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Physiology Flashcards

1
Q

Order of the GI Tract

A

Oral cavity-UOS Oesophagus- LOS_Stomach- Pyoric Sphincter- Duodenum- Jejunum- Illeum- Illeocaecal Valve- Appendix + caecum- A. Colon- T. Colon- D. Colon-Sigmoid Colon- Rectum- Anus

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2
Q

Venous Drainage of the Stomach

A

Gastric Veins- Hepatic Portal Vein- Central Vein (Liver)- Hepatic Vein- (out)- IVC

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3
Q

Venous Drainage of The Pancreas

A

Splenic Veins- Hepatic Portal Veins- Central Vein (Liver)- Central Vein- Hepatic Vein- (out)- IVC

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4
Q

What drains into the Superior Mesenteric Vein?

A

Small Intestine (lower 2/3 of duodenum, Jejunum, Ileum), Caecum, A. Colon, 2/3 of T. Colon

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5
Q

What drains into the Inferior Mesenteric Vein?

A

Descending Colon, S. COlon, Rectum

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6
Q

NERVOUS CONTROL- Autonomic Control of the GI Tract?

A

Long Fibres from CNS

Short Fibres from ENS (small brain, it’s own modulator/ control)

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7
Q

Parasympathetic Control of the GI Tract?

A

Via the Facial Nerve (CN7), Glossopharngeal (CN9) + Vagus Nerve

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8
Q

Function of parasympathetic nervous system in GI control?

A

Increases secretion

Increases Motility

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9
Q

Sympathetic Control of the GI Tract

A

Via Splanchnic Nerves

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10
Q

Function of the Sympathetic Nervous System in GI control?

A

Decrease secretion
Decrease Motility
NOTE- Increases salivatory secretion (more viscous due to more mucus and amylase poduction)

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11
Q

1st Epithelial Layer (Outside)

A

Serosa (Below Diaphragm) / Adventitia (Above Diaphgram). Connective tissue layer

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12
Q

2nd Epithelial Layer

A

Musculares Externa
Longditudinal Muscle layer (most external)- Shortens Tube
Circular Muscle Layer- Constrict Lumen
= Perislaltic Segmentation

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13
Q

3rd Epithelial Layer

A 
Submucosa- Thick, Irregular, Connective Tissue.
Contains Glands (oesophagus mucus, duodenum bicarb), Neurones, BV + lympth
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14
Q

4th (inner most) epithelial layer

A

Mucosa

  1. Muscularis Mucosae (Thin, Smooth Muscle Layer)
  2. Lamina Propria (loose connective tissue)
  3. Epithelium -Stratified Squamous (Mouth, oesophagus + anus)
    - Simple Collumnar 9everywhere else)
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15
Q

3 Areas of Salivatory Secretion

A

Parotid, Sublinguial + Submandibular Glands

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16
Q

Where does the Coelic Artery/ Trunk come from and what does it supply?

A

Bifurcates from the aorta at T12

It supplies the stomach, upper duodenum, pancreas and liver= FOREGUT

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17
Q

Where does the Superior Mesenteric Artery come from and what does it supply?

A

SMA bifurcates from the aorta at L1

It supplies the lower duodenum, jejunum, ileum, caecum, appendix, a.colon + 2/3rds of t.colon= MIDGUT

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18
Q

Where does the Inferior Mesenteric Artery come from and what does it supply

A

IMA bifurcates from the aorta at L3

It supplies last 1/3 of the t. colon, d. colon, s. colon, rectum + anal canal

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19
Q

What mucosal layer contains the Enteric Nervous Plexus

A

The Submucosa (Meissners Plexus) has the extensive network of parasympathetic neurones= own control

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20
Q

How do nutrients from the GI Tract get to the circulation?

A

The Hepatic Artery from the heart carries highly oxygenated but low nutrient content blood from the heart to the liver.
The Hepatic Portal Vein carries low oxygenated but high nutrient blood from the GI system.
These 2 supplies mix in the liver producing a blood supply high in oxygen and nutrients to be recirculated out via central vein- hepatic vein-IVC and back to heart

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21
Q

What makes the liver unique?

A

It has a arterial and venous supply

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22
Q

What are the contents of saliva and what re their function?

A
  1. Water- Dilution and Moistening
  2. Mucins- Protein + Water= Mucus (Lubricant)
  3. Alpha Amylase- polysaccharides to disaccharides (via alpha 1,4 glycosidic bond breaking)
  4. Electrolytes- release ions to control tonicity/ pH
  5. Lysosome- cleaves polysaccharides off bacteria= renders ineffective
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23
Q

Give an example of the use of reflex control of salivation?

