietary requirements do breastfeeding women have?

A 
Limit caffeine, inc energy & vitamins
Daily Vit D
Restrict oily fish to x2 / week - pollutants
Peanuts ok
If vegan - Zn can be low.

Remember psychological impact of breastfeeding.

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18
Q

What additional dietary requirements do children have?

A

No eat well plate under 2.
Need Vitamin A, C & D supplements every day.
Growth spurts - big energy requirement increases.
Adolescents - higher Ca and P requirements than adults

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19
Q

What is the landmark division between upper & lower GIT?

A

Suspensory ligament of duodenum = ligament of Treitz.

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20
Q

What are the accessory organs of the GIT?

A 
Tongue
Teeth
Salivary glands
Gall bladder
Pancreas
Liver
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21
Q

What forces propel food?

A

Peristalsis, gravity + lower abdominal pressure - intraoesophageal pressure is higher than in abdomen - creates pressure for food to move down.

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22
Q

What is the anticipatory phase of digestion called?

A

The cephalic phase - salivary & parietal glands stimulated.

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23
Q
A
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24
Q

Name the four layers of GIT wall

A

Mucosa
Submucosa
Muscularis externa
Serosa

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25
Q

What are the three layers of the mucosa - and what is in each?

A

Epithelium - enteroendocrine & exocrine glands - lubricate & chemical breakdown
Lamina propria - CT (thin), GALT for immunity
Muscularis mucosae - circular and longitudinal muscle - moves substances in lumen in right direction

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26
Q

What is in the submucosa?

A

Dense layer of CT - contains BVs, lymph, mucus glands & Submucosal nerve plexus (controls gland secretions and localised blood flow).

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27
Q

What is in the muscularis externa layer?

A

Circular muscle, Myenteric nerve plexus (controls the muscles here) & Longitudinal muscle

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28
Q

What is the function of the serosa?

What is the serosa called in the oesophagus?

A

Secretes serous fluid into abdominal cavity - lubricates to prevent friction from adjacent organs.
Serosa in oesophagus = adventitia (thick & fibrous CT).

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29
Q

How do substances move through the GIT?

A

Coordinated smooth muscle contraction - synchronised & autonomic process

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30
Q

Which parts of the GIT are under voluntary control?

A

Upper oesophagus & external anal sphincter - both made of striated skeletal muscle.

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31
Q

How is the GIT adapted for motility?

A

Has smooth muscle w/gap junctions - fast - contracts as syncytium.

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32
Q

What are the 3 phases of swallowing & which CN controls each phase? Describe what happens in each.

A

Oral (Voluntary) - tongue - formation of bolus

Pharyngeal (pharynx) - autonomous - bolus stimulates receptors –> CN9 - triggers swallowing centre in medulla oblongata –> CN5, 9 & X –> muscular contraction of pharynx, propelling bolus down. Epiglottis closes over larynx, respiration inhibited. UOS (at pharyngoesophageal junction) relaxes for food to move into oesophagus, closes once it has passed.

Oesophageal - autonomous - intraoesophageal pressure is higher than abdominal = pressure for food to move down. Sphincters remain constricted to prevent air entering.
First peristalsis wave - bolus reaches oesophagus - receptors - muscularis externes circular muscle contracts and squeezes, longitudinal relaxes and lengthens - pulls bolus down.

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33
Q

Which cranial nerve supplies the roof of the mouth?

A

CN5

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34
Q

Which cranial nerve supplies the pharynx?

A

CN9 - GP nerve

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35
Q

Which cranial nerve supplies the oesophagus & stomach?

A

CNX - Vagus nerve

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36
Q

Which nerves supply the visceral organs?

A

Splanchnic nerves

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37
Q

What is the enteric nervous system?

A

Is the myenteric nerve plexus (motility + contraction) + submucosal nerve plexus (glandular secretions & local blood flow).

Functions independently of CNS - truly autonomous

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38
Q

How can the enteric nervous system be modified?

A

By the Autonomic nervous system:

  • PSS - postganglionic fibres innervate the SM & Secretory cells (using ACh) - stimulates rest & digest via CNX
  • SS - innervate ganglia - inhibits the enteric nervous system (F&F response) but stimulate BV and sphincter contraction.
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39
Q

Which vertebral level does the oesophagus penetrate the diaphragm?

A

T10

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40
Q

Which types of muscle are in the oesophagus?

A

Upper 1/3 - striated muscle - voluntary control
Lower 1/3 - smooth muscle - involuntary
Middle - mix of both

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41
Q

What stops air entering the oesophagus?

A

Contraction of sphincters.

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42
Q

What happens during the primary peristaltic oesophageal wave?

A

Primary peristaltic wave - bolus reaches oesophagus - receptors - muscularis externis - circular muscle contracts and squeezes, longitudinal relaxes and lengthens -> moves bolus downwards. Receptors sense pressure change - info to CNX - causes release of vasoactive intestinal peptide - VIP - causes relaxation of LOS & SM - relaxes and opens (and closes).

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43
Q

What happens during the secondary peristaltic wave?

A

Remaining bolus is detected by mechanoreceptors in mucosal layer -> ENS —> myenteric plexus coordinates contraction above and relaxation below - initiates 2 peristaltic wave which removes any remaining food.

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44
Q

Where does the oesophagus meet the stomach?

A

At the cardiac orifice via the cardiac sphincter - = oesophagogastric junction.

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45
Q

What happens to the lining of the GIT at the oesophagogastric junction?

A

Changes from stratified squamous epithelium (oesophagus) to columnar epithelium of stomach.

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46
Q

Which cells are in the pyloric part of the stomach?

A

Mucous neck cells and enteroendocrine cells

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47
Q

What controls gastric secretions and blood flow in the stomach?

A

The submucosal plexus

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48
Q

Which level of lining of stomach is responsible for peristalsis?

What is it used for?

A

Muscularis externa - has 3 layers of SM - outer longitudinal, middle circular and inner oblique layer.

Mixing, digestion and emptying

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49
Q

What are the stomach muscles innovated by?

A

Myenteric nerve plexus (ENS)
PSS - CNX - increases gastric secretion and motility
SS - celiac ganglion - inhibits secretion and motility

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50
Q

Which reflex mediates receptive relaxation when food enters the stomach?

What does it allow?

A

The vagovagal reflex - reduces muscle tone and allows reservoir function.

CNX

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51
Q

What do propulsion & retropulsion in stomach cause?

A

Mixing of the contents in cycles.

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52
Q

What stimulates and inhibits transfer of contents from stomach to duodenum?

A

Regulated by signals from SI.

Stimulated by ENS, ANS or hormones (motilin)

Inhibited by ANS, duodenal enterogastric reflexes and hormones (CCK)

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53
Q

Which is the gene responsible for CF?

A

CFTR

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54
Q

What causes CF on a cellular level?

A

CFTR - gene involved with Cl ion transport - can be completely blocked or partially impaired. Result = less Cl to outside of cell - therefore less water and HCO3 follows. Creates sticky mucus - can affect whole body inc. lungs, gut & fertility

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55
Q

How does neonatal meconium ileus occur?

A

CFTR gene irregularity = tubes in GIT fail to “canalise” - are either narrowed or completely obstructed. Means baby cannot poo - meconium remains in ileum.

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56
Q

How does CF affect the GIS?

A

Causes strictures / blockages in development. Sticky mucus can later cause obstruction.
Also causes blockages in liver, biliary tree & pancreas.

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57
Q

If a P with CF presents with vomiting, stress diarrhoea, distension & then absence of poo - what could be the diagnosis?

A

Blockage of the intestinal tract

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58
Q

What is creon?

A

Digestive pancreatic enzymes

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59
Q

Why do CF ps have greater risk of C Diff?

A

Are often on ABs for long time.

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60
Q

Will calprotectin by high or low in CF?

A

High

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61
Q

What is DIOS?

What causes it?

Treatment?

A

Distal Intestinal Obstruction Syndrome - thickened stool with mucus blocks intestinal tube - completely or partially.

Can be caused by too little Creon, dehydration or narrow intestine.

Rehydration, laxatives, enzymes + poss surgery.

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62
Q

P presents with distension, vomiting, constipation. AXR = distended proximal bowel + tinkling bowel sounds. Diagnosis?

A

DIOS

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63
Q

What is Cholecystitis?

What causes it in CF?

A

Inflammation of the gallbladder.

Lots of CFTR genes in gallbladder - may mean that ducts are too narrow. Lots of sticky mucus can also inc formation of gall stones + inc risk from bacteria with the mucus.

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64
Q

Why does GERD worsen respiratory status in CF Ps?

What can be done to prevent GERD in CF Ps?

A

Acid into lungs - aspiration - can cause more infections.

Fundoplication procedure + change in chest physio position.

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65
Q

P presents with dyspepsia, reflux, early satiety & regurgitation. Diagnosis?

A

GORD

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66
Q

P presents with RUQ + umbilical deep pain (to back). Have raised serum amylase & raised blood glucose.

Diagnosis?

A

Pancreatitis

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67
Q

What is the difference between pancreatic sufficiency and insufficiency?

A 
PS = pancreas working efficiently
PI = pancreas not working efficiently - sticky mucus has built up and blocks the exocrine glands.
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68
Q

What is CFLD?

A

Cystic Fibrosis associated Liver Disease

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69
Q

How prevalent is CFLD in Ps with CF?

A

Common - about 1/3 develop - can be made worse by oestrogen (so in F after puberty).

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70
Q

What does CFLD do?

A

Causes general dysfunction of the liver. Can have hepatic steatosis (FLD), biliary cirrhosis (focal or multilobular) & neonatal cholestasis (rare - dec in bile flow).

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71
Q

What are ALT, AST & GGT

A

Liver enzymes in blood serum.

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72
Q

Is colorectal cancer more prevalent in CF Ps?

A

CF Ps are x5-x10 more likely to develop CRC - should have screening from 40+

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73
Q

What are surgery risks to CF Ps?

A

CF Ps = hyper metabolic - drugs need to be calculated differently. CF Ps can also have reduced lung function - riskier for GA.

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74
Q

How does CF affect P’s nutrition?

A

Less absorption -

  • Pancreas, biliary + intestinal loss = dec absorption of fats - dec ADE&K absorption
  • Gastric, pancreatic + intestinal loss = dec absorption of carbs
  • Pancreatic + intestinal loss = dec protein absorption
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75
Q

If a P has terminal ileum removed / lack of IF - what cannot be absorbed?

A

B12

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76
Q

What determines whether a reaction will proceed?

A

Gibbs free energy - whether the reaction is endothermic or exothermic - if exothermic (GFE neg) - reaction can spontaneously occur.

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77
Q

Are catabolism and anabolism positive or negative energy?

A 
Catabolism = negative free energy (exothermic) - breaking bonds
Anabolism = positive free energy (endothermic) - making bonds
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78
Q

What does coupling of reactions with ATP allow?

A

Reactions to proceed that require an input of energy - taken from the breaking of ATP bonds.

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79
Q

What are the two methods of phosphorylation that make ATP?

A

Substrative level phosphorylation (glycolysis)

Oxidative phosphorylation (ETC)

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80
Q

What do cofactors do? Name two types

A

Help the enzyme function efficiently - metal ions and coenzymes (substrates & prosthetic groups)

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81
Q

What are coenzymes that are covalently bound to the enzyme called?

A

Prosthetic groups

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82
Q

Name 3 coenzymes involved in respiration

A

NAD, FAD & CoA

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83
Q

How many ATP are produced from oxidative phosphorylation of NADH & FADH

A

NADH - 2.5

FADH - 1.5

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84
Q

What does CoA do?

A

Transfers acetate between molecules

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85
Q

Name the four stages of respiration. Why is it divided into stages?

A

Glycolysis, Pyruvate Oxidation (Link Reaction), Citric Acid Cycle + ETC

Provides lots of control points to prevent overly rapid breakdown, excess heat loss & non-utilisation of ATP that is made.

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86
Q

What are the products of glycolysis?

A

4 ATP are made, 2 are used in stage 1 - so is a net gain of 2 ATP.

2 NADH are produced

2 Pyruvate are produced

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87
Q

What is glycolysis controlled by?

A

Kinases - which are inhibited by the products of the steps:
Hexokinase - inhibited by too much G6P
Phosphofructokinase - inhibited by too much ATP or citrate (activated by ADP & AMP high levels)
Pyruvate kinase - inhibited by high levels of pyruvate, ATP or CoA.

