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1
Q

What are 6 differences between smooth and skeletal muscles?

A

1) Smooth: non-striated; Skeletal: striated

2) Smooth: Fusiform; Skeletal: Cylindrical

3) Smooth: Involuntary; Skeletal: Voluntary

4) Smooth: Slow contraction; Skeletal: fast

5) Smooth: phasic; Skeletal: deliberate

6) Smooth: sustained tonic contraction; Skeletal: unsustained tonic

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2
Q

Smooth activity of stomach and intestines are _________ active.

A

Phasically active

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3
Q

What are 4 functions of mastication?

A

1) Dissolve chemicals in saliva (taste)
2) Lubricate food to ease swallowing
3) Mix food with salivary enzymes (α-amylase)
4) ↑ SA of food by breaking into smaller pieces

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4
Q

Primary peristalsis is (voluntary/involuntary) while secondary peristalsis (voluntary/involuntary).

A

Primary: voluntary
Secondary: involuntary

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5
Q

What are the 3 phases of swallowing?

A

1) Oral (voluntary) phase
- chewing reflex
- food bolus formation

2) Pharyngeal phase (1-2s)
- swallowing reflex start
- respiration inhibited

3) Oesophageal phase
- 1° peristalsis
- 2° peristalsis

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6
Q

What happens during the pharyngeal phase of swallowing?

A

1) Soft palate pushes against nasopharynx
2) Food moves downwards → pushes against epiglottis to close trachea
3) Larynx moves up to meet bolus and close off airway
(respiration inhibited)
4) Upper oesophageal sphincter opens

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7
Q

What induces secondary peristalsis?

A

Stretching of esophageal wall by food bolus

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8
Q

What are 4 functions of the stomach?

A

Secretory:
1) Acid, mucous, enzymes, hormones

Motor:
2) Reservoir (proximal, fundus)
3) Churning (distal, antrum)
4) Antrum-pylorus-duodenum unit for emptying

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9
Q

What are 3 types of modalities of gastric relaxation?

A

1) Receptive (swallowing signal)
2) Adaptive (Vago-vagal)
3) Feedback (Small intestines)

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10
Q

Describe the pathway of adaptive gastric relaxation.

A

Vago-vagal:
Gastric stretch receptors → vagal afferents
→ medulla
→ vagal efferents
→ enteric nervous system
→ interneuronal circuits → inhibitory motor neurons (NO and VIP)
→ muscle relaxation

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11
Q

How does a vagotomy affect gastric filling?

A

Limits vago-vasal/adaptive gastric relaxation
→ ↑Intraluminal pressure @ ↑volumes

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12
Q

What are the 3 processes of gastric churning and trituration?

A

1) Propulsion
- bolus pushed towards closed pylorus

2) Grinding
- antrum churns the trapped material

3) Retropulsion
- bolus pushed back into proximal stomach

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13
Q

What are 3 intragastric factors that inhibit gastric emptying?

A

1) low pH
2) hypertonicity
3) fatty acids

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14
Q

The pyloric sphinter:
regulates ________
prevents ________

A

regulates gastric emptying
prevents duodenal-gastric reflux

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15
Q

Gastric motility is under what 2 mechanisms of control?

A

1) Neural
- Vagal nerve (eg. stress, nausea)
- vaso-vagal reflex

2) Hormonal
- gastrin (+)
- CCK, Secretin, GIP (-)

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16
Q

What are 3 hormones that affect gastric motility?

A

1) CCK (cholecystokinin)
2) GIP (Gastric inhibitory peptide)
3) Secretin

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17
Q

What is the most effective method of eliciting intestinal mobility/peristalsis?

A

Radial stretch of intestinal wall

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18
Q

What is segmentation in intestinal motility?

A

Local reflex
- bidirectional propulsion in propulsive segments
- mixing of bolus in receiving segments

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19
Q

What are migrating motor complexes?

A

Phases of 90-120mins of contractions
- stimulated by motilin
- occur during interdigestive period (no food)
- sweeps food and bacteria down towards colon
- inhibits migration of colonic bacteria into distal ileum

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20
Q

What hormone triggers the migrating motor complex during interdigestive period?

A

Motilin

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21
Q

What are the 3 phases of MMC?

A

Phase 1: No spike potential, no contraction

Phase 2: Irregular spike potentials, no contractions

Phase 3: Regular spike potentials, contractions

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22
Q

Where is the ileocaecal sphincter?