A

presence of food alerted via chemoreceptors and pressure

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24
Q

Muscle of the oesophagus

A

Top 1/3= Skeletal Muscle for swelling/ reflex/ stop regurgitation (UOS)
Bottom 1/3= smooth muscle, involuntary control (LOS)

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25
Q

Is there any keratin in the oesophagus?

A

No

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26
Q

Phase 1 of swallowing- oral phase

A

Oral Phase- Bolus pushed to back of mouth by tongue

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27
Q

Phase 2 of swallowing- pharyngeal phase

A

Pharyngeal Phase

  1. Reflex contraction of the pharyngeal muscle (via medulla).
  2. Soft pallet goes back and up to close the nasopharynx
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28
Q

Phase 3 of Swallowing- bolus approaches oesophagus

A
  1. UOS relaxes
  2. Epiglottis covers larynx
  3. UOS contracts, food enters and breathing resumes
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29
Q

Phase 4 of Swallowing- Oesophageal Phase

A

Peristaltic wave via Muscular Externa propelled bolus to stomach. As food gets near stomach LOS (smooth muscle) relaxes to allow it to enter the stomach.

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30
Q

List the 5 functions of the stomach

A
  1. Sterilising Food
  2. Dissolving food
  3. Temporary store of food
  4. Controls delivery of food
  5. Produces intrinsic factor (for B12)
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31
Q

Why does the histology of the stomach differ from that of the rest of the GI Tract?

A

In the stomach the Muscularis Externa has 3 layers-

  1. Longditudinal Muscle Layer- shortening
  2. Circular Muscle Layer- peristaltic grinding
  3. Oblique Muscle Layer- squeezing
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32
Q

What does the lumental surface of the stomach contain?

A
  • Mucus Cells
  • Gastric Glands
  • Parietal Cells- HCL + Intrinsic Factor (Pepsin)
  • Chief Cells- Zymonogens (pepsinogen)- activated by pepsin (intrinsic factor) produced by parietal cells
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33
Q

Where is the fungus of the stomach and what is its function?

A

The fundus lies directly after the LOS and is thin and stretchy with folds of ruggae to accommodate incoming food

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34
Q

Where is the body of the stomach and what is its function?

A

The body of the stomach lies between the funds and atrium and is vital for storage and release of mucus, HCL, intrinsic factor & pepsinogen

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35
Q

Where is the atrium of the stomach and what is its function?

A

The Atrium lies just before the pyloric sphincter and is responsible for dissolving food via it’s thick muscle

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36
Q

In what order do cells lie in crypts of the stomach?

A

Chief cells sit at the bottom of crypts
Parietal Cells sit in the middle of crypts (this makes sense as they have to access pepsinogens coming up from chief cells)
Mucus cells sit sit at the top/neck and move up to shed with age

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37
Q

Production of stomach acid

A
  1. Carbon Dioxide (blood) –stomach lumen + water= bicarbonate (via carbonic anhydrase)
  2. BiCarb splits
    - carbonic acid is pumped back out into blood in exchange for Cl- ions (brought straight through cell to stomach lumen)
    - the other H ion is taken to the stomach lumen via K+H+ATPase pump (water out of cell via osmotic gradient)
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38
Q

What happens to CNS and ENS when bolus enters the stomach?

A

Via vagus activated by distension (CNS) + local reflex (ENS) resulting in an increased tone

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39
Q

What mechanisms are in place to increase stomach acid secretion (HCl)?

A

Increase Tone

  1. G- Cells produce Gastrin (stomach)
  2. Increase Ca levels and Release Histamine via g-protein coupling (converts ATP–cAMP)
  3. Protein Kinases- turn H-K pump
  4. Increase production of HCl
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40
Q

What mechanisms are in place to inhibit stomach acid production?

A 
Decreased Tone
Stomach distended (bolus has entered)= 
Decrease in pH= Increase in HCl= Decrease in Gastrin (-ve feedback)

Acid, hypertonic, fat, monoglycerides in duodenum (stomach emptying)= ENTEROGASTRONES (secretin, CCK, GIP) release= Decrease gastrin secretion= Decrease HCl (parietal cells)

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41
Q

What mechanisms are in place to increase stomach acid secretion (HCl)

A

Increased Tone

1. Releases ACh= Increase Ca production= protein kinases= turns H-K pump= more HCl produced

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42
Q

What do chief cells secrete?

A

Pepsinogen (zymogen) is secreted by chief cells

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43
Q

What is a zymogen?

A

Inactive precursors of digestive enzymes in acinar cells.

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44
Q

Under what circumstance is pepsinogen activated to pepsin?