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88
Q

What is the link reaction? Is it reversible or irreversible?

What are the products from this reaction?

A

Carrier protein in mitochondrial membrane that undergoes oxidative decarboxylation via pyruvate dehydrogenase.

Is irreversible.

Pyruvate is converted to ACoA (controlled by pyruvate dehydrogenase)

Products: 2 ACoA, 2 CO2 + 2 NADH

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89
Q

What are the control points of Krebs cycle?

A
  • Link reaction (pyruvate dehydrogenase)
  • Entry of ACoA into cycle (citrate synthase)
  • Isocitrate dehydrogenase
  • Ketoglutarate dehydrogenase

Many of these enzymes are activated by Ca - therefore inc levels of Ca during exercise in muscles stimulates and drives Krebs.

Are all inhibited by high levels of ATP & NADH

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90
Q

What are the products from Krebs?

A

Each glucose molecule makes Krebs x2

Therefore -

  • 6 NADH
  • 2 ATP
  • 2 FADH
  • 1 CoA
  • 2 CO2
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91
Q

How does the ETC work?

A

H released split into H+ and e-. Electrons move across - lose energy at each carrier - used to pump H+ into inter membrane space –> electrochemical gradient. H+ moves back via ATP synthase (chemiosmosis). In matrix - H+ + e- + O2 = H2O.

O2 is final electron acceptor

Regenerated coenzymes are used in Krebs.

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92
Q

What are the 3 pathways into the ETC? How does each work.?

A

Complex I, II & Coenzyme Q

Complex I - NADH release - forms QH2 - moves to Complex III. 4H+ pumped in.

Complex II - succinate - fumarate from Krebs releases FADH2 - releases e and forms QH2. No H+ pumped.

CoQ - NADH from glycolysis directly drives formation of QH2 via CoQ in inter membrane space without using a complex (uses G3P shuttle).

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93
Q

Which 2 methods allow NADH to be brought into mitochondria?

A

G3P shuttle

Malate-aspartate shuttle

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94
Q

What happens at Complex III in ETC?

A

Receives electrons from I, II & glycolysis - in doing so 4 H+ are pumped into the intermembrane space before passing to cytochrome C in the inter membrane space - uses Fe to transfer electrons from III to IV (Fe2+ <> Fe3+).

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95
Q

What happens at Complex IV in ETC?

A

Accepts donated electrons - and attaches to O2 molecules - then uses H+ from matrix to produce H2O whilst also pumping more H+ into inter membrane space.

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96
Q

Which complexes in the ETC pump H+ into inter membrane space?

A

I, III & IV

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97
Q

Which enzyme creates ATP in the ETC?

A

ATP synthase

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98
Q

What do uncoupling reagents do?

Where are they found in the body?

A

Allow transport of H+ back into matrix bypassing ATP synthase - allows energy to be released as heat. Found in thermogenin in brown adipose tissue.

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99
Q

Why do muscles hurt after exercise at times?

A

Due to build up of lactic acid. When O2 is short - anaerobic respiration takes place - just glycolysis - pyruvate –> Lactate (NAD) + CO2 + H2O.

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100
Q

How many ATP are produced by lactate production?

A

2

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101
Q

What can be used in place of ATP during strenuous exercise?

A

Creatinine phosphate

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102
Q

How are fatty acids utilised in respiration?

A

Are changed from FA to ACoA for entry into Krebs via β-oxidation,

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103
Q

How is mitochondrial DNA inherited

A

From the mother only - father the mitochondria are in the flagella of sperm.

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104
Q

Why do mitochondrial DNA suffer greatest exposure and damage?

A

Because they are close to the ETC = greatest exposure to ROS.

Mitochondrial DNA is also less effective at correction & repair

Happens x10 more than nuclear DNA.

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105
Q

Which diseases have mitochondrial DNA damage over time been associated with?

A

Alzheimers, Parkinsons & T2 diabetes

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106
Q

Name some ROS

A

O2-, HO-, O22-, H2O2 & HOCl

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107
Q

Why are mitochondrial diseases from birth rare?

A

Affect the ETC - most are incompatible with life.

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108
Q

What are the implications of mitochondrial disease?

Which cells are most affected?

A

Reduces the capacity of cells to produce ATP.

Affects neurons, skeletal muscle and β cells of pancreas the most.

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109
Q

What are the symptoms of mitochondrial disease?

A

Exercise intolerance
Muscle weakness

Also - HF, arrhythmias, dementia, blindness & seizures

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110
Q

What are the two ways that mitochondrial disease can occur?

A

Threshold effect - threshold of mutated mitochondrial via damage that you need for pathology

Genetic bottleneck effect - randomness of mitochondrial division during ovum formation - means some will have resultant pathology whilst others wont.

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111
Q

What are the 5 classifications of mitochondrial disease?

A
  • Mitochondrial transport system defects
  • Substrate utilisation defects
  • Krebb’s cycle defects
  • Oxidative phosphorylation coupling defects
  • Oxidative phosphorylation defects
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112
Q

What is LHON?

A

Lebers Hereditary Optic Neuropathy

Single base change in Complex I (or similar in III) - leads to reduced transport to Ubiquinone - less ATP produced (although some still produced via succinate and glycolysis) - but not enough to support neuronal activity = damage to optic nerve - blindness

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113
Q

What is MERRF?

A

Myoclonus Epilepsy with Ragged-Red Fibre

Mutation in tRNA - disrupts synthesis of proteins needed for oxidative phosphorylation = skeletal fibres with abnormal shaped mitochondria (clump together).

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114
Q

What possible treatments are there for mitochondrial myopathies to prevent inheritance?

A

Replacing defective mitochondria in ovum - can merge DNA from 2 eggs - use IVF and transfer pronuclei of fertilised eggs to a zygote with normal mitochondria.

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115
Q

How do infections directly cause diarrhoea?

A

Cell death –> loss of absorptive area

+

Increase inflammatory response - causes fluid to leak into the bowel

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116
Q

How do infections indirectly cause diarrhoea?

A

Toxins (cytotoxic or pro inflammatory)
Mimic endogenous cell signalling mechanisms (act upon ion channels)
Form pores in cell membrane (cholera) or inc permeability at tight junctions

End result = fluid and electrolyte loss

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117
Q

Which medications can cause diarrhoea?

A

Metformin
ABs
Omeprazole
Ace Inhibitors

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118
Q

What are the main bacteria that cause diarrhoea?

A

Salmonella
Campylobacter
C. Diff
Cholera

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119
Q

What is the main virus that causes diarrhoea?

A

Norovirus

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120
Q

What are the causes of acute diarrhoea?

A

Infection - Viral, Bacterial
Meds
Parasites (unusual in UK)

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121
Q

Do you test for acute diarrhoea?

A

If P well - doesn’t usually need tests. Only test of symptoms persist and seems more chronic pathology.

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122
Q

What percentage of pop have diarrhoea?

A

7%

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123
Q

How do you define acute, persistent & chronic diarrhoea?

A 
Acute = < 14 days
Persistent = > 14 days
Chronic = > 4 weeks
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124
Q

How do drugs cause diarrhoea?

A

Osmotically active
Affect ion absorption
Inc Transit time
Alter absorption (causing malabsorption of fluid)
ABs - can cause overgrowth –> bugs like C Diff

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125
Q

When should you investigate acute diarrhoea?

A 
P is unwell
Blood/pus in stool
Recent ABs
Recent hospital admission
On PPI
Recently been abroad
Immunocompromised

Start with stool microscopy

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126
Q

What is in diarrhoea?

A

H20
Na
HCO3
K

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127
Q

What can bad diarrhoea affect?

A

Fluid and electrolyte levels

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128
Q

What can persistent diarrhoea cause?

A

Dehydration, hypokalaemia & acidosis (due to dehydration)

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129
Q

What is the treatment for acute diarrhoea?

A

Usually none if P remains well.

If unwell - fluids inc saline & glucose - reduces Na loss from proximal small bowel + improves water absorption via Na/Glu transporter.

V rare for ABs unless serious infection.

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130
Q

What is the commonest cause of chronic diarrhoea?

A

IBS

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131
Q

What defects of the colon can cause chronic diarrhoea?

A

Cancer
Diverticulitis
IBD

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132
Q

What defects of the SI cause chronic diarrhoea?

A 
Coeliac disease
IBD
Lactose intolerance
Bile salt malabsorption
Short bowel / intestinal failure
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133
Q

What defects of pancreas cause chronic diarrhoea? What will it cause?

A

Exocrine failure
CF

Causes steatorrhea (not digesting fats)

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134
Q

What defects of endocrine system can cause chronic diarrhoea?

A

Hyperthyroidism
Addison’s
Hormone Secreting Tumours

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135
Q

Which parasites can cause chronic diarrhoea?

A

Threadworms

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136
Q

Name 4 mechanisms of diarrhoea

A

Osmotic - fluid is drawn into lumen (lactose intolerance, steatorrhea)
Secretory - fluid is secreted into lumen (infection, gut hormone excess, post radiation)
Failure of absorption (coeliac, short gut syndrome)
Mechanical narrowing - overflow diarrhoea (neoplasia, stricture)

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137
Q

What faecal analysis tests can you do for diarrhoea?

A

Stool microscopy - infection, parasites
Faecal calprotectin level
qFIT
Faecal elastase (pancreatic exocrine levels)

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138
Q

What blood tests can you do for chronic diarrhoea?

A 
Thyroid
FBC
CRP
tTG
B12
Folic Acid & Folate
Gut Hormones
Minerals & Vitamin levels if worried about malabsorption
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139
Q

How can you examine the colon?

A

Colonoscopy
Virtual colonoscopy
Capsule colonoscopy

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140
Q

How can you examine the small intestine?

A

MRI
Capsule endoscopy
OGD
Colonoscopy for extreme end of bowel (can reach terminal ileum)

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141
Q

How does IBS present?

A

Abdo pain with possible painful defecation
+/- Altered stool frequency & appearance + 2 of:
- Altered stool passage
- Bloating/distension (worsened by eating)
- Rectal mucus
+ ALTERNATIVES EXCLUDED

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142
Q

Is mucus more common with IBS or BC?

A

IBS

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143
Q

How much of global pop have IBS? Which ppl is it most common in?

A

20% (probably underreported)

20-30 yr olds, F>M (underreporting?)

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144
Q

What is the cause of IBS?

A

Unknown - but possibly psychosocial influence, genetic link or infection link.

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145
Q

What is the management of IBS.

A

Rule out alternatives, reassure.
Dietary changes - avoid triggers - poss low FODMAP diet. Probiotics help.
Avoid stress

If symptoms persist = do tests and poss colonoscopy.

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146
Q

What are the medical treatments for IBS?

A

Diarrhoea - Loperamide (Immodium)
Buscopan (hydroscine butyl bromide) - antimuscarinic for cramps
Constipation - Laxatives (bulk-forming)
Tricyclic antidepressant - Amitriptyline (90% respond)

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147
Q

How does loperamide work? What are its SE?

A

Agonist for opioid receptors = anti motility. Opioid receptors in the bowel = mu receptors. When stimulated - inhibit GI motility and inc tone in sphincters. Loperamide only binds to SI mu receptors in the large intestine.

SE: Constipation, arrhythmia in high dose

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148
Q

How much of the pop has constipation?

A

1-2% - poss underreported. F>M.

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149
Q

What is the definition of constipation?

A

Less than 3 poos per week, excessive straining, abdominal pain / bloating. Look for change in intrinsic pattern and symptoms.

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150
Q

What are the functional causes of constipation?

A 
IBS
Behavioural
Slow transit
Pregnancy
Diet (poor fluid +/- fibre)
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151
Q

What are the colonic causes of constipation?

A

Cancer
Extrinsic compression
IBD w/ stricture

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152
Q

What medications cause constipation?

A

Opioids
Loperamide
Iron tablets

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153
Q

What endocrine condition can cause constipation?

A

Hypothyroidism

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154
Q

What neurological conditions can cause constipation?

A

Parkinsons
MS
Hirschsprung’s disease

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155
Q

What acute pathology causes constipation?

A

Bowel obstruction

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156
Q

What is Hirschsprung’s disease?

A

Congenital absence of ganglia in the bowel –> failure of peristalsis.

90% diagnosed in infancy as baby doesn’t pass meconium.

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157
Q

What are the possible consequences of chronic constipation?