A

Terminal ileum

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23
Q

What are 2 functions of the ileocaecal sphincter?

A

1) regulate flow past ileocaecal junction
2) prevent reflux of colonic bacteria

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24
Q

What are 2 stimuli that affect the contraction and relaxation of the ileocaecal sphincter?

A

Relaxation: Ileum distension
Contraction: Proximal colon distension

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25
Q

The large intestine partakes in (propulsive/non-propulsive) segmentation.

A

Non-propulsive
- mix colonic contents
- slow progressive of contents
- retrograde movements

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26
Q

When would there be mass peristalsis within the large intestine?

A

1) after meal (gastrocolic reflex)
2) Defecation
3) Opiates (morphine, codeine, pethidine)

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27
Q

How is the gastrocolic reflex initiated?

A

Distension of stomach and duodenum
(vago-vagal gastro/duodenal colic reflex)

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28
Q

What happens when defecation is not desired?

A

Involuntary reflex by sacral nerves → keep external sphincter contract

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29
Q

What happens when defecation is desired?

A

1) Relaxation of external sphincter
2) Relaxation of pelvic wall muscles
3) Contraction of abdominal muscles

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30
Q

What happens as feces move towards the rectum?

A

rectum distension →
1) rectosphincteric reflex
→ relaxation internal sphincter

2) sensation to “void” (defecate)

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31
Q

Differentiate between active and passive distention of the rectum.

A

Passive: by filling of rectum

Active: triggered by threshold pressure in rectum by passive distention → active contraction of rectal smooth muscles

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32
Q

Differentiate within the internal and external anal sphincter.

A

Internal: ANS
- circular and longitudinal muscle
- high resting tone

External: voluntary
- striated muscle

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33
Q

What is the term for problems with swallowing?

A

Dysphagia

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34
Q

What is the term for pain on swallowing?

A

Odynophagie

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35
Q

What are 4 causes of dysphagia?

A

1) Abnormal coordination
2) Obstruction
3) Stricture
4) Dysmotility
5) Achalasia

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36
Q

What are 4 gastric secretions that are secreted into the gastric lumen?

A

1) HCl (Parietal)
2) Pepsinogen (Chief)
3) Intrinsic factor (Parietal)
4) Mucous and electrolytes

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37
Q

What are 2 gastric secretions secreted into the blood stream?

A

1) Gastrin
2) Ghrelin

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38
Q

When is ghrelin secreted?

A

When stomach is empty

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39
Q

What is the difference between satiety and satiation?

A

Satiety: lack of desire to eat between meals

Satiation: “fullness” after a meal

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40
Q

What is the effect of destruction of the ventromedial nucleus?

A

Ventromedial nucleus: Satiety signals
Destruction → Hyperphagia → Obesity

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41
Q

What is the effect of destruction of the lateral nucleus?

A

Lateral nucleus: Hunger center
Destruction → starvation

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42
Q

What is the effect of ghrelin?

A

Travels in bloodstream to hypothalamus → ↑ appetite

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43
Q

What is the effect of gastrin?

A

Travels in bloodstream to hypothalamus → ↑acid secretion and antral motility

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44
Q

How do the different parts of the stomach differ in their function?

A

Proximal → reservoir function
Distal → Churning function
Antrum-pylorus-duodenum unit → gastric emptying

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45
Q

What do parietal cells secrete?

A

HCl and intrinsic factor

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46
Q

What do enterochromaffin-like cells secrete?

A

Histamine

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47
Q

What do the chief cells secrete?

A

Pepsinogen and lipase

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48
Q

What do D cells secrete?

A

Somatostatin

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49
Q

What do G cells secrete?

A

Gastrin

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50
Q

How are parietal cells stimulated and what are the morphological changes to the cells?

A

Stimulated by:
i) Gastrin (CCK-B → Ca2+)
ii) ACh (M3 → Ca2+)
iii) Histamine (H2 → cAMP)

Changes:
↑ expression of apical H+/K+ ATPase (from tubulovesicles)
↑ expression of canaliculi

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51
Q

What is an alkaline tide in gastric acid production?

A

Activation of carbonic anhydrase:
H2CO3 → ↑H+ and ↑HCO3-

H+ pumped out by H+/K+-ATPase to gastric lumen (apical)

HCO3- pumped out by HCO3-/Cl- ATPase to blood (basolateral)

**all pumps driven by Na+/K+ ATPase

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52
Q

What are the factors that promote the activation of pepsinogen?