A

Pepsinogen is activated to pepsin (digests everything) via a low ph (less than 3)

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45
Q

Control of Pepsin

A

In high levels pepsin acts back to cleave itself returning to pepsinogen

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46
Q

Role of gastric mucus

A

cytoprotective role to

  • protect mucosal surface from mechanical injury
  • pH 7 from cells (compared to pH 2 of gastric juice) cleaves pepsin and renders it ineffective
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47
Q

Where is gastric mucus produced?

A

Surface epithelial and mucus neck cells

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48
Q

How is the peristaltic wave produced

A

By pacemaker cells in longitudinal muscle layer

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49
Q

How are the number of peristaltic waves in the stomach controlled?

A

Hormones control the amount of AP produced

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50
Q

AP levels in the stomach

A

Slow (constant AP) wave= electrical rythm - Vgated threshold reached- movement

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51
Q

Is AP firing constant in the stomach?

A

Yes, have a slow base rhythm brought to depolarisation (movement) by an increase in APs

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52
Q

Gastrin role in AP

A

Gastrin increases AP levels= Increases contractions

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53
Q

Distensions role in AP

A

Distension activates CNS + ENS= increases contractions

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54
Q

Fat, Acid, AAs, hypertonicity role in AP

A

When fat, acids, AA, hypertonicity reaches the DUODENUM= decrease AP= Decrease contractions

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55
Q

How do you stop gastric acid entering the duodenum?

A

Acid entering duodenum triggers short (ENS) and long (CNS) reflex that releases secretin from S Cells (enterogastrone) - pancreas + liver- triggers HCO3 release- SI = neutralises acid.
Secretin also increases CCK into BS- gallbladder (release bile)- intestine

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56
Q

How are zymonogens activated?

A

Released from pancreas during digestion and turned into their active form when coming into contact with their enterokinase (bound at the brush border of the duodenum)

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57
Q

What is the difference between endocrine and exocrine?

A

Endocrine is delivered to another site via the blood stream, endocrine is produced and targets in its immediate area

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58
Q

Are acinar cells endocrine or exocrine?

A

Exocrine

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59
Q

Structure of the pancreas

A

Acinar cells (enzyme secretion) in lobules- intercalculated ducts- pancreatic duct (mix with bile duct)- sphincter of oddi- duodenum

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60
Q

What do proteases cleave?

A

peptide bonds

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61
Q

What to nucleases cleave?

A

DNA/ RNA

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62
Q

What do Elastases cleave?

A

Elastic/ collagen/ connective tissue

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63
Q

What does phospholipase cleave?

A

Phospholipids- fatty acids

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64
Q

What do lipase cleave?

A

TAG- FA + glycerol

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65
Q

What does a- amylase cleave?

A

Starch- Maltose + Glucose

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66
Q

What nutrients does the liver remove from the circulation?

A 
Glycogen
Fat
Vit A,D,E, K, B12 (diet)
Cu
Fe
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67
Q

Shape of liver?

A

Heaxgonal

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68
Q

What are the 6 components of bile?

A 
Bile Acid
Billirubine (bile pigment)- from haemoglobin breakdown) 
Bicarbonate
Cholesterol
Toxic Metal
Lecithin
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69
Q

What colour is bilirubin?

A

yellow —modified by bacteria— brown (faceless)/ Yellow (urine)

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70
Q

Where is bile produced?

A

Bile is produced in the liver

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71
Q

What addition turns the products of bile synthesis into Bile Acids?

A

Cholestrol

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72
Q

How do you turn bile acids (in liver) to bile salts

A

Conjugate bile acids with glycine/ taurine

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73
Q

Why do you change bile acids- bile salts

A

Bile salts are more soluble

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74
Q

How is bile released into the duodenum?

A

CCK (enterogastrone) production relaxes the sphincter of oddi releasing bile and its contents into the duodenum

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75
Q

What happens if sphincter of oddi is close?

A

If closed bile backs up via the common bile duct- cystic duct- gallbladder

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76
Q

Function of the gallbladder

A

Store and dehydrate bile

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77
Q

How does the gallbladder dehydrate bile?

A

Dehydrates via active transport of NaKATPase (pulls water out) as water follows Na gradient

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78
Q

How many layers does the gallbladder have and what are they?

A
  1. Ruggae Mucosa
  2. Muscularis- smooth muscle
  3. Serosa- Connective Tissue
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79
Q

Structure of a villi in the small intestine (5 layers)

A
  1. Arterial Supply
  2. Venous Drainage
    NOTE: 1+2 via anastomose capillary beds
  3. Lacteal- take away products of fat digestion
  4. Goblet Cells- secrete mucus to surface to act as HCl/ Acid microclimate barrier
  5. Crypts- stem cell production, secrete Cl + water
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80
Q

Function of the Duodenum

A

1st in small intestine

  • Acid neutralisation
  • Digestion
  • Iron Absorption
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81
Q

Function of the Jejunum

A

2nd in SI

Absorption

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82
Q

Function of the Ileum

A

3rd in SI

  • NaCl absorption
  • H20 absorption
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83
Q

What products does the Small Intestine absorb?