A 
Haemorrhoids
Anal fissures
Painful defecation
Rectal prolapse
Abdo pain
Bloating
Diverticular disease
Urinary retention
Faecal impaction 
Overflow diarrhoea
Stercoral perforation
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158
Q

What investigations should you do for constipation?

A

Bloods - thyroid, FBC, inflammatory markers
qFIT
Calprotectin

Acute - AXR, CT (rule out BO), colonoscopy, virtual colonoscopy

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159
Q

What is diverticular disease?

A

Protrusions of mucosal pouches through the bowel wall.

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160
Q

What is thought to cause diverticular disease?

A

Thought to be closely linked to constipation + poor dietary fibre.

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161
Q

Which part of the bowel has the highest incidence of diverticular disease?

A

Sigmoid colon (where the intra-luminal pressure is highest)

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162
Q

What are the symptoms of bowel obstruction?

A

Absolute constipation - no passage of stool or wind.

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163
Q

What are the causes of bowel obstruction?

A

Extrinsic compression (mass, adhesions, hernias)
Bowel wall problem (neoplasia, inflammation, stricturing)
Luminal blockage

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164
Q

What is the management of a bowel obstruction?

A

Resus (if needed) = CT to decide whether intervention needed.

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165
Q

How do bulk forming laxatives work? Give an example of one.

A

Attract fat and water into lumen - incs mass - causes distension - triggers enteric reflex - causes peristalsis. Also softens stool.

Eg. Ispaghula hulk

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166
Q

How do osmotic laxatives work? Give an example of one.

A

Draws water into the lumen of the bowel - inc faecal mass & softens - enteric reflex - peristalsis.

E.g. lactulose, phosphate enemas, Movicol, Moviprep

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167
Q

How do stimulant laxatives work? Give an example of one.

A

Stimulate bowel nerves for peristalsis + have osmotic agent - softer stool.

E.g. Senna

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168
Q

How do stool softeners work? Give an example of one.

A

Allows fat and water to penetrate the stool - makes easier passage & reduced straining.

E.g. Docusate sodium

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169
Q

What are 1st and 2nd line treatments for constipation?

A

1st = Ispaghula hulk

2nd = Docusate sodium

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170
Q

What are possible side effects of laxatives?

A

Electrolyte imbalances, diarrhoea, wind, bloating (bulk-forming & osmotic), cramps (osmotic & stimulant), bowel obstruction.

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171
Q

How do we treat constipation?

A

Suggest high fibre diet + inc fluid + laxatives. If it doesn’t resolve - further testing.

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172
Q

What is Coeliac Disease? Which genes cause it?

A

Gluten - broken into gliadin - causes inflammation of small intestine (enteropathy) - means surface cant effective absorb. Because villi are inflamed - they shorten and atrophy.

Caused by DQ2 & DQ8 genes.

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173
Q

What percentage of pop have coeliac?

A

1% - F>M.

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174
Q

What is gluten found in?

A

Wheat, barley, rye & possibly oats if contaminated

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175
Q

What are the symptoms of coeliac disease?

A

Diarrhoea, steatorrhea, weight loss, anaemia, abdominal pain, malabsorption.

Malabsorption -> anaemia -> glossitis (B12 def), mouth ulcers, dermatitis herpetiformis, pale eye, angular stomatitis & chelitis.

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176
Q

How does coeliac present histologically?

A

Decreased folds of the intestine, villous atrophy (smooth shiny surface) & scalloping of the folds. Can form lots of crypts with large presence of inflammatory cells (trying to stop gliadin crossing into bowel wall). Also increased intraepithelial lymphocytes.

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177
Q

Why does gliadin cause coeliac disease?

A

It crosses enterocytes & forms a complex with tTG - binding to T cells - causes them to produce antibodies - anti-tTG, anti-endomysial & anti-gliadin.

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178
Q

Why does coeliac disease cause dermatitis herpetiformis?

A

The tTG complex can react to epidermal TG causing the rash.

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179
Q

What are the three antibodies produced in response to tTG in coeliac Ps?

A

Anti-tTG
Anti-gliadin
Anti-endomysial

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180
Q

What is the gold standard investigation for coeliac disease?

A

Endoscopy biopsy (OGD).

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181
Q

What is the Marsh criteria?

A

For coeliac disease - 3 things observed:

Raised intraepithelial lymphocytes, crypt hyperplasia + villous atrophy

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182
Q

What is the treatment for coeliac disease?

A 
Gluten free diet (oats ok)
Vaccination against pneumococcus 
Screen for osteoporosis
Supplements - iron, B12 & folate
Screen for other AI disease & thyroid disease
Annual FBC
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183
Q

Why are coeliac Ps vaccinated against pneumococcus?

A

Because for many the spleen becomes inept.

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184
Q

How does Crohn’s appear on histology?

A

Patchy, transmural ulceration - anywhere from mouth to anus. Inflammation is full depth - can form fistulae, ulcers & strictures. Granulomas can be seen. Perianal disease may also be seen.

Can spread to adjacent bowel & organs - can also cause localised abscesses.

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185
Q

Who is more likely to get Crohn’s?

A

Younger adults & children - bimodal peak at mid-20s and mid-60s.
Strong link to smoking
Higher in Western & Jewish Ps

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186
Q

What causes Crohn’s?

A

Not known - combo of genetic, immune, environment, diet, smoking & NSAIDs. Strong genetic link.

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187
Q

What happens to the mucosal barrier in Crohn’s?

A

Defects in the mucosal barrier allow pathogens and antigens to invade.

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188
Q

Which gene is most commonly identified in Crohn’s?

A

Chromosome 16, NOD2 - most common. 200+ others have also been identified.

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189
Q

What is the treatment for Crohn’s?

A

Acute - nil by mouth, IV ABs (if abscess) & HCS, liquid diet for 1 month (modulen).
Meds: Thiopurines, Biologics, Prednisolone

Surgically - 50% will need - of these 70% will need a second op within 5 years. Remove infected patches.

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190
Q

How does Ulcerative Colitis present?

A

Continuous inflammation, superficial to mucosa only (unlike Crohn’s), only affects colon. Lesions start at rectum and extend proximally with no breaks. Does not affect small intestine.

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191
Q

What does ulcerative colitis look like on histology?

A

No deep ulcers, continuous inflammation.
Crypt abscesses but no granulomas.
Affects only mucosal layer.

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192
Q

Which disease is more at risk for perforation and why - Crohn’s or UC?

A

UC - lumen can become so narrowed with inflammation that air cannot pass - causes toxic megacolon.

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193
Q

What is the risk of colectomy in Ps with UC?

A

20-30%

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194
Q

In UC - what are the following?

  • Proctitis
  • Left-sided disease
  • Pancolitis
A

Proctitis = inflammation of rectum only
Left-sided disease = rectum and sigmoid colon only
Pancolitis = entire colon inflammation

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195
Q

What are the statistics regarding progress of UC?

A

First year - 1/3 remission, 1/3 symptomatic, 1/3 progressive to extensive disease.

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196
Q

What does extensive UC put Ps at risk of developing?

A

More flares, perforation and colorectal cancer.

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197
Q

What is the treatment for UC?

A

Acute - IV HCS, LMWH, Mesalazines, Thiopurines then Biologics. Use corticosteroids for flares in between.

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198
Q

What are mesalazines?

A

5-aminosalicyclic acids (5-ASAs) = are pH dependant capsules - can alter release timing along passage.

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199
Q

What is Barrett’s oesophagus?

A

Changes in the lining of oesophagus from squamous epithelium to columnar with goblet cells.

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200
Q

What is the progression of Barrett’s oesophagus?

A

GORD –> Reflux oesophagitis –> Metaplasia

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201
Q

What are the signs of Barrett’s oesophagus?

A

Dysphagia & heartburn

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202
Q

What is metaplasia?

A

Replacement of one adult cell type to another adult cell type.

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203
Q

What is dysplasia?

A

Increased cell numbers - can be low or high grade - is a pre-malignancy stage.

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204
Q

What is the biggest risk factor for oesophageal adenocarcinoma?

A

Barrett’s oesophagus

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205
Q

What is the pathogenesis of Barrett’s Associated Adenocarcinoma?

A

Normal squamous –> Reflux / Oesophagitis –> Metaplasia (Barrett’s) –> Low grade dysplasia –> High grade dysplasia –> Adenocarcinoma

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206
Q

What functions do secretions perform?

A

Lubrication
Digestion
Protection

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207
Q

What are the 3 major salivary glands, what percentage of saliva do they make and what does their saliva contain?

A

Parotid - 25% - serous + high conc salivary amylase
Submandibular - 70% - mixed mucous and serous.
Sublingual - 5% - mucus

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208
Q

What are dispersed salivary glands?

A

Smaller salivary glands found in the mucosa of mouth & tongue.

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209
Q

What are the components of saliva?

A 
Water
Electrolytes - Na, Cl, HCO3 & K
Enzymes
IgA
Mucin 
Urea & Uric acid (waste for removal)
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210
Q

What does α-amylase in saliva do?

A

Hydrolyses α 1-4 glycosidic bonds in starch

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211
Q

What do lysozymes in saliva do?

A

Hydrolyses peptidoglycan in G-ve bacteria.

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212
Q

When is lingual lipase activated?

A

In low pHs - stomach acid.

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213
Q

What does lactoferrin in saliva do?

A

Antibacterial - chelates iron - stops microbes from multiplying.

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214
Q

What does IgA do in saliva?

A

Prevents microbial attachment to the epithelium.

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215
Q

What do myoepithelial cells around acinar cells do?

A

They contract and force more saliva from the acinar cells into the acinus & duct.

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216
Q

What are the two stages of saliva formation?

A

1) . NKCC1 co-transporter transports Na & Cl into the acinus - water follows - forms isotonic fluid.
2) . Fluid flows into the duct of the salivary gland - reabsorption of Na and Cl occurs, water cannot follow as ductal cells are relatively impermeable to water - K and HCO3 flow into the ductal fluid = hypotonic fluid.

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217
Q

What happens to the components of saliva when flow rate increases?

A

Becomes more isotonic - BUT is always slightly hypotonic - Na & Cl levels inc.

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218
Q

What is the pH of saliva?

A

6-7

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219
Q

How does the ANS control salivary secretions?

A

PSS - stimulates via CN7 (submandibular and sublingual) and CN9 (parotid) = inc saliva production and vasodilation.

SS - superior cervical ganglion & sympathetic postganglionic nerves - INHIBIT - vasoconstriction & reduced saliva = dry mouth (e.g. nervous)

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220
Q

Which cranial nerve innervates the submandibular and sublingual salivary glands?

A

CN 7 - Facial nerve

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221
Q

Which cranial nerve innervates the parotid salivary gland?

A

CN9 - GPG

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222
Q

Which AI disease destroys exocrine glands - leading to reduced tear and saliva production?

Which test is used to determine?

A

Sjorgren’s syndrome

Schirmer’s test (filter paper to eyes)

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223
Q

Which disease causes lack of adequate saliva leading to tooth decay & halitosis, difficulty speaking, dysphagia & bacterial overgrowth in the mouth?

A

Xerostonia

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224
Q

Where are gastric glands in the stomach? What do they contain?

A

In the mucosa.

Exocrine and endocrine glands

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225
Q

Which cell produces mucus?

A

Mucous neck cells

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226
Q

Which cell produces HCL in the stomach?

A

Parietal cells

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227
Q

Which cell produces intrinsic factor in the stomach?

A

Parietal cells

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228
Q

What is the function of HCL in the stomach?

A

It converts pepsinogen to pepsin.

Denatures proteins - allowing easier protein breakdown

Kills microbes

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229
Q

What is the function of Intrinsic factor?

A

Needed for B12 absorption in the SI - needed for erythropoiesis.

Absence of IF = pernicious anaemia.

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230
Q

Which cells produce pepsinogen?

A

Chief cells

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231
Q

Which cells produce gastric lipase?

A

Chief cells

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232
Q

Which cells produce rennin?

A

Chief cells

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233
Q

What does pepsinogen do?

A

Used to break down proteins (activated in the presence of HCL and covered to pepsin).

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234
Q

What does gastric lipase do?

A

Breaks down 3Gs to FAs and 2Gs.

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235
Q

Name 3 exocrine glands in the stomach.

A

Mucous neck cells
Parietal cells
Chief cells

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236
Q

Name 3 endocrine cells in the stomach

A

G-cells
D-cells
ECL cells

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237
Q

Which cell in the stomach can be endocrine or paracrine.