A

1) Low pH (optimal <3)
2) Pepsin (autocatalytic)

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53
Q

Which part of the stomach are the cells producing intrinsic factor found?

A

Parietal cells mainly in fundus

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54
Q

What is the function of intrinsic factor?

A

Absorption of vit. B12
- forms complex with B12 in intestine → resistant to digestion
- IF-B12 absorbed at terminal ileum

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55
Q

What are the factors that stimulate intrinsic factor secretion?

A

1) Gastrin
2) Histamine
3) ACh

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56
Q

Do PPIs reduce intrinsic factor secretion?

A

No

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57
Q

What are the neuronal factors involved in the stimulation of gastric secretion?

A

1) CNS (vagal): 30%
2) Local gastric(local reflex, vagal, gastrin-histamine): 60%
3) Intestines (nervous and hormonal): 10%

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58
Q

What are 4 effects of gastrin?

A

1) ↑HCl secretion
2) ↑Gastric and intestinal motility
3) ↑pancreatic secretion
4) Growth of GI mucosa (Trophic effect)

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59
Q

How does smelling good food stimulate gastric acid secretion?

A

Olfactory receptors → higher centers in CNS
i) ACh to parietal via vagus
ii) Vagus stimulate gastrin → parietal

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60
Q

How does distension of the antrum stimulate gastric acid secretion?

A

Local reflex → gastrin → parietal

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61
Q

How do gastrin related peptides/amino acids stimulate gastric acid secretion?

A

Stimulate G cells → gastrin → parietal cells

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62
Q

How does somatostatin reduce gastrin acid secretion?

A

Inhibits G cells → ↓gastrin

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63
Q

What is the functions of mucin in the gastric mucosal barrier?

A

Large molecules → R to digestion
→ Coat and lubricate mucosal surface

64
Q

What are 2 factors that physiologically stimulate mucin expression on the gastric mucosa?

A

1) ACh
2) Mechanical (food)

65
Q

What are 4 functions of prostaglandins in the gastric mucosal barrier?

A

1) Epithelial restitution (stem cells)
2) Regulate mucosal HCO3- and mucosa
3) Inhibit parietal cell secretion
4) Mucosal blood flow

66
Q

What is the main defence of the gastric mucosal barrier against abrasion, HCl and pepsin?

A

Thick mucous layer (mucins, HCO3-)

67
Q

The unstirred later of the gastric mucosal barrier, there is an inward diffusion of _______ and an outward diffusion of __________.

A

Inward: H+
Outward: HCO3-

68
Q

What are 3 exocrine secretions of the pancreas, and the cells that secrete them?

A

1) Enzymes (Acinus cells)
2) Electrolytes (Ductal cells)
3) Mucin (Goblet cells)

69
Q

What are 4 endocrine secretions of the pancreas, and the cells that secrete them?

A

Islets of Langerhans
1) Glucagon (α)
2) Insulin (ß)
3) Somatostatin (δ)
4) Pancreatic polypeptide (F cells)

70
Q

Describe the 4 factors that contribute to the “autoprotection” of the pancreas.

A

1) Package as zymogens (inactivated)
2) Protease inhibitors (pancreatic trypsin inhibitor)
3) Compartmentalisation
4) Condensation of secretory proteins @ low pH

71
Q

Acinar cell secretions are stimulated by _________.

A

CCK (cholecystokinin) from I cells

72
Q

Ductal cell secretions are stimulated by ___________.

A

Secretin from S cells

73
Q

What are 3 active enzymes secreted by the pancreas (do not require trypsin for activation)?

A

1) Pancreatic α-amylase (polysaccharide (except cellulose) → disaccharides)

2) Pancreatic lipases
- water-insoluble esters → need bile salts to work
- water-soluble esters dont need

3) Nucleases

74
Q

What 4 examples of zymogens secreted by the pancreas and how are they activated?

A

Activated by: Enterokinase in pancreatic juice
→ cleave trypsinogen → trypsin
→ activates other enzymes

1) Trypsinogen
2) Chymotrypsinogen
3) Proelastase
4) Procarboxypeptidase A/B

75
Q

What are 4 functions of CCK in the GIT?

A

TLDR: match nutrient delivery to digestive and absorptive capacity
1) Gall bladder contraction
2) Pancreatic acinar secretion
3) ↓ stomach emptying
4) Sphincter of Oddi relaxation

76
Q

Describe the hormonal control of pancreatic secretions.