A 
NaCl
Water
Monosaccharides
Amino Acids
Fats
Peptides
Vitamins
Minerals
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84
Q

How are products of the Small Intestine absorbed?

A

via SECONDARY TRANSPORT

NaKATPase pulls in more Na from lumen along with glucose/ galactose/ AAs (out of BS)

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85
Q

How is intestinal fluid secreted?

A

For every 2Cl in 1 goes out to intestinal lumen
Additionally K out via leaky channels + Na out via NaKATPase (recycling K)
Water follows Cl out other side passively into intestinal lumen

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86
Q

Where is intestinal fluid secreted?

A

From epithelial cells lining crypts

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87
Q

Need for fluid secretion in the Small Intestine

A
  1. Keeps luminal contents in liquid state
  2. Promotes mixing of nutrients with digestive contents
  3. Aids nutrient presentation to absorbing surface
  4. Dilutes/ washes away potentially injures substances
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88
Q

What is the physiological condition associated with absence of Cl channel on villi

A

Cystic Fibrosis

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89
Q

What is segmentation

A

contraction and relaxation of adjacent pieces of bile to move chyme up and down

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90
Q

When does segmentation occur?

A

After eating

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91
Q

Are digestive enzymes involved in segmentation?

A

Yes

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92
Q

Purpose of segmentation

A

Bring chyme into contact with digestive surface (enzymes)

93
Q

How is segmentation generated?

A

Via contraction generated by pacemakers in longitudinal muscle

94
Q

Is there any autonomic effect on segementation?

A

No

95
Q

Parasympathetic affect on segmentation

A

increase contraction via vagus nerve

96
Q

Sympathetic affect on segmentation

A

Decrease contraction

97
Q

When does peristalsis occur?

A

During eating

98
Q

Are digestive enzymes involved in peristalsis?

A

No

99
Q

Purpose of segmentation

A

Move undigested material to Large Intestine

100
Q

Why, in respect to bacteria, is movement in the SI necessary?

A

Limit bacterial colonisation of SI

101
Q

How is peristalsis generated?

A

Via increased Motilin levels in the blood starts Migrating Motility Complex (gastric antrum- LI) Waves

102
Q

Law of the Intestine

A

oral (before bolus) CONTRACTS-bolus- anal (after bolus) RELAX medicated by neurones in myenteric plexus (ENS)

103
Q

What is the name of the enteric nervous system of the GI tract?

A

Myenteric Plexus (small brain)

104
Q

Gastroileal Reflex

A

gastric emptying opens the ileocaecal valve allowing chyme into the LI- colon distenses- REFLEX contraction to shut Ileocaecal valve = prevents reflux

105
Q

What is the caecum?

A

Blind sac between the ileum and colon. Ends with the appendix

106
Q

Epithelia of the colon

A

Simple, columnar epithelium

107
Q

What is different about the longitudinal muscle layer in the colon?

A

It is not complete

108
Q

What are the bands in the colon called? What are their use?

A

Teniae coli- span entire length, allow the colon to contract

109
Q

What are the pouches in the colon called?

A

Haustra

110
Q

What makes the crypts in the LI different? What is their function?

A

Crypts are larger and longer than SI and are used for lubrication of faeces (make it move along tract)

111
Q

Epithelia in the rectum

A

simple, columnar epithelia

112
Q

Muscle in the rectum

A

Thick muscular externa

113
Q

Muscle in the anal canal

A

Muscular externa even thicker than that of the rectum

114
Q

Epithelia in anus

A

Stratified squamous epithelia

115
Q

What types of muscle in the external anal sphincter? Therefore what kind of control is it under?

A

Skeletal Muscle

Under voluntary control

116
Q

What type of muscle is the internal anal sphincter? Therefore what kind of control s it under?

A

Smooth Muscle

Under involuntary control

117
Q

How does the colon produce solid faecal pellets?

A

The Large Intestine brings in sodium via NaKATPase and water follows gradient= dehydrates chyme= solid faecal pellets

118
Q

Does chyme spend a long time in the LI? Why?

A

Yes it has a long residence time to allow bacteria to act on it

119
Q

How do solid faecal pellets move from the colon to rectum?