A

D cells

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238
Q

Which cells in the stomach produce gastrin?

A

G cells

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239
Q

In what 3 ways are G cells in the stomach stimulated?

A

CNX

Distension of the stomach

Presence of peptides

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240
Q

What does gastrin do?

A

Activates parietal and chief cells.

Causes lower oesophageal sphincter contraction

Increases motility of the stomach

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241
Q

Which cells produce somatostatin?

A

D Cells

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242
Q

When is somatostatin produced?

What does it do?

A

When the H+ levels in the duodenum are too high.

It inhibits H2 receptors on parietal cells - prevents H+ release into the stomach.

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243
Q

Which cells produce histamine in the stomach?

A

The enterochromaffin-like cells

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244
Q

What is the membrane of parietal cells like?

A

Branched canaliculi with lots of villi

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245
Q

In which 3 ways can parietal cells be stimulated?

A

1) . CNX (via ACh)
2) . Gastrin from blood stream - binds to their basolateral membrane.
3) . Histamine binds to H2 receptors and stimulates.

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246
Q

What happens inside parietal cells when they are stimulated?

A

ACh/Gastrin simulate and activate PLC - releases Ca2+ or histamine –> H2 receptor –> AC –> cAMP –> PKA.

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247
Q

Name 2 ways that parietal cells can be inhibited?

A

1) . Somatostatin (paracrine & endocrine action) - inhibits H2 receptors.
2) . Mucosal prostaglandins - antagonist of H2.

248
Q

How to NSAIDs cause gastric damage?

A

They inhibit prostaglandins - means the H2 receptor is no longer blocked - histamine continuously produced and H+ secreted.

249
Q

How are parietal cells adapted for acid secretion?

A

+++ Mitochondria & Tubulovesicles - fuse to form microvilli when stimulated - these contain H+ K+ ATPase & carbonic anhydrase needed for H+ secretion.

250
Q

Name 3 pharmacological inhibitors of gastric acid & how they work.

A

PPIs - inhibit the H+/K+ ATPase pump = less H+

H2 receptor antagonist (Cimetidine)

Atropine - inhibits M receptors & CNX stimulation of acid secretion.

251
Q

What are the three phases of gastric secretion?

A

1) Cephalic
2) Gastric
3) . Intestinal

252
Q

What happens in the cephalic phase of gastric secretion?

A

Sight, smell etc - excites vagal centre in medulla –> CNX –> stimulates parietal, chief & G cells to release.

253
Q

What happens in the gastric phase of gastric secretion?

A

Bolus in the stomach - causes distension - excites CNX and also neurosensory reflexes (ENS) = secretions from parietal, chief, mucus & G cells

254
Q

What happens in the intestinal phase of gastric secretion?

A

Can be excitatory or inhibitory of gastric juices + controls rate which chyme enters duodenum.

Excitatory = high pH or peptides - triggers further gastric secretions via CNX and gastrin.

Inhibitory = low pH, protein products or change in osmolarity = triggers production of CCK - inhibits gastric secretions

255
Q

Why does the gastric mucosa not get damaged?

A

Mucin - physical barrier from acidity.

HCO3 - secreted by surface epithelial cells - pH remains near 7 close to tissue - pepsinogen not activated - prevents digestion of tissue proteins.

Tight junctions - stop acid damaging underlying tissue.

256
Q

Most common causes of gastritis?

A

H pylori
Smoking
Alcohol
NSAIDs

257
Q

How is acute damage to the gastric lining repaired?

A

Through rapid division of stem cells found in neck of gastric glands.

258
Q

What secretions are found in the small intestine?

A

Intestinal juice
Pancreatic juice
Bile

259
Q

What is in intestinal juice?

A

Mucus
Electrolytes & water
Lysosomes
Alkaline mucosal fluid

260
Q

What cell produces mucus of the intestinal juice?

A

Goblet cells

261
Q

Which cells produce electrolytes and water of intestinal juice?

A

Secretory enterocytes

262
Q

Which cells produce lysozymes in intestinal juice?

A

Paneth cells

263
Q

Which cells produce alkaline mucosal fluid in the small intestine?

A

Brunner’s glands

264
Q

What does pancreatic juice contain?

A

Digestive enzymes & HCO3

265
Q

What are the 3 components of the small intestine and what does each do?

A

Duodenum - receives chyme & neutralises via Brunner’s glands secretions.

Jejunum - chemical digestion and absorption takes place

Ileum - B12 absorption takes place via Peyer’s patches

266
Q

Which endocrine hormones are secreted into the small intestine from the duodenum?

A

CCK
Secretin
GIP (Gastric Inhibitory Peptide)

267
Q

What makes CCK and what does it do?

A

From I cells - stimulates pancreatic and gallbladder secretions. Also inhibits gastric emptying.

268
Q

What makes secretin and what does it do?

A

S cells - stimulates pancreatic and biliary HCO3 secretions

269
Q

Which cell makes GIP (Gastric Inhibitory Peptide) and what does it do?

A

Made from K cells - inhibit acid secretion / stimulate insulin release.

270
Q

What is present in the base of intestinal glands?

What are they vulnerable to and why?

A

Daughter cells - differentiate and migrate to become goblet, enteroendocrine, Paneth or enterocytes.

Have rapid regeneration (3-6 days) - therefore are vulnerable to chemo and radio.

271
Q

How do secretions from the pancreas get to the duodenum? What is their flow controlled by?

A

Pancreas –> pancreatic duct –> accessory pancreatic duct –> joins CBD from gallbladder –> hepatopancreatic sphincter - controls secretions into the duodenum.

272
Q

What percentage of the pancreas is exocrine and endocrine?

A

99% Exocrine acinar clusters

1% Endocrine islets

273
Q

How do secretions from acinus of exocrine glands get to the main pancreatic duct?

A 
Acinus -->
Intercalated duct -->
Intralobular duct -->
Interlobular duct -->
Main duct
274
Q

What stimulates the pancreas to release exocrine pancreatic juice?

A

Presence of chyme with fat and protein in the duodenum - stimulates CNX to release ACh - simulates ducts to release CCK = production of lower vol, enzyme rich juice.

275
Q

Which electrolytes are in exocrine pancreatic juice?

A

High in Na & HCO3

Low in Cl & K

276
Q

Which electrolytes are in pancreatic endocrine secretions?

A

High in Na and Cl, lower in HCO3 and K.

277
Q

What triggers the secretion of endocrine pancreatic secretions?

A

Highly acidic chyme - stimulates production of secretin from S cells - stimulates endocrine pancreatic secretions.

278
Q

Name 4 types of cells in the Islets of Langerhans and name what they produce.

A

Αlpha cells = glucagon
Βeta cells = insulin
Delta cells = Somatostatin
F cells = pancreatic polypeptides

279
Q

How does the pancreas avoid auto-digestion?

A

Secretes proteolytic enzymes in inactive form.

Also secretes trypsin inhibitor - prevents activation of trypsin in the pancreas.

280
Q

Which digestive enzymes does the pancreas secrete?

A 
Proteolytic enzymes
Amylase
Lipases
Nucleases
Trypsin inhibitor
281
Q

What are zymogens?

A

Inactive proteolytic enzymes.

282
Q

What are zymogens activated by?

A

Kinases in the small intestine brush border.

283
Q

How is HCO3 pancreatic produced by the pancreas?

A

Chyme in duodenum = fall in pH - stimulates secretin release.

Secretin causes HCO3 to leave pancreatic duct cells in exchange for Cl entering. CFTR channel then pumps Cl back into the lumen - allows more HCO3 to be pumped out into lumen.

Na follows HCO3 into lumen (down the electrochemical gradient) water then follows sodium by osmosis.

Result = high vol HCO3 pancreatic juice.

284
Q

How does the cephalic phase stimulate pancreatic juices?

A

PSS - CNX - ACh –> VIP - stimulates enzyme secretion by acinar cells of pancreas.

285
Q

How does the gastric phase of digestion stimulate production of pancreatic juices?

A

Distension = vagovagal reflex via CNX - causes production of gastrin by G cells - stimulates enzyme secretion by acinar (exocrine) cells in pancreas.

286
Q

In what 2 ways does the intestinal phase of digestion stimulate the production of pancreatic juices?

A

1) . Protein & fat in duodenum - stimulates secretion of CCK by I cells = enzyme secretion by exocrine cells in pancreas.
2) . Low pH in duodenum - stimulates secretin secretion (S cells) = endocrine duct cells to produce HCO3 rich juice.

287
Q

What happens to pancreas in Ps with CF?

A

Lack CFTR gene - therefore defective ductal secretion - ducts become blocked with enzymes & mucus - causes fibrosis.

Lack of enzyme secretions to duodenum from pancreas = malabsorption. Need Creon.

288
Q

What is pancreatitis caused by?

A

Gallstones and alcohol - can cause pancreatic enzymes to activate in the pancreas. V painful.

289
Q

What do bile salts do?

A

Emulsify fats for digestion (with lipase) - and turn them into micelles for absorption.

290
Q

How is bile made?

A

Hepatocytes in liver acinus - produce bile and drain into canaliculi.

291
Q

How does bile get from the liver to the gallbladder?

A 
Acinus -->
Canaliculi -->
L & R Hepatic bile ducts -->
Common hepatic duct -->
Cystic duct -->
Gallbladder
292
Q

Where is bile stored?

A

Gallbladder

293
Q

How does bile get from gallbladder to duodenum?

What controls it?

A 
Gallbladder -->
Cystic duct -->
Common Bile Duct -->
Pancreatic Duct -->
Duodenum

Controlled by hepatopancreatic sphincter (Sphincter of Oddi)

294
Q

What stimulates release of bile?

A

CCK (released when fat is in duodenum) - causes gall bladder contraction & relaxation hepatopancreatic sphincter (Oddi).

Acidic chyme in duodenum –> secretin = liver ductal cells to secrete watery HCO3 into the bile.

295
Q

How is the gallbladder controlled by the PSS?

A

CNX - minor role in bile flow and gall bladder contraction.

296
Q

What causes gallstones?

A

XS water & bile salt reabsorption or XS cholesterol in bile - causes precipitation = gallstones.

297
Q

What is biliary colic?

A

Blockage of the cystic duct.

298
Q

What is enterohepatic circulation of bile salts?

A

Recycling of bile salts from the ileum (94% are returned through portal vein to liver).

299
Q

What effect does enterohepatic circulation of bile salts have upon hydrophobic drugs?

A

Hydrophobic drugs - are deactivated by liver and secreted into bile - of there is recirculation of bile salts then it slows the rate at which the drugs are totally eliminated from the body.

300
Q

What drives water and electrolyte homeostasis?

What is it controlled by?

A

Na and Cl transport.

Controlled by ENS, ANS, endocrine & immunogenic systems.

301
Q

What can disruption of absorption of water cause?

A

Diarrhoea
Dehydration
Electrolyte imbalances

302
Q

Which ions are dominant extracellularly?

A

Na and Cl

303
Q

Which ion is dominant intracellularly?

A

K

304
Q

What can cross the cell surface membrane?

What cannot cross the CSM?

A

Non-polar, hydrophobic molecules (O2, CO2) or small, uncharged molecules.

Non-permeable to large, charged molecules (ions & glucose)

305
Q

Which cellular processes enable larger molecules to cross the cell surface membrane?

A

Endocytosis & exocytosis

306
Q

What does the Na/K ATPase pump do?

Where is it found?

A

Moves 3 Na out and 2 K in. Found in epithelial cells.

Creates a negative Na electrochemical gradient intracellularly - allows Na to be drawn in from the lumen via channel or co-transporter - and water flows into the lumen to follow the high conc of Na.

307
Q

Give an example of a symporter that uses secondary active transport.

A

Na/Glu symporter.

308
Q

What is the difference between primary and secondary active transport

A

Primary - uses ATP to move a molecule across the membrane.

Secondary - uses the concentration gradient of one molecule in a symporter to move the other molecule.

309
Q

Give an example of facilitated diffusion across the CSM.

A

Ion channels - e.g. aquaporins that allow water to move across.

310
Q

What are enterocytes?

What is found between them?

A

Intestinal epithelial cells

Between them = tight junctions .

311
Q

What is the purpose of tight junctions between enterocytes?

Where are they found to be more permeable?