A

1) Cephalic and gastric (30%)
- ACh to M3 on ductal and acinar cells
- gastrin → CCK-A on acinar cells

2) Intestinal (70%)
- H+ → S cells → secretin
- protein/lipids → I cells → CCK

77
Q

Describe the neuronal control of pancreatic secretions.

A

Vagal (+)

78
Q

Where do CCK-RP and Monitor peptides come from and how do they regulate pancreatic secretion?

A

CCK-RP: stimulated by digested AA/FA
Monitor peptide: secreted by pancreas

Both can bind to I cells → ↑CCK secretion
- broken down by trypsin
- so when ↑food → ↓trypsin →↑CCK-RP/Monitor peptide → ↑CCK from I cells
- vice versa

79
Q

In the liver, _____ cell-thick epithelial hepatocytes separates two fluid compartments: ________________

A

One-cell thick
- canalicular lumen (bile)
- sinusoids (blood)

80
Q

The apical membrane of hepatocytes face the ___________ while the basolateral membrane faces the ___________.

A

Apical: canalicular lumen
Basolateral: peri-sinusoidal space (space of Disse)

81
Q

The blood flow in the sinusoids and the bile flow in the cannaliculi is (parallel/countercurrent).

A

Countercurrent flow

82
Q

Describe the flow of bile from the liver to the intestines.

A

Produced in liver → R/L hepatic ducts →common hepatic duct
→ gallbladder (via cystic duct)

Cystic + Common hepatic duct → common bile duct

common bile duct + pancreatic duct → sphincter of oddi → duodenum

83
Q

What are 2 sources of bile secreted into the duodenum?

A

Hepatic and gall bladder

84
Q

What are 5 components of bile?

A

1) Bile acids
2) Bile pigments (bilirubin)
3) Lecithin/phospholipids
4) Cholesterol
5) Proteins
6) Electrolytes

85
Q

Describe the regulation of bile release.

A

FA in duodenum → ↑CCK
i) gall bladder contraction → ↑ bile into common bile duct
ii) sphincter of oddi relaxation → bile flow into the duodenum

86
Q

What are 2 classes of bile acids?

A

1) 1° bile acids (cholic, chenodeoxycholic acid)
- produced in liver

2) 2° bile acids (deoxycholic, lithocholic acids)
- converted from 1° by intestinal bacteria

87
Q

How are bile acids converted to bile salts?

A

Bile acids conjugated to glycine/taurine

88
Q

What is the difference between conjugated and unconjugated bile acids?

A

1) More amphipathic
- easier to form micelles → aid fat absorption
- poor reabsorption → stays longer in gut

2) R to hydrolysis by pancreatic enzymes

89
Q

What are 3 functions of bile acids?

A

1) Promote bile flow
2) Solubilse cholesterol, phospholipids in gall bladder
3) ↑ dietary lipid digestion and adsorption by mixed micelle formation

90
Q

Where and how are bile acids reabsorbed?

A

@ terminal ileum by active Na+ dependant process

91
Q

Why is bile acid reabsorption so important?

A

80-90% is reabsorbed (too much loss, synthesis cant keep up → ↓fat absorption)

92
Q

Where is most of dietary fluid absorbed?

A

Small intestine
(much less in colon, very little normally excreted in feces)

93
Q

What are 2 ions that are secreted in the small intestine?

A

1) Cl- secretion
2) HCO3- secretion

94
Q

How does Cl- secretion occur in the small intestine?

A

Basolateral Na/K/Cl co-transporter
- driven by Na/K ATPase

Apical CFTR (Cystic fibrosis transmembrane conductance regulator)

  • water follows the change in osmolarity via paracellular transport (space between cells)
95
Q

How does HCO3- secretion occur in the small intestine?

A

HCO3- and H+ from carbonic anhydrase

HCO3- also from NBC1 (HCO3-/Na+ co-transporter)
- driven by Na/K ATPase

Apical:
1) CFTR HCO3-/CL- co-transporter
2) PAT (HCO3-/Cl- antiport)

96
Q

What are 2 functions of small intestinal secretions?

A

1) Maintain fluidity of chyme
2) Akalinise contents (enzyme activity)

97
Q

What are the components of intestinal juice, where does it come from and what is it driven by?

A

Intestinal juice: water, electrolytes, mucous
- driven by CFTR (Cl-secretion)

98
Q

What are 4 stimulants of intestinal juice secretion?