A

A wave of intense contraction results in a mass movement of solid faecal pellets to the rectum

120
Q

Defectaion reflex

A

Via mechanoreceptors- contracts rectum

121
Q

Control of mechanoreceptors in defecation

A

Via parasympathetic control via pelvic splanchnic nerves

122
Q

At what age can you control the External Anal Sphincter?

A

2 years of age

123
Q

Expellation of faeces

A

Relax internal sphincter
Increase peristaltic activity in colon
Increases pressure on external sphincter
= relax voluntary control and expel faeces

124
Q

What is constipation?

A

Long period of retension- no absorption of toxins from faecal material

125
Q

Symptoms of constipation

A

Headache
Nausea
Loss of appetite
Abdominal distension

126
Q

What is diarrhoea?

A

Too frequent passage of liquid faeces

127
Q

Cause of diarrhoea

A 
Stress
Food
Allergy eg./ lactose intolerance
Virus
Protezoans
Pathogenic Bacteria eg./ Entereotoxigenic Bacteria
128
Q

Example of enterotoxigenic bacteria

A

vibes cholera, escherichia coli

129
Q

What do enterotoxigenic bacteria do?

A

Increase water secretion via cAMp,cGAMP, Calcium Channel Defect- water moves out into the colon, villi can’t cope
= profuse watery diarrhoea, no absorption of vitamins/ minerals
NOTE: can’t get this if have CF

130
Q

Treatment for Diarrhoea

A

Oral rehydration therapy (glucose + sodium)

131
Q

Does diarrhoea damage villus cells?

A

No

132
Q

What is triacyglycerol made up of?

A

Glycerol + 3 stearic Acids

133
Q

Is Triacyglycerol solubale

A

No, it’s insoluable

134
Q

What/ how is TAG broken down to?

A

Pancreatic lipase breaks TAG down (only on cell surface) to a monoglyceride and 2FAs

135
Q

Why can pancreatic lipase only act of the aqueous phase of emulsification?

A

Water soluble

136
Q

How are large lipid droplets (monoglyeride + 2FAs) broken down?

A

Smooth muscle grinds + mixes lumen contents

137
Q

What is the purpose of breaking droplets down during esterification?

A

Larger surface area for digestive enzymes (lipase) to act on

138
Q

What is emulsification?

A

Process of dividing larger droplets into smaller ones

139
Q

What makes up an emulsification agent?

A

Bile + Phospolipids

140
Q

How does an emulsifying agent stop droplets from reforming?

A

non-polar to centre and polar to outside so droplets repel each other= smaller micelles

141
Q

How are smaller micelles broken down?

A

Smaller micelles randomly gravitate towards brush border where acid microclimate makes them unstable and causes a breakdown

142
Q

How do the contents of micelles diffuse across the membrane?

A

Uncharged so pass through apical membrane

143
Q

What happens to the products of micelles what don’t diffuse?

A

Taken back up by micelles and the process begins again

144
Q

What happens to FAs when they enter the cell?

A
  1. Enter sER where they are turned back into TAGS
  2. Emulsification= coated with amphiphatic proteins
  3. Transported in vesicles to Golgi Apparatus
  4. Exocytosed into extracellular fluid at serosa
145
Q

What are chylomicrons?

A

Extracellular fat

146
Q

Products of TAG digestion

A

Chylomicrons, phospholipids, cholesterol, + fat soluble vitamins

147
Q

Where do the products of fat digestion go after entering extracellular fluid?

A

Pass into lacteals (terminal branch of lymph) - Thoracic Duct- IVC

148
Q

Water soluble vitamins

A

Vit B, C + Folic Acid

149
Q

How are water soluble vitamins absorbed?

A

Via passive diffusion/ carrier mediated transport

150
Q

What is B12

A

Large, charged molecule

151
Q

How is B12 Absorbed?

A

Binds to intrinsic factor (stomach-parietal cells)= complex that absorbs via specific transport (in distal ileum) - taken up by liver

152
Q

How long of a supply of B12 is stored in the liver

A

3 year supply

153
Q

What is the name of B12 deficiency?

A

Pernicous Anemia (NOT iron deficiency)

154
Q

Why must iron be bound?

A

Detrimental if left on its own (highly reactive)= free radicals + lipid damage

155
Q

How is iron bound

A

Iron (also lead + cadmium) transported across via DMT1 into duodenal enterocytes- unbound across the serosal membrane-blood- binds to transferin

156
Q

What is the intracellular store of iron?

A

Ferritin (12) is the intracellular iron store

157
Q

What happens during hyperaemia?

A

Hyperaemia (too much iron) resulting in an increase in ferritin- excreted- dark faeces

158
Q

What happens during anaemia?