A

Keeps the gut contents away from the tissues underneath.

More permeable in the duodenum.

312
Q

What is bi-directional fluid flux?

A

Absorption of water + secretion of secretory agents at the same time.

313
Q

What affects the rate of the bidirectional fluid flux?

A

The tonicity of chyme.

314
Q

What is the difference between the enterocytes in crypts and the enterocytes in villi?

A

Crypts = secretory function

Villi = absorptive function

315
Q

What are the routes of transport in enterocytes?

A

Transcellular - across CSM

Paracellular - moves between cells through tight junctions - no energy required.

316
Q

What is solvent drag? Give an example.

A

Water moves via osmosis and takes ions with it.

E.g. Tight junctions in the proximal SI - Na, K and Cl move paracellularly with H2O.

317
Q

What’s happens in the duodenum to the osmolality of chyme?

A

There is rapid equilibrium to form isotonic chyme - H20, Na & Cl move through permeable tight junctions.

318
Q

What does the jejunum reabsorb?

A

Na, K, Cl & H20

319
Q

What does the ileum secrete?

A

HCO3

320
Q

What does the large intestine reabsorb and secrete?

A

Reabsorbs Na, Cl & H20

Secretes K+ and HCO3

321
Q

How much water is lost through the rectum each day?

A

100ml

322
Q

How does sodium drive absorption in the small intestine?

A

Na is pumped out of enterocytes in the basolateral membrane by the Na/K ATPase pump (3 Na out, 2 K in) = creates a negative electrochemical gradient within the enterocytes. Na then moves down the electrochemical gradient from the lumen, through the apical membrane and into the enterocytes - uses carrier proteins to do so - this drives the absorption of other ions and organics.

323
Q

Which cell within intestinal villi secretes mucus to provide a protective layer to the apical surface?

A

Goblet cells

324
Q

What do I cells do?

A

Secrete CCK when there is fat or protein in the duodenum. Also modulate bile secretions and exocrine pancreatic secretions.

325
Q

Which are the only three sugars that can be absorbed through the small intestine wall?

A

Glucose, fructose & galactose - all monosaccharides.

326
Q

What is the mechanism that allows water to be reabsorbed in the duodenum?

A

Duodenum contains brush border microvilli, which increases the surface area available for absorption.

Diffusion – there is some diffusion of water directly through the membrane, aquaporins are membrane proteins that form selective water channels (facilitated diffusion).

Facilitated diffusion – ions (channel), glucose (carrier), water via aquaporin channels.

Duodenal tight junctions are more permeable (cf. jejunum/ileum), allowing them to respond more quickly to the tonicity of the chyme.

327
Q

How is sodium absorbed in the large intestine?

A

Driven by Na/K ATPase pump in basolateral membrane – Na then enters intracellularly via FD through protein channels (this is regulated by aldosterone which increases Na channels & absorption at expense of K+) – allows K+ secretion when lumen concentration is low.

Cl & HCO3 mechanism provides buffer for acid (produced by bacteria) – Cl moves transcellularly into BV & paracellularly through tight junctions (no backflow through these – are less permeable than in proximal duodenum). HCO3 is secreted into lumen for excretion.

328
Q

What are the bonds between glucose molecules in starch?

A

α 1-4 and α 1-6 glycosidic bonds. α 1-6 creates the side branches.

329
Q

What does amylase in saliva do?

A

Begins carbohydrate digestion - hydrolyses the α 1-4 glycosidic bonds - creates maltose, maltotrose & α dextrins.

330
Q

When is salivary amylase inactivated?

A

When it reaches the stomach - cant work in low pH - therefore starch digestion cannot occur in the stomach.

331
Q

After swallowing - where is starch broken down?

A

Duodenum contains

1) pancreatic α amylase
2) enterocyte brush border enzymes (inc maltase & sucrase).

332
Q

How is glucose absorbed in the small intestine?

A

Enterocytes absorb glucose via the Na-GLUT co=transporter on their apical surface (2 Na: 1 Glucose).

333
Q

What happens to glucose once it is absorbed by enterocytes?

A

It is transported via GLUT 2 transporters on basolateral membrane into the blood stream.

334
Q

Where does digestion of fats commence?

A

In the mouth - mastication + lingual lipase.

335
Q

What secretes lingual lipase?

A

Dispersed salivary glands of the tongue.

336
Q

What does lingual lipase do?

A

Converts 3Gs to 2Gs and FAs.

337
Q

Where does lingual lipase work best and why?

A

In the stomach - works better in low pH.

338
Q

How are fats broken down in the stomach?

A
  1. Gastric lipase secreted - hydrolyses 3Gs to FAs and glycerol.
  2. Lingual lipase works better in low pH
  3. Contractions of stomach disperse fat molecules and prevent clumping.
339
Q

How are fats broken down in the duodenum?

A

Chyme moves through pyloric sphincter - bile emulsifies fat goblets.

Segmentation of SI breaks down large fat molecules = micelles.

340
Q

How are fats absorbed in the small intestine?

A

Micelles cross apical membrane of enterocytes via passive diffusion + lipid transporter mechanisms (FA transporter protein).

341
Q

What happens to lipids inside enterocytes?

A

FAs & glycerides –> ER –> Golgi - used to make 3Gs before being attached to cholesterol and lipoproteins = chylomicrons.

Chylomicrons are then removed from the cell in golgi vesicles via exocytosis through basolateral membrane of enterocyte - are discharged into lacteals.

342
Q

What are lacteals?

A

The lymph vessels of the small intestine.

343
Q

What catalyses proteolysis?

A

Proteases.

344
Q

What breaks down proteins in the stomach?

A

Pepsoinogen is released from chief cells - is converted to pepsin in the acidic environment (needs pH 2-3).

345
Q

How are proteins broken down in the duodenum?

A

Trypsin and chymotrypsin = pro-enzymes (zymogens) - secreted into SI from pancreas and are activated by mucosal membrane of duodenum (are enterokinases on the brush border of the duodenum).

346
Q

How are AAs absorbed into the duodenum?

A

Utilise the electrochemical gradient of Na across the epithelium. Protein transporters bind AAs after binding Na (is a symporter - conformational change occurs when Na binds that then attaches AA) - deposits both Na and AAs into the cytoplasm.

347
Q

How do AAs get into the blood?

A

There are transporters on enterocyte basolateral membrane that export AAs from the cell into the blood - is not dependant on the Na gradient here.

348
Q

What does bile do?

A

Emulsifies fats into chylomicrons - solubilises for transport across the CSM.

Also involved in elimination of waste products - bilirubin is made from haem degradation.

Bile also needed for cholesterol and drug transport around the body.

349
Q

Where are fat soluble vitamins stored?

A

In the liver and adipose tissue until needed.

350
Q

What is absorption?

A

Transfer of drug from administration site to blood circulation.

351
Q

What factors affect absorption of drugs?

A

Pharmaceutical properties of the drug (pill/liquid)

Physiochemical properties of the drug (solubility, pH, molecular weight - bigger = harder to cross CSM)

Physiological properties (SA, contact time, concentration of drug, absorption site, interactions, transport systems)

352
Q

What happens to diffusion rate with a higher concentration?

A

It increases - higher concentration = faster diffusion as stronger concentration gradient

353
Q

Where is best for the absorption of alkaline drugs?

A

Small intestine

354
Q

Where is best for the absorption of acidic drugs?

A

Stomach

355
Q

Where do enteric coated drugs dissolve?

A

Small intestine - will not dissolve in low pH

356
Q

How does gastric emptying / motility affect drug absorption?

A

If the stomach empties too fast, or of the small intestine works too quickly - there is not enough time for the drugs to be broken down and absorbed.

357
Q

What do antacids or enzymes do drug absorption?

A

They can affect absorption and drug stability by changing pH or rate of reaction - meaning that drugs are absorbed too quickly / slowly / in the wrong place.

358
Q

What things can affect drug absorption?

A 
pH of GIT
Enzymes in GIT
Gastric emptying / motility rate
Presence of food 
Other drugs 
Formation of complexes
Chelation
359
Q

How does chelation or formation of a drug complex affect absorption?

A

It can prevent the drugs from working as it should or even prevent its absorption into the blood stream.

360
Q

What is bioavailability?

How is it worked out?

A

The fraction of the drug which reaches the blood circulation compared to the IV dose administered. Is given as a percentage

Bioavailability = Oral AUC / IV AUC

361
Q

If the bioavailability of a drug is 20% - how many times higher do you need to make the IV dose?

A

x5 higher

362
Q

Why does bioavailability of a drug occur?

A

First pass metabolism in the liver means some of the drug is absorbed and degraded without reaching the blood stream.

363
Q

If you avoid first pass metabolism do you still need to do bioavailability?

A

No

364
Q

Which drug administration routes bypass the liver?

A

IV
Sublingual
Buccal
Suppository

365
Q

What are the pros and cons of enteral administration of drugs (i.e. through GI tract).

A

Simple & inexpensive

GIT - harsh environment, needs to be absorbed - can be slow delivery to site of action.

366
Q

What are the pros and cons of parenteral (IV, IM & SC) drug administration?

A

Rapid, no first pass or harsh GI environment.

Difficult to reverse, infection risk, pain, fear, training required,

367
Q

What are the pros and cons of mucous membrane drug administration?

A

Rapid, direct delivery, no first pass, painless, convenient, low infection risk.

Limited drugs can be given this way, not all Ps have dexterity for inhalers.

368
Q

What are some examples of drug administration methods via mucous membranes?

A

Inhalers
Suppositories
Sublingual

369
Q

What are the pros and cons of the transdermal route of drug administration?

A

Simple, painless, convenient, good long term use, no first pass.

Requires highly lipophilic drug, slow delivery, irritation.

370
Q

What is distribution of drug in the body?

A

Transference of the drug to other parts of the body and tissues.

371
Q

Which types of drugs reach the following body compartments following absorption?

  • Total body water
  • Extracellular water
  • Blood plasma
  • Adipose tissues
  • Bones & teeth
A

Total body water - small, water-soluble drugs

Extracellular water - large water-soluble drugs

Blood plasma - protein-bound molecules, large molecules, highly charged molecules

Adipose tissue - lipid soluble

Bones & teeth - certain ions

372
Q

What is the volume of distribution of a drug?

How is it calculated?

A

A measure of how widely a drug is distributed in body fluid and tissues compared to plasma conc.

Vd = amount of drug in body / measured plasma concentration (Cp).

373
Q

If there is 25mg of drug in the tissues and 10mg/L in the plasma - what is the volume of distribution?

A

25/10 = 2.5 Vd

374
Q

If there is 25mg of drug in the tissues and 0.5g in the plasma - what is the volume of distribution?

A

25/0.5 = 50 Vd

375
Q

What factors influence distribution of drugs?

A

Physiochemical properties of the drug.

Drug protein binding affinity

Drug particle size

Blood flow

pH

376
Q

What causes higher rates of Vd - water soluble or lipid soluble drugs?

A

Water soluble drugs mainly staying the blood & water compartments of the body = low Vd.

Lipid soluble drugs are widely distributed to the tissues = higher Vd.

377
Q

Why does protein binding prolong the half-life of drugs?

A

Drug binds to the protein (reversibly). When the proteins in the blood are saturated - the remaining unbound drug has the clinical effect.

The bound drug is not active until released. When the unbound drug is metabolised and excreted - then the bound drug can be released and utilised - this prolongs the half-life of the drug.

A small difference in protein binding can have large affects on free drug concentration & drug effect.

378
Q

What affects how much drug binds to blood proteins?

A

The concentration of the drug
Its affinity for the binding site
The concentration of the proteins.

379
Q

Which is the most important plasma protein and why?

A

Albumin - binds to may different drugs - therefore competition between drugs for the binding site on albumin can occur.

380
Q

When is protein binding clinically relevant?

A

When there is high protein binding (>90%)
When there is a change in protein binding
When there is a low Vd

381
Q

Why does saturability inc the amount of unbound drug?

A

If the blood protein is saturated by other things - then the amounts of free drug increase.

382
Q

Why does displacement increase the amount of unbound drug?

A

If there is competition for the protein binding then this can increase the amount of free drug.

383
Q

What can late pregnancy increase the amount of unbound drug?

A

Because it affects the concentration of albumin.

384
Q

Why does renal impairment increase the amount of unbound drug?

A

Renal impairment = toxins accumulate and can bind to albumin - reduces saturation via competition.