A

1) Mechanical irritation of mucosa
2) Distension of gut
3) ACh (vagal), prostaglandin, guanylin
4) 2nd messenger (cAMP, cGMP, Ca)

99
Q

What are 3 ions secreted in the colon?

A

1) Cl-
2) HCO3-
3) K+ secretion

100
Q

How does the intestinal fluid in the colon differ from that of the small intestine?

A

Higher K+ and HCO3- secreted in colon (to buffer H+ produced by bacterial fermentation)

101
Q

What are 2 stimuli that promote colonic secretion?

A

1) Parasympathetic nerve impulses
2) Mechanical/chemical irritation of mucosa

102
Q

How is K+ secreted in the colon?

A

Aldosterone → Na+ influx from lumen into colonic epithelial cells

change in electrical gradient → K+ efflux into colonic lumen

103
Q

What is the main driver of water and electrolyte absorption in the small intestine?

A

Na

104
Q

What are the differences between the ions absorbed and secreted in the small vs large intestine?

A

Small intestine
net abs: H2O, Na, Cl, K
Secrete: HCO3

Large intestine
net abs: H2O, Na, Cl
Secrete: K, HCO3

105
Q

Paracellular transport of solutes and water in the intestines is highest in ________ and decreases in __________ direction. The greatest limiting factor is the __________________.

A

Paracellular transport highest in duodenum, decreases arborally (down the GIT).

Limiting factor: permeability of tight junction

106
Q

In transcellular transport of solutes and water in the intestines, there is higher _________________ R than in paracellular transport and may require ______________.

A

Higher transepithelial R, need active processes (co-transporters, exchangers: secondary active)

107
Q

What is solvent drag absorption?

A

Solute movement coupled to fluid movement for absorption

108
Q

How is K+ absorbed in the GIT?

A

In small intestine
- via paracellular (solvent drag)

109
Q

What is the difference between the water and solvent absorption in the distal ileum/proximal colon vs the distal colon?

A

Distal ileum/proximal colon
- driven by electroneutral Na/Cl absorption

Distal colon
- driven by electrogenic Na absorption (aldosterone)
(tighter tight cell junctions → ↓paracellular)

110
Q

How is iron absorption in the GIT adaptive?

A

↑Fe in Liver/Reticuloendothelial system → ↑Hepcidin production

Hepcidin → ↓ferroportin activity → ↓Fe in blood/↑Fe in ferritin in enterocytes (can be excreted in feces if enterocyte is sloughed off)

111
Q

What are the 2 ways iron can be absorbed in the the GIT?

A

1) Heme → heme transporter → broken down into Fe2+

2) Fe3+ → reductase → Fe2+ (if needed) → DMT1

Then either:
1) Fe2+ → Ferroportin → blood → Fe3+ → Fe3+-Transferrin

2) Fe2+ → Fe3+-ferritin (stored in cell

112
Q

How is B12 absorbed in the GIT?

A

B12 bound to food → released by enzymes/acid
→ haptocorrin from gastric glands bind to B12
→ transported to intestines
→ B12 released from haptocorrin by proteolysis
→ B12 bound to IF from parietal cells to form complex
→ IF receptors on terminal ileal enterocyte → endocytosis

113
Q

What are 2 specific parts of the GIT where carbohydrate digestion occurs, each with their specific enzymes?

A

1) Luminal: salivary and pancreatic amylase
2) Mucosal: disaccharidases

114
Q

What are the 3 products of luminal digestion of carbohydrates?

A

1) α-limit dextrins
2) Maltose
3) Maltotriose

(α-1,4 and 1,6 linkages that cannot be cut by amylase)

115
Q

What are the 2 key transported in brush border digestion of carbohydrates?

A

1) SGLT (sodium-linked glucose transporter)
2) GLUT (glucose transporter)
- eg. GLUT 5 → fructose

116
Q

How are (i) lactose, (ii) sucrose and (iii) amylase products (eg. maltose, maltotriose, α-limit dextrins) broken down and absorbed in the GIT?

A

i) Lactose → Lactase → Glucose + Galactose → SGLT1

ii) Sucrose → Sucrase → Glucose (SGLT1) + Fructose (GLUT5)

iii) Maltose, Maltotriose, α-limit dextrins → Isomaltase → glucose →SGLT1

117
Q

Which part of the GIT has the highest capacity for carbohydrate absorption?