A

Anaemia (not enough iron) resulting in a decrease in ferritin- kept in body- more in blood
NOTE- the surface of the small intestine is replenished after 5 days so ferritin is lost

159
Q

What are the 3 monosaccharides

A

Glucose, Galactose + Fructose

160
Q

How many carbons in a monosaccharide?

A

6 Carbons

161
Q

What are the 3 disaccharides?

A

Lactose, Sucrose + Maltose

162
Q

What is Lactose broken down to?

A

Glucose + Galactose via the lactase enzyme

163
Q

What is Sucrose broken down to?

A

Glucose + Fructose via sucrase

164
Q

What is Maltose broken down to?

A

2 x Glucose via maltase

165
Q

What are the 3 polysaccharides?

A

Starch, Cellulose + Glycogen

166
Q

What is starch?

A

Linked by a 1,4 glycosidic bonds
- Plant glucose
-in saliva and pancreas
NOTE: Hydrolysed by amylase

167
Q

What is cellulose?

A

Linked by b 1,4 glycosidic bonds
-Plant cell walls
NOTE: No enzyme digestion, bacterial digestion only

168
Q

What is glycogen?

A

Linked by a 1,4 glycosidic bonds

-Animal storage of glucose

169
Q

How are glucose and galactose transported?

A
  1. SGLT1 on the Apical Membrane (lumen of SI) brings in Na + glucose/galactose (as long as both are bound)
    • GLUT2 on the Basal Lateral Membrane transports glucose into the blood stream
      - NaKATPase pumps out Na to the blood stream and brings K in, this also aids in the movement of H20 from lumen (SI) to blood
170
Q

What is the transport mechanism for glucose and galactose?

A

Secondary Active Transport (via NaKATPase)

171
Q

How is fructose transported?

A
  1. GLUT5 on the Apical Membrane (lumen of the SI) brings fructose in.
  2. GLUT 2 on the Basal Lateral Membrane (same as glucose + galactose) transports fructose into the blood stream
172
Q

What is the normal level of blood glucose?

A

5mm/L (any higher than this is linked to obesity)

173
Q

What are proteins?

A

AA polymers linked by peptide bonds

174
Q

What does post-translational modification do to proteins?

A

Shortens them to 3-10 AAs in length

175
Q

What does endopeptidase do to a protein/peptide?

A

Cleaves Internally

176
Q

What does exopeptidase do to a protein/ peptide?

A

Cleaves at terminal ends (reduce chain 1 AA at a time)

177
Q

How are proteins/peptides broken down to amino acids?

A

via endo/exopeptidases (cleavage) and hydrolysation via proteases/ peptidases

178
Q

What are proteins broken down by endo/exo peptidases and hydrolysation to form?

A

Amino Acids

179
Q

How are peptides transported?

A

PEPT1 on the Apical Membrane (lumen of SI) brings in Di+Tripeptides via coupling (bringing in H+) ions. These H+ ions are recycled back out to the lumen and bring na in via NHE3
NOTE: As hydrogen is being put back into the lumen an acid microclimate of pH less than 6 is produced at the brush border as compared to the lum (pH greater than 7)
At the Basal Lateral Membrane the NaKATPase pulls in K from the blood and pushes out Na. Additionally an unknown transporter moves the peptide through

180
Q

Why is there a difference in pH at the brush border?

A

As hydrogen is being put back into the lumen an acid microclimate of pH less than 6 is produced at the brush border as compared to the lum (pH greater than 7)

181
Q

How are Amino Acids transported?

A

SAAT1 on the Apical Membrane (lumen of SI)brings in both Na and an Amino Acid.
NaKATPase pulls the sodium out of the cell into the blood stream in exchange for K.
The amino acid is pulled into the blood stream by its SPECIFIC transporter

182
Q

is there a concentration of fructose in the blood?

A

No, fructose is always metabolised

183
Q

What kind of transport mechanism transports Amino Acids?

A

Secondary Active Transport

184
Q

What 3 ways are small/ non-polar molecules transporter?

A
  1. Transcellular- Through the cell
  2. Paracellular- Down the side (proteins) where junction is less tight
  3. Vectorial- Needs minimum of 2 transport proteins
185
Q

What is transcellualr transport?

A

Through the cell

186
Q

What is paracellular transport?

A

Down the gaps between cells (where junctions are less tight)

187
Q

What is vectorial transport?

A

Need a minimum of 2 transport proteins

188
Q

What is the difference between food and diet?

A

Food is the individual items ingested that make up a diet

189
Q

What are nutrients?

A

Chemically defined compounds required by the body

190
Q

How does malnutrition occur?

A

When intake is less than demand

191
Q

What are the FIXED demands on the body which require calorific intake?