385
Q

How do low plasma albumin levels affect the amount of unbound drug?

A

Increases the amount of unbound drug - less albumin = more free drug.

386
Q

What intake do we look at when assessing malnutrition?

A

Intake of energy and protein.

387
Q

Of under 5s - how many deaths are linked to malnutrition?

A

Over half.

388
Q

How prevalent is malnutrition in the UK?

A

Very - over 3m ppl affected

Esp - care homes, hospital inpatients (oncology, respiratory, geriatrics).

389
Q

What impact does malnutrition have economically?

A

Huge burden - 15% of health & care pending - 50% >65s - inc dependancy, GP visits, prescriptions, referrals, admissions, readmissions, complications in infections, inc length of hospital stay and DEATH…

390
Q

What is the malnutrition carousel?

A

Revolving hospital door idea - Hospital stay puts Ps at risk of malnutrition - longer stay, more complications, more support needed after, more likely to need care (70% of Ps weigh less after discharge) - more GP visits and prescription & care needs on release - greater chances of hospital admissions as a consequence.

391
Q

Name some of the consequences of malnutrition on a P’s health.

A

Reduced muscle mass & strength (= less independent Ps)
Inactivity = pressure ulcers & blood clots
Falls
Reduced ability to cough = chest infections & pneumonia
Heart failure (catabolised heart muscle)
Impaired temp regulation - hypothermia
Increased osteoporosis / rickets
Decreased immunity & resistance = impaired healing

392
Q

What do Ps often report as weight loss?

A

Looser clothes, jewellery, dentures,
Sunken cheeks & temples
Tiredness, low energy, inability to do what they did previously, low mood, poor concentration.

393
Q

Which Ps are at most risk of malnutrition?

A

> 65s
Long-term condition Ps (diabetes, renal, chronic lung)
Chronic progressive conditions (dementia, cancer)
Cancer or GI conditions
Drug or alcohol abuse Ps

394
Q

How long can Ps survival in starvation?

A

Rare after 3 months, 40% body weight loss or BMI <10 F / <11 M

395
Q

What happens in short term starvation?

A

Inc ++ glycogenolysis, + lipolysis and +++ protein catabolism. Energy expenditure is elevated.

396
Q

What happens in long term starvation?

A

Glycogen stores depleted, +++ lipolysis, + protein catabolism. Dec energy expenditure. Adaptive response to conserve protein.

397
Q

What is stress starvation?

A

Associated with metabolic stress (trauma/injury/sepsis) - normal adaptive response of conserving protein is override by neuroendocrine & cytokine responses to the injury.

398
Q

What happens during stress starvation?

A

Metabolic rate increases, ketosis is minimal and protein catabolism +++ to meet demands for tissue repair and gluconeogenesis.

Is hyperglycaemia & glucose intolerance, oedema & hypoalbuminaemia, N levels decrease and ketone bodies increase.

Difficult to get enough calories and protein into P as requirements are so high.

399
Q

What is the difference between short, long and stress starvation.

A

Short - glycogen used, proteins broken down, not so much fat breakdown for energy.

Long - glycogen gone, shift from protein breakdown to fat breakdown.

Stress - proteins broken down to repair the damage, not as much fat breakdown as in long term starvation. Huge protein requirements for repair.

400
Q

Why do Ps not eat well / may be malnourished in community living?

A

Finances, poverty, inability to self-feed, inability to cook, mobility issues, dexterity, grief, depression, food timings, prescriptions, detention.

401
Q

What are the causes of malnutrition?

A
  • Altered nutritional requirements (increase due to illness etc)
  • Inadequate intake
  • Impaired nutrient digestion and processing
  • Excess losses (D&V, fistulae, drains etc - fluid leaking).
402
Q

What does B12 deficiency cause?

A

Pernicious anaemia & nerve problems

403
Q

What does Vit D deficiency cause?

A

Rickets in children, osteomalacia in adults (brittle bone)

404
Q

What does thiamine deficiency cause?

A

Wet or dry beriberi

405
Q

What is Beriberi?

A

SOB, rapid HR, oedema (wet), nerve damage, pain, confusion, asphagia, vomiting (dry)

406
Q

What does vitamin C deficiency cause?

A

Scurvy

407
Q

What does Vitamin A deficiency cause?

A

Night blindness, dry mouth.

408
Q

What is malabsorption?

A

A deficiency of nutrients such as energy, protein, vitamins and minerals causes measurable adverse effects on body composition, function or clinical outcome.

409
Q

What screening tool is used to determine risk of malnutrition in Ps?

A

MUST score

410
Q

What does the MUST score measure?

A

Step 1 - BMI
Step 2 - Weight loss - % of total body weight in past 3-6m
Step 3 - Acute disease effect score
Step 4 - Calculate overall score
Step 5 - 0 - Low Risk, 1 - Medium Risk, observe, 2+ - High risk, treat

411
Q

How can you estimate height?

A

Ulnar length

412
Q

How can you estimate BMI?

A

Mid Upper Arm Circumference - MUAC

413
Q

What is the definition of obesity?

A

Excess body fat has accumulated sufficiently to adversely affect health.

414
Q

What does NICE suggest as alternative to BMI.

A

Hip to waist ratio in Ps <35 BMI

415
Q

What is BMI measured in?

A

Kg / m2

416
Q

What are the BMI cut off points?

A

18-25 Normal
25-30 Overweight
30+ Obese

417
Q

What are the obesity waist measurements?

A

> 37 inches men 94cm
31.5 inches women 80cm

Slightly less in asian pops.

418
Q

What is worse - central obesity or general obesity - and why?

A

Central obesity worse - is associated with higher risk of diabetes, elevated lipids & CVS M&M.

419
Q

What percentage of adults are overweight and obese globally?

A

40% overweight, 13% obese.

420
Q

What are the health impacts of obesity?

A

Changes at cellular & metabolic levels.
Wear & tear of joints
Fat around airways
Altered insulin response due to fat

421
Q

Is obesity a lifestyle choice?

A

No - more than that - need policy interventions.

422
Q

Name some recent campaigns to reduce obesity levels in the UK

A 
Traffic light on foods
Sugar tax
Calories at restaurants
Junk off checkouts
Change 4 Life
One You
TV Adverts
423
Q

What can double the chances of weight loss for patients?

A

Interventions at primary care level - weight loss management clinics.

424
Q

What weight loss should you aim for?

A

1-2 lb / week (0.5kg) - need long term rather than short term changes.
Aiming for 5% overall.

425
Q

What percentage of weight loss can reduce health risks?

A

5%

426
Q

What causes malabsorption?

A

Alterations to:

  • Secretions
  • Structure / absorptive capacity
  • Motility
  • Blood flow (reduction)
427
Q

What are the symptoms of malabsorption?

A

Diarrhoea, change in stool
Abdo distension
Flatulence
Loss of weights / growth failure (children)
Hypoproteinaemia
Iron deficiency anaemia / Low serum ferritin

428
Q

What are the long term signs of malabsorption?

A

Osteoporosis, B12, folate deficiency

429
Q

What is the stool like with fat malabsorption?

A

Steatorrhea

430
Q

What is the stool like with carbohydrate malabsorption?

A

Watery, frothy diarrhoea (due to fermented sugars in the bowel)

431
Q

How do we treat malabsorption?

A

Replace fluid & electrolytes
Treat primary disorder
Symptom relief
Supplements if needed (oral may not lead to inc absorption)

432
Q

What do Ps need if they have their terminal ileum removed?

A

B12 injections

433
Q

Who is most at risk of dehydration due to acute diarrhoea?

A

Elderly, infants & young children

434
Q

What deficiencies do you get with alcoholic liver disease?

A

B1 (Thiamine) and Vitamin D deficiency

435
Q

What deficiencies can you get with IBD?

A

Iron, Vits D, L, B6, B1, B12, folic acid, selenium, zinc

436
Q

What is dumping syndrome caused by?

A

Malabsorption of fluids and nutrients –> diarrhoea. Caused by overly rapid absorption of glucose. Two types - early and late.

437
Q

How can the GIT cause malabsorption?

A 
Rapid emptying / motility 
Rapid absorption of glucose = dumping syndrome
Reduced secretion of IF
Inadequate mixing 
Reduced secretion of pancreatic enzymes
Abolition of normal pH gradient in SI
438
Q

What are the symptoms of early dumping? What are they caused by?

A

Happens soon after eating - sweating, dizziness, faint, rapid pulse, hypotension.

Caused by rapid early delivery of hyperosmolar load into the jejunum.

439
Q

What are the symptoms of late dumping? What causes it?

A

Weakness, cold, faintness & sweating - happens 2 hours after a meal - is caused by overproduction of insulin in response to rapid absorption of glucose.

440
Q

What are absorption problems in the small intestine caused by?

A

Alterations to:-

  • Secretions
  • Structure
  • Blood flow (reduced)
441
Q

What types of secretion change cause malabsorption problems in the small intestine?

A

Change of secretions can cause enzyme deficiencies, overly high pH or low pH.

442
Q

What is lactose malabsorption caused by? What are its symptoms?

A

Caused by lactase deficiency - lactose remains in intestine - causes watery, frothy diarrhoea due to fermentation - leads to distension, flatulence and explosive diarrhoea.

443
Q

What are the three causes of lactase deficiency?

A

Congenital alactasia - absence of lactase - genetic (autosomal recessive) - needs total lactose exclusion.

Primary lactase deficiency - gradual reduction in production

Secondary lactase deficiency - temporary - result of damage to intestinal brush border.

444
Q

How does coeliac disease cause malabsorption?

A

Inflammation of SI mucosa (gluten AI) - cant cause poor absorption of calcium - leads to anaemia & osteoporosis.

445
Q

What deficiencies are likely with Crohn’s?

A

Ileal resection or bacterial overgrowth = B12 and lactase deficiency. Can get iron deficiency anaemia.

446
Q

If the tail of the pancreas is not working - what is more likely?

A

Tail impaired - more likely endocrine insufficiency - therefore diabetes more likely.

447
Q

What symptoms does pancreatic exocrine insufficiency present with?

A

Variety - inc steatorrhea, bloating, flatulence, weight loss, micronutrient deficiencies.

448
Q

How do you treat pancreatic insufficiency?

A

Digestive enzymes - Creon

449
Q

Which is the most clinically significant vitamin deficiency?

A

VItamin D - is associated with osteopenia and osteoporosis.

450
Q

What do you need to be concerned about with fat malabsorption?

A

Ps tend to eat a low fat diet as a consequence for symptom control - need to ensure that the fat soluble vits, Ca & iron are absorbed and the P is not deficient in these.

Supplements may be needed.

451
Q

What can bile salt deficiency cause?

A

Malabsorption of fats.

452
Q

What does a colon resection mean for the P?

A

There is a loss of absorptive capacity for fluids & electrolytes - especially sodium! Means that some bile acid reabsorption may not take place.

Should adapt within 8 weeks.

453
Q

What is the definition of malnourished?

A

BMI <18.5 + >10% weight loss (unintentional) over 3-6m

BMI <20 + >5% unintentional weigh loss over 3-6m

454
Q

If a P is malnourished and you SUSPECT reduced oral intake - what is the most appropriate initial intervention?

A

Red tray meals - directly observed meals + food diary - to assess his nutritional intake.

Dont necessarily start on oral nutritional supplementation until you are sure his malnutrition is due to inadequate intake.

455
Q

How does long-term nutritional support impact on a P’s long-term health?

A

Want to prevent malnutrition and thereby reduce risks of:

  • Falls (due to sarcopenia and weakness)
  • Pressure sores
  • Osteomalacia and anaemia
  • Low energy levels
  • Better quality of life
456
Q

If Ps have inadequate oral intake - how long does NICE advocate an NG feeding trial for?

A

2 weeks

(Although in practice this isn’t undertaken unless there is a clear reversible cause that can be treated).

457
Q

Which food intake route is preferred?

A

Oral

458
Q

When is a patient at risk of malnutrition?

A

When they have eaten little or nothing for >5 days and are likely to continue not eating much/anything for the next 5 days OR have poor absorptive capacity +/- high nutrient losses +/- increased nutritional needs.

459
Q

When do we not use oral route for nutrition?

A

P cannot swallow safely

P has inadequate GIT function

No benefit is anticipated (EOL)

460
Q

Is NG tube feeding usually long or short term solution?

A

Usually short-term and < 4 weeks.

461
Q

What are complications of NG tube feeding?