A

Duodenum and upper jejunum

118
Q

How do the absorption of glucose and fructose differ?

A

Glucose: SGLT (2° active transport)

Fructose: GLUT5 (facilitated diffusion)
- most fructose rapidly converted into glucose and lactic acid within epithelial cells

119
Q

How are absorbed sugars transported into the bloodstream?

A

Via basolateral GLUT2 (facilitated diffusion)

120
Q

What are 3 types of proteases that aid in the digestion of proteins in the GIT and where are they located?

A

1) Gastric luminal pepsin
2) Pancreatic luminal proteases
3) Enterocyte peptidases

121
Q

Where is most of dietary protein absorbed?

A

Duodenum and jejunum (50%)

  • 20-50% in ileum
  • 10% colon → digested by micro-organisms
122
Q

True or false: most of the protein found in stools is a result of inefficient protein digestion in the GIT.

A

False.
- protein in stools is from bacterial and cellular debris

123
Q

What are 2 methods of apical peptide/amino acid absorbtion?

A

1) Na+-dependent for L-amino acids
2) Carrier transport for Tri/Dipeptides → broken down by intracellular peptidases

124
Q

How are oligopeptides absorbed in the GIT?

A

Via PEPT1 (peptide transporter 1)
- oligopeptide/H+- symport

125
Q

What are 2 cells that partake in whole protein absorption?

A

1) Enterocytes
- 10% direct → intact protein
- 90% indirect → processed proteins

2) M cells
- 50/50 direct/degradative

126
Q

How does lecithin and bile aid in the digestion and absorption of fats?

A

Bile → detergent → emulsify fats
lecithin → ↑detergency of bile

127
Q

What are 3 parts of the GIT where lipases are secreted?

A

1) Pancreas
2) Stomach
3) Mouth (lingual lipases)

128
Q

Gastric lipases work under what conditions compared to pancreatic lipases?

A

Gastric lipase: acidic (pH 4.5-6)

Pancreatic lipase: basic (pH >7)

129
Q

Lipolysis by pancreatic lipase (glycerol ester hydrolase) is enhanced by __________ because _________

A

Colipase dependent
- bind tgt to form complex
→ btr access to lipids in emulsion & micelle
→ expose active site to substrate
→ target fat-water interface

130
Q

What are 3 pancreatic lipases?

A

1) Glycerol ester hydrolase (main lipase)

2) Cholesterol esterase

3) Phospholipase A2

131
Q

Micelles are very small (5nm in diameter) and contain ________________ within the interior, requiring a minimum amount of _______________.

A

Interior: extremely hydrophobic material (cholesterol, fat soluble vit.)

Need min. amount of bile salts

132
Q

Why are micelles crucial in fatty acid absorption??

A

Fatty acids are highly insoluble in water
→ cannot pass through aqueous “unstirred” layer of eg. mucous

Micelles have ↑solubility in water → can pass through the “unstirred” layer to come into contact with the enterocyte membrane and diffuse into cells

133
Q

What is the rate limiting step of lipid absorption from micelles?

A

Migration of micelle from chyme to microvilli surface

134
Q

Once the micelles come into contact with the microvilli surface, lipid absorption can occur by:______________

A

Diffusion or carrier proteins

135
Q

True or false: most of the lipid found in stools is a result of inefficient protein digestion in the GIT.

A

False.
Fat in stools is physiologically from colonic bacteria and desquamated intestinal cells

136
Q

Where are short chain fatty acids derived from?

A

Synthesised by bacteria in the colon (not dietary)
- eg. acetate, propionate, butyrate
- butyrate is primary nutrient for colonic epithelial cells

137
Q

Absorption of short chain fatty acids by colon also stimulate ______________.

A

Na and water absorption

138
Q

Rank the fatty acid (short, medium, long chain) by their solubility in water.

A

Short > Medium > Long

139
Q

True or false:
Medium chain fatty acids do not require micelle formation, hydrolysis, re-esterification nor chylomicrons and are found in the portal blood.

A

True

140
Q

Describe the re-esterification/post-absorptive phase of long chain fatty acids.

A

1) Hydrolysed lipids in lumen in micelles absorbed at brush border

2) Re-esterification of free fatty acids to form cholesterol, triglycerides, phospholipids → chylomicrons

3) Exocytosis of chylomicrons into interstitial space → lymphatics (lacteals) → systemic circulation

141
Q

Describe the structure of chylomicrons.

A

Phospholipid sphere (