A
  1. Basal Requirements- Membrane functioning, transporting + signalling
  2. Mechanical Work
  3. Substrate Turnover eg./ Bones, gut etc (huge)
192
Q

What are the VARIABLE demands on the body which require calorific intake?

A
  1. Processing dietary intake
  2. Physical Activity
  3. Maintaining body temperature
  4. Growth
193
Q

What are the causes of undernutrition?

A
  1. Appetite failure- eg./ illness, Anorexia Nervosa
  2. Access failure- teeth, stroke, NG/PEG tube, cancer, head injury
  3. Intestinal Failure- reduction in functioning gut/ inadequate digestion/ inadequate absorption eg./ IBD
194
Q

How do you treat Nutritional Failure?

A

Protein, Calorie, trace elements + vitamins needed
Diabetic Assessment
IV feed (percutaneous endoscopic gastrostomy)
Deal with sepsis

195
Q

What is Marasmus?

A

Protein Calories malnutrtion

196
Q

What is Kwashiokor?

A

Severe ascites (H20 + salt retention)

197
Q

What are the 2 types of liver injury and how are the classified/ separated?

A

Type A- Predictable/ Intrinsic.

Type B- Bizzare, idiosyncratic. Inc LFTs- failure. Factors: Older, Female, Alcoholic, Genetic, Malnourished.

198
Q

What are the main differences between the small and large bowels?

A
  1. SB is absorptive, LB is absorptive(water+electroylets) + secretive
  2. SB mucosa has tons of villi, NO vili in LB
  3. SB- crypts of Lieberkühn(goblet cells, stem cells, endocrine + paneth cells). LB- tubular crypts (goblet, endocrine + stem)
  4. BOTH have columnar epithelia
  5. SB is larger but LB is wider
  6. No peyers patches in LB but in SB
  7. Muscle in the SB is in a continuous band whereas in the LB taenia coli are the muscle.
  8. NO hormones secreted in LB.
  9. Both mediated by myenteric plexus (intrinsic), autonomic NS (extrinsic) + Auerbach plexus
199
Q

How do you get from the small intestine to the large intestine?

A

Ileum (small intestine)- Ileocaecal Valve- Caecum (blind ended sack with appendix at end)- colon- rectum- anal canal- internal anal sphincter (smooth muscle)- external anal sphincter (skeletal muscle)

200
Q

What it the difference in innervation between the internal and external anal sphincter?

A

Internal- Autonomic Control- smooth muscle via pelvic splanchnic (can’t control it)
External- Voluntary control- skeletal muscle

201
Q

What kind of epithelia is found in the colon? What is its muscularity?

A

Columnar- Absorption (water+electrolytes) + Secretion.
Brings in Na via NAKATPase (water follows) to dehydrate chyme.
Incomplete muscle layer- taeniae coli when they contract produce hausfrau pouches.
Crypts Leiberkun filled with goblet cells (mucus to pass foecal matter) no paneth cells

202
Q

What kind of epithelia is found in the rectum?

A

Columnar epithelia

203
Q

What kind of epithelia lines each area of the GI tract?

A

Mouth- Oesophagus= Non- keratinised stratified squamous
Stomach- LI= simple columnar
Rectum= Non- keratinised stratified squamous

204
Q

How does defecation occur?

A

NaKATPase movement- water follows- dehydrates chyme- solid faecal pellets + a long residency time for bacterial action

  1. Mass movement to rectum via taeniae coli contraction- distension of rectal wall- moves faecal matter into rectum.
  2. Mechanoreceptors- defecation reflex (parasympathetic control via pelvic splanchnic nerves)= rectum contraction + relax internal sphincter
  3. Increase peristaltic activity in colon- inc pressure on external sphincter= relax and voluntary expel (learn at age 2)
205
Q

What is constipation? What happens?

A

Long period of retention- no absorption/ removal of faecal material toxins
=Headaches, nausea, loss of appetite, abdominal distension

206
Q

What is Diarrhoea? What happens?

A

Too frequent passage of (liquid) faeces
Caused by stress, food, toxins, viruses, protezoalis, pathogenic bacteria eg./ Enterotoxigenic bacteria (e.coli)
Inc H20 secretion via cAMP,CGAMP + Calcium (cant get if CF)
Doesn’t damage villas cells
Give oral rehydration (sodium + glucose gets pump turning bringing water in)

207
Q

What is the purpose of the bacterial populations in the LI?

A

Breakdown of undigested carbohydrates to short chain FAs + Vit K + gasses (hydrogen, methane, carbon dioxide etc)

208
Q

What are the main functions of the liver?