A

Sinusitis
Sore throat
Difficulty swallowing
Candidasis

VERY BAD - Aspiration pneumonia, tube - displacement, blockage or knotting

462
Q

What are pros and cons of gastrostomy feeding?

A

Pro - daycare, GA not needed, few complications.

Complications - poss tumour seeding, refeeding syndrome, aspiration, diarrhoea, tube blockage, accidental removal, stoma site problems (leakage, infection, peritonitis, overgranulation, buried bumper syndrome).

463
Q

In which Ps is gastrostomy contraindicated?

A

Severe obesity, portal hypertension / oesophageal varices, coag abnormalities, gastric ulceration, gastric malignancy, total or partial gastrectomy, ascites, peritoneal dialysis, P must be able to lie still and flat - MND, dementia problematic.

464
Q

When do we use post-pyloric route?

A

When there are risks with gastrostomy or risk of aspiration (e.g. P immobile and cant sit up).

465
Q

Name two types of post-pyloric feeding.

A

Nasoduodenal + nasojejunal

466
Q

When is the parenteral route of nutrition used?

What are the risks of parenteral nutrition?

A

When the enteral route is inaccessible / inadequate.

Infection, deficiencies/excess, electrolyte disturbances, liver dysfunction, hyperglycaemia/hyperlipidaemia, insertion complications (pneumothorax, haemothorax, thrombosis, arrhythmias, nerve injury, thrombus, catheter occlusion, catheter fracture, thrombophlebitis etc).

467
Q

How does the post-pyloric route of nutrition work?

A

Pump feeding for set number of hours OR bolus feeding OR combo of both.

Water flushing required to prevent blockage.

468
Q

How does the parenteral nutrition route work?

A

Into vein - initially 24 hours by pump, can be dropped to 16. BUT needs close monitoring - 4 hourly obs, daily FBC etc.

469
Q

What is refeeding syndrome?

A

Severe electrolyte & fluid shift causing metabolic abnormality in Ps that are malnourished & food is reintroduced. Can lead to fluid retention, low serum K, Mg & P. Can cause MI.

Malnourished/starved P -> lipid & protein catabolism suppression + insulin suppression -> glucose then introduced -> inc insulin secretion -> intracellular shift of PO4, K & Mg -> CAUSES hypophosphatemia, hypokalaemia & hypomagnesemia.

470
Q

Who is (a) high risk and (b) v high risk for refeeding syndrome?

A

High risk -
- little or no food for > days (esp if BMI <20 + unintentional weight loss of >5% in past 3-6m)

  • or 2 or more of BMI <18.5, UWL of >10% in 3-6m, no food > 5days, Hx of alcohol abuse or using insulin, chemo, antacids or diuretics

V high risk - BMI <16, UWL >10% in 3-6m, no food >10 days + low P, K, Mg prior to feeding.

471
Q

What is Wernicke-Korsakoff’s syndrome?

A

Wernicke’s encephalopathy
Korsakoff’s psychosis

Acute & chronic phases of same disease - due to shortage of thiamine = dementia like symptoms.

472
Q

Which patient’s are most at risk of WKS?

How can it be given in this group?

A

Alcoholics

Preventative thiamine

473
Q

How long does it take to die if you withhold nutrition?

If you withhold hydration?

A

Nutrition - up to 10 weeks

Hydration - 3-14 days

474
Q

What does the Dementia & Alzheimer’s society recommend about nutritional support in old age?

A

Focus should be on quality of life, not length of life - gastrostomy feeding in advanced dementia should only occur in exceptional circumstances.

475
Q

What is risk feeding?

A

Feeding Ps orally who are at risk of choking / aspirating.

476
Q

What are the 2 objectives of swallowing?

A

1) . Food bolus to stomach

2) Protection of airway from aspiration.

477
Q

What is difficulty swallowing termed?

A

Dysphagia

478
Q

How is food prevented from entering the airway?

A

Vocal cords close, epiglottis occludes, hyoid & larynx move up & forward.

479
Q

How is reflux prevented in healthy Ps?

A

Lower oesophageal sphincter
Diaphragmatic sphincter
Gravity
Position of stomach (abdominal not thorax = no negative pressure)

480
Q

How is acid production stimulated by the PSS?

A

CNX - can

1) directly stimulate parietal cells
2) stimulate ECL cells - release histamine - attach to H2 receptors on parietal cells –> inc H+ release

481
Q

How is acid production in the stomach stimulated by hormones?

A

Gastrin (from G cells of gastric antrum, duodenum & pancreas) - in response to peptides in lumen - stimulates parietal cells directly and indirectly (histamine release).

482
Q

What causes hiatus hernia?

A

Failure of the diaphragmatic sphincter.

483
Q

What are the causes of GORD?

A

Failure of LOS (can be permanent or frequent relaxations)

Failure of diaphragmatic sphincter

Increased intra-abdominal pressure (obesity, pregnancy, ascites).

H. Pylori

Lifestyle, age, meal timings

484
Q

What is the commonest cause of GORD?

A

H. pylori

485
Q

What are the symptoms of GORD?

A

Dyspepsia (heart burn), reflux, chest pain, globus sensation in the throat, cough, wheeze, SOB.

Can be worse lying down,
Nausea & vomiting possible
Poor dentition

486
Q

How can we diagnose GORD?

A 
Endoscopy 
X-Ray contrast swallow / meal
Oesophageal manometry
pH studies
Faeces / breath testing for H pylori
487
Q

H pylori cannot tolerate acidic conditions - how does it overcome this?

A

Expresses urease - converts urea to NH3 + CO2 - thereby raising environmental pH.

488
Q

What conditions are linked to H pylori?

A

Gastritis
Dyspepsia
Peptic ulceration
Gastric cancer - adenocarcinoma & MALT lymphoma

489
Q

What types of peptic ulcer are there?

A

Gastric and duodenal

490
Q

What causes most cases of peptic ulceration?

A

H pylori

491
Q

How do we treat GORD?

A

Lifestyle advice
PPIs
H2 receptor antagonists

492
Q

What do we do to eradicate H pylori in a patient?

A

Triple therapy - PPI + 2 ABs (amoxicillin and metronidazole)

493
Q

How does omeprazole work?

What are its side effects?

A

Inhibits the H+/K+ ATPase pump in parietal cells.

SE: Diarrhoea, inc risk of infection (C Diff)

494
Q

Give an example of a H2 receptor antagonist.

How do they work?

A

Ranitidine

Blocks H2 receptor - reduces histamine stimulation of parietal cells.

495
Q

When is surgery performed for GORD? What can be done?

A

V rarely - usually when Ps dont want medication or haven’t responded.

Repair of hiatus hernia or fundoplication procedure can be effective.

496
Q

What is a hernia?

A

It is a profusion of part, or all, of a viscus through its coverings into an abnormal position.

497
Q

Name two types of hiatal hernia and how freq they are.

A

Rolling (5-15%)

Sliding (85-95%)

498
Q

What happens in a sliding hiatal hernia?

A

GOJ is mobile - stomach slides upwards into thorax - negative pressure then causes reflux.

499
Q

What happens in a rolling hiatal hernia?

A

GOJ remains below the diaphragm, - instead the funds herniates.

Both diaphragmatic and LOS are still working.

500
Q

What are complications of a rolling hiatus hernia?

A

If big enough - can compress oesophagus.

Is a 1% risk of strangulation.

501
Q

How are hiatial hernias repaired?

A

Surgery - reduce hernia + close defect.

Can do fundoplication to strengthen.

502
Q

What is gastritis?

A

Mucosal injury to the lining of the stomach.

503
Q

What can chronic gastric cause?

A

Ulceration

Cancer

504
Q

What is the main cause of gastritis?

A

H pylori

505
Q

What is the management of gastritis?

A

Remove cause if possible

PPI

506
Q

What are the causes of gastritis?

A

Many causes inc. lifestyle, NSAIDs, caustics, AI, infection, IBD, sarcoid, vasculitis.

507
Q

Why do NSAIDs cause gastric problems?

A

NSAIDs - inhibit COX enzymes (these breakdown arachidonic acid into prostaglandins).

COX1 - produces protective prostaglandins in GIT - gastric mucus, HCO3 & blood flow - therefore reduced protection and ability to repair if inhibited.

COX2 - produces prostaglandins which mediate pain and inflammation

With inhibition of these - have less protection of lining + increased pain and inflammation.

508
Q

What do you need to use if on long-term NSAIDs?

A

PPIs

509
Q

What are the causes of peptic ulceration?

A

H Pylori

NSAIDs

510
Q

What causes peptic ulceration?

A

Stress (metabolic stress)
Malignancy
Zollinger-Ellison syndrome
Medications (steroids, biphosphonates, chemo)

511
Q

Which syndrome causes a rare tumour of G cells in the pancreas?

What does it do?

A

Zollinger-Ellison syndrome

G cells secrete uncontrolled gastrin - lots of acid = multiple GI ulcers.

512
Q

Which part of the duodenum most commonly develops ulcers?

A

The first part

513
Q

Which part of the stomach most often develops ulcers?

A

The lesser curve

514
Q

Which is more common - duodenal or gastric ulceration?

A

Duodenal - x4 more common than gastric.

515
Q

Where is peptic ulceration more likely to be associated with cancer - gastric or duodenal?

A

Gastric is more likely to be malignancy associated.

516
Q

How can you tell the difference between gastric and duodenal ulcers by presentation?

A

Gastric - pain occurs 2-3 hours after eating (during eating acid production increases)

Duodenal - pain is often reduced after eating (eating inc pancreatic juice which neutralises acid and reduces pain)

517
Q

What are the symptoms of chronic peptic ulceration?

A

Upper abdo pain, iron deficiency anaemia, weight loss

518
Q

Why does chronic ulceration cause iron deficiency anaemia?

A

From chronic blood loss

519
Q

How can acute peptic ulceration present?

A

Haematemesis - fresh blood / coffee grounds

Melaena

520
Q

How do you diagnose peptic ulcers?

A

Hx, Ex, OGD & H Pylori test

521
Q

How do you treat peptic ulcers?

A

PPI
Triple treatment for H Pylori if needed
Lifestyle
Some NSAIDs or other implicated meds

522
Q

Where does upper GI bleeding come from?

A

Oesophagus, stomach or duodenum

523
Q

What is upper GI bleeding divided into?

A

Variceal (11%) and non-variceal bleeding

524
Q

What causes variceal bleeding?

A

Inc portal venous pressure

525
Q

How do we treat variceal bleeding?

A

Stop bleeding
Reduce portal hypertension (β blockers)
Radiological or endoscopic treatment

526
Q

How do we treat non-variceal bleeding?

A

Ps can be very unwell

Resuscitation,
Transfusion
Reverse anticoags
Endoscopy - clip or cauterise 
Radiological 
Surgery

Test for H Pylori

527
Q

What is a possible complication of duodenal ulcers?

A

Ulceration through to the gastroduodenal artery which passes behind D1.

528
Q

How can perforation sometimes be managed without surgery?

A

If the omentum spontaneously seals the hole

529
Q

How can perforation sometimes be managed without surgery?

A

If the omentum spontaneously seals the hole - is no need for surgery.

530
Q

If a P has high grade dysplasia in Barrett’s oesophagus - what percentage likelihood is it that they already have cancer?

A

50%

A significant % of the remaining 50% will also develop cancer at a later stage.

531
Q

What are the chances that a P with low grade dysplasia in Barrett’s oesophagus will progress to cancer?

A

Much lower than high grade - some will progress to high grade dysplasia, however most will not progress or will revert to non-dysplastic mucosa.

532
Q

Which gene is involved with dysplasia in Barrett’s oesophagus?

A

P53

533
Q

What is the management of Barrett’s oesophagus?

A

If metaplasia and no dysplasia - monitor.

Low grade dysplasia - mostly surveillance

High grade dysplasia - treatment, surgery, radio etc.

534
Q

What medical intervention can reduce the progression of Barrett’s?

A

PPI treatment

535
Q

What is 1st line maintenance treatment of new diagnosis of mild - moderate Crohn’s?

A

Thiopurines (but also start steroids in meantime).

536
Q

What is bowel cancer 10 year survival rate?

A

50%

537
Q

Which is the 3rd most common cancer in the UK?

A

Bowel cancer

538
Q

Which Ps are most at risk of bowel cancer?

A

Over 60s
M=W
High incidence West, lower incidence Asia & Africa.

539
Q

What are the risk factors for bowel cancer?

A 
Age
Genetics
Lifestyle
Processed meats
Low fibre diet
Socioeconomic (greater incidence of other risk factors?)
IBD - esp UC
Previous bowel cancer
540
Q

Why does fibre stop incidence of bowel cancer?

A
  1. Increases the formation of short-chain fatty acids = more healthy gut bacteria = reduces proliferation of neoplastic cells.
  2. Reduces transit time = less exposure to carcinogens
  3. Reduces secondary bile acid formation = carcinogenic
541
Q

What is a polyp?

A

A protrusion into a hollow viscus.

542
Q

What is neoplasia?

A

A new growth - can be benign or malignant

543
Q

How common are lower GI polyps?

A

V common - 25% of pop.

544
Q

What is the link between lower GI polyps and bowel cancer?

What are the majority of polyps in the lower GIT?

A

Polyps are a precursor for the majority of bowel cancers. Need to look at degree of dysplasia - are they low grade or high grade (pre-malignant).

Majority are adenomas.

545
Q

What types of polyp exist in the lower GIT?

A

Pedunculated
Sessile
Semi-pedunculated

546
Q

Which is most common gene involved in adenoma?

A

TP53 - tumour suppressor gene

547
Q

What is the carcinoma sequence?

A

Normal mucosa –> early adenoma –> high grade dysplasia + further mutations –> carcinoma.

548
Q

Where do 60% of adenomas and bowel cancer occur?

A

Left hand side of the colon - sigmoid and rectum.

549
Q

What is the peak age for polyps forming?

A

60

550
Q

What is the peak age for bowel cancer incidence?

A

71

551
Q

What is the screening criteria for bowel cancer?

A

Wilson’s criteria - screening test must

  • Identify pre-malignant phase = polyp
  • Have good & acceptable test = colonoscopy
  • Have agreed treatment = polypectomy
  • Prevention must be better than cure
552
Q

What is the most common type of bowel cancer?

A

Adenocarcinoma

553
Q

What is Familial Adenomatous Polyposis?

A

Genetic mutation (autosomal dominant) - in APC gene - Chr 5Q21.

1% of PCs - causes lots of polyps - >100 by late teens. Is 100% risk of bowel cancer by 30.

554
Q

What is the Knudson 2-hit hypothesis? How does it explain why FAP causes cancer by 30.

A

Hypothesis that tumour suppressor genes need both alleles to be inactivated in order for tumours to occur.

In FAP - one allele already damaged so only one remaining copy need a mutation to develop cancer - hence cancer develops earlier than in normal Ps.

555
Q

What is Lynch syndrome also known as?

A

HNPCC - Hereditary Non-Polpyposis Colorectal Cancer

556
Q

What is Lynch syndrome?

A

Genetic abnormality in mismatch repair genes - no checking system = tumours easier to acquire.

Still need 2 hits for cancer but happens more quickly because of the malfunctioning MMR genes.

Is also greater risk of non-GI tract tumours due to this defect.

557
Q

Which side does Lynch syndrome cancer tend to occur in?

A

RHS of colon.

558
Q

What percentage of cancers are caused by Lynch syndrome?

A

3%

559
Q

What percentage of bowel cancers are caused by FAP?

A

1%

560
Q

What criteria is used to identify families at risk of Lynch syndrome?

A

Amsterdam criteria - 3+ relatives with Lynch, 1 must be 1st degree, 2+ generations affected, cancer before 50 & FAP has been excluded.

561
Q

How are most bowel cancers identified?

A

Screening - 33-50%
Symptoms - 50-66%
Small minority - emergency or incidental presentation

562
Q

When do Ps have a screening sigmoidoscopy? How much of the bowel does it look at?

A

At 55 - reaches the splenic flexure - so misses 25% of bowel.

563
Q

What screening happens for bowel cancer between 60-74?

A

QFIT (Quantitative Faecal Immunohistochemical Test) - every 2 years - much better specificity and sensitivity.

>10 = 6% chance of bowel cancer
>150 = 33% chance of bowel cancer
564
Q

What are the clinical symptoms to investigate for bowel cancer?

A

Iron deficiency anaemia in Ps >60
Unexplained change in bowel habit in Ps >60
Unexplained rectal bleeding in Ps >50
PR bleeding + abdo pain + CIBH + weight loss + iron deficiency anaemia at ANY age
Weight loss + abdo pain >40
Abdo / rectal mass at any age

565
Q

What is the gold standard test for bowel cancer?

A

Colonoscopy

566
Q

What are the pros and cons of colonoscopy for bowel cancer?

A

Cons: Have to cleanse bowel - prep needed, sedation needed, high perf and mortality rate.

Pro: Better for seeing polyps - virtual colonoscopy wont see polyps under 6mm.

567
Q

Which Ps are more at risk for colonoscopy?

A

Frail
Immobile
Diabetics - can they tolerate the fluid loss?

568
Q

What are the benefits and disadvantages of a sigmoid colonoscopy?

A

Pros: Enema needed rather than full cleanse, no sedation needed, lower perf rate - gives good view of LHS of colon.

Cons: Limited to splenic flexure.

569
Q

What are the pros and cons of a virtual colonoscopy?

A

Involves: CT scan, oral contrast and rectal insufflation.

Pros: better tolerated than invasive procedures, low perf rate, can identify non-GI pathology - shows inside and outside of bowel. Can be used for Ps who cannot tolerate colonoscopy. Good for emergencies or frail Ps who cannot tolerate anything else.

Cons: Not under 40s - high radiation dose (3-4 years background).

570
Q

What is poorly differentiated cancer a sign of?

A

Tumour aggression - cell development has stopped at early stage - therefore quite immature cells which rapidly divide = aggressive cancer.

571
Q

If there are mets in the liver from bowel cancer, does this mean that the cancer has spread elsewhere?

A

Not necessarily - because of the portal system is possible for tumour to spread to liver from bowel without infiltrating the lymph or other tissues.

572
Q

What are emergency presenting symptoms of bowel cancer?

A

Acute lower gastro intestinal symptoms = obstruction, perforation, fistulae, infection/asbcess.

If presenting as emergency - is more likely to be a poor prognosis for the patient.

573
Q

What are the main risk factors for bowel cancer?

A 
Older age
Genetics / Family history
Processed Meats
Smoking 
Longstanding IBD - esp UC
574
Q

What percentage of Ps with hereditary polyposis have no family history of bowel cancer?

A

25%

575
Q

What percentage of Lynch syndrome is due to new mutations rather than genetics?

A

20%

576
Q

What percentage of patients who have bowel cancer have previously had it?

A

2%

577
Q

Which ethnicity has a higher prevalence of Crohn’s?

A

Ashkenazi Jews

578
Q

How can you differentiate coeliac from Crohn’s disease?

A

Coeliac - should not cause bloody diarrhoea or intense abdo pain. It can have stomatitis and glossitis - but is not associated with oral ulcers (unlike Crohn’s).

579
Q

Whilst awaiting review by a surgeon - what tests & treatments should a patient with acute Crohn’s receive?

A

FBC - check infection, blood loss, inflammatory markers & dehydration, electrolytes

Stool culture - rule out infectious causes

Treatments:
IV Fluids
IV hydrocortisone
Nil by mouth if bowel obstructed
Analgesia
LMWH
AXR - rule out perf / obstruction / toxic megacolon
Monitor stool output & blood loss
580
Q

Where does Crohn’s most frequently affect in the bowel?

A

The terminal ileum and ileo-caecal valve.

581
Q

After IV hydrocortisone for IBD - what should patients be discharged with?

A

A weaning course of oral steroids - prednisolone.

582
Q

What are the main long-term complications of Crohn’s?

A 
Short bowel syndrome following surgery
Abscess formation
Fistula formation
Malnutrition, Iron, B12 or Folate deficiency
Strictures
Perianal disease
Stoma necessity
Colon cancer
Drug side effects
Depression
Infertility
583
Q

What are mitochondria with wild and mutant DNA called?

A

Hetereoplasmy

584
Q

What is it called when all the mtDNA in a cell are identical?

A

Homoplasmy

585
Q

What are fats stored in the body as?

A

Triacylglycerols in adipocytes

586
Q

What are excess carbohydrates stored in the body as?

A

Some are stored in the liver as glycogen.

Remainder converted into fatty acids from ACoA and stored as triacylglycerols.

587
Q

How can amino acids be utilised in the body?

A

Can be used to:

  • Make protein
  • Make pyruvate, ACoA & Oxaloacetate - all used in Kreb’s cycle.
588
Q

How are triglycerides utilised in the body?

A

They are broken into fatty acids - then used to make ACoA (reversible).

ACoA - can be used to make FAs which are then turned into tricylglycerols for storage.

589
Q

What are the main fuels that are used to produce ATP in the body?

A

Glucose
Long-chain FAs
Amino acids

590
Q

What is the division between the upper and lower GIT?

A

Suspensory muscle of the duodenum = ligament of Trieitz.

591
Q

What does the mesentery house?

A

Blood vessels, nerves & lymph

592
Q

What is the shortest part of the small intestine?

A

Duodenum

593
Q

Which is the longest part of the duodenum?

A

Ileum

594
Q

How long does digestion take in the small intestine?

A

3-5 hours

595
Q

How is the small intestine adapted for absorption?

A

Circular folds, villi projections of mucosa, brush border on villi.

596
Q

What is the apical surface of the small intestine?

A

The side of enterocytes which face into the lumen.

597
Q

What are the two types of motility in the small intestine?

A

1) . Mixing and circulation = max absorption to epithelium

2) . Propulsion of chyme aborally

598
Q

What is motility in the small intestine controlled by?

A

ENS - modified by ANS and hormones.

599
Q

What happens in segmentation in the small intestine?

A

Stretch receptors in ENS –> stimulation of muscle contraction - however NO NET MOVEMENT of contents.

600
Q

What happens in propulsive peristalsis in the small intestine?

A

Stretch receptors –> ENS stimulation –> contraction behind bolus, relaxation in front = peristalsis and net movement through the SI.

601
Q

Which hormones excite propulsive peristalsis?

A

Gastrin, CCK, Insulin, Motilin

602
Q

Which hormones inhibit propulsive peristalsis?

A

Secretin and glucagon

603
Q

Which reflex is caused by gastric distension activating the myenteric plexus to promote peristalsis throughout the small intestine?

A

Gastroenteric reflex

604
Q

Which reflex is caused by gastric distension promoting peristalsis in the ileum forcing chyme through the ileocecal valve into the caecum?

A

Gastroileal reflex

605
Q

How does the ileocaecal valve control emptying of chyme into the colon?

A
  • Pressure and chemical irritation in ileum relax ileocaecal sphincter and excite peristalsis.
  • Fluidity of contents in ileum promotes emptying
  • Pressure or chemical irritation in caecum inhibits peristalsis of ileum and excites sphincter
606
Q

What is the series of frequent peristaltic contractions between meals which move SI content to the large intestine called?

A

Migrating motor complex

607
Q

What is the migrating motor complex controlled by?

A

Intrinsic enteric control & hormone (motilin)

608
Q

What problem can arise in the absence of sufficient peristalsis in the small intestine?

A

Bacterial overgrowth

609
Q

What are folds in the large intestine called?

A

Haustra

610
Q

What happens in the proximal large intestine?

A

Absorption of water and electrolytes

611
Q

What happens in the distal large intestine?

A

Formation and storage of faeces.

612
Q

How does motility arise in the large intestine?

A

Is a combo of mixing and propulsion.

Is under ENS control - modified by neural and hormonal control.

613
Q

How does mixing occur in the large intestine?

A

Via haustral churning

614
Q

How does movement occur within the large intestine?

A

Via propulsive peristalsis.

615
Q

What are mass movements in the large intestine and how often to they occur?

A

Forceful peristaltic contractions - force contents of large intestine into sigmoid colon and rectum.

Requires a lot of energy - so only happens x2-x3 per day

616
Q

How does defecation occur?

A

Mass movements push faecal matter into the rectum - stretch receptors are stimulated - leading to activation of ENS and PSS.

Involuntary contraction of longitudinal muscle in rectum opens the internal anal sphincter.

Constricted external anal sphincter is then voluntarily relaxed to allow defecation.

617
Q

What can AAs make?

A

Pyruvate, ACoA & Oxaloacetate - power Krebs

NME (2 decks)

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