A
  1. Glucose Synthesis- Glycogenolysis (break down stores) + Glycogenesis (storage)
  2. Fat (lipid) Metabolism- break down fats to produce phospholipids + cholesterol
  3. Protein Metabolism- Deamination + Transamination of AAs; albumin synthesis; urea synthesis to remove ammonia (by products of aa metabolism)
  4. Storage- Glucose, iron, copper, vitamins
  5. Synthesis- fibrinogen (fibrin for clotting) + thrombopetin (platelet production in bone marrow)
  6. Bile production (fat breakdown)
  7. Metabolises alcohol + drugs
209
Q

What affect does the liver have on glucose?

A

Metabolism
Glycogenesis- build up for storage (when high BGL)
Glycolysis- break down for use (when low BGL)

210
Q

What affect does the liver have on fats?

A

Metabolism

Breaks fats- phospholipids + cholesterol

211
Q

What affect does the liver have on proteins?

A

Metabolism
Deamination- removing aas
Transamination- adding aas+ ammonia (by-product the liver metabolises via urea)

212
Q

What does the liver store?

A

Glucose, Iron, Copper + vitamins

213
Q

How is alcohol processed in the body?

A

Drink- absorbed into the blood- hepatic circulation- liver
Converted from ethanol- acetylaldehyde- acetate via alcohol dehydrogenase (AHD) + acetyldehydrogenase (ALDH)
Acetate- fatty acids +C20 + H20

214
Q

How much alcohol can a healthy liver process?

A

1 unit of alcohol per hour

215
Q

What is acetaldehyde? Why is it dangerous?

A

Produced when the liver metabolises ethanol via ADH and ALDH. It is a carcinogen

216
Q

What are the physiological affects of chronic, excessive alcohol consumption on the liver?

A

Fatty liver, fibrosis, hepatocyte injury/ cell death, inappropriate activation of kupffe (collect bacteria, old cells etc)r + stellate cells

217
Q

What is the recommended allowance of alcohol per week for males and females?
What level can result in serious liver damage?

A

<14 units per week is the recommended allowance of alcohol for males and females.
>100 units per week gives a 20% chance of developing serious liver disease.

218
Q

What groups of people are more susceptible to damage by high alcohol consumption?

A
  1. Poor dietary status- nutritional deficiencies
  2. Exposure to other drugs can affect metabolism
  3. Genetic variations/ polymorphisms of enzymes eg./ fast acting ADH or slow acting ALDH builds up acetaldehyde
  4. Females more vulnerable
  5. Coexisiting viruses damaging the liver eg./ hep C
219
Q

What is the progression of alcohol related liver disease?

A

Normal Liver- Fatty Liver (steatosis)- Steatohepatitis- fibrosis- liver cirhosis

220
Q

What is steatosis?

A

Fatty Liver due to-
Alcohol metabolism (alcohol-acetaldehyde-acetate-fatty acids). Fat then deposited in central veins + parenchyma.
REVERSIBLE with alcohol abstinence

221
Q

Is steatosis reversible?

A

Fatty liver due to alcohol metabolism is reversible with abstinence

222
Q

What indicated a patient is a chronic abuser of alcohol?

A
  1. Elevated gamma GT (liver enzymes)
  2. Macrocytosis (large RBC)
  3. Low Platelets
  4. Elevated Ferritin
  5. Enlarged, smooth edged liver of AUSS
223
Q

How does alcoholic hepatitis differ from steatosis?

A

Is ALSO a fatty change within the liver +
infiltration with leucocytes + hepatic necrosis
It results in- hepatomegaly, jaundice, abdo pain, fever, hepatic decompensation

224
Q

What scale is used to measure alcoholic hepatitis? Give a brief overview of the markers used in this scale and the survival rate

A

Takes into account age, markers of inflammation and liver function to produce a 28 day survival rate
GAHS<9= 87%
GAHS>9= 46%

225
Q

What is liver fibrosis?

A

liver damage- steatosis/ alcoholic hepatitis- LIVER FIBROSIS=
Chronic inflammation
Activation of stellate cells
Collagen Production

226
Q

What is the difference between fibrosis and cirrhosis?

A

Fibrosis come before cirrhosis, it is damaged to the liver causing fibrous scar tissue to develop. It can be reversed as long as it doesn’t develop into cirrhosis- pan lobular and destroys function of liver, it is irreversible

227
Q

What are the complications of cirrhosis?

A

Cirrhosis- irreversible scaring of the liver that reduces its function, it is irreparable.
Can results in- variceal haemorrhage, encephalopathy, ascites

228
Q

What affect can abstinence have on liver disease?

A

5 year survival 65% as a pose to 35%

GI (6 decks)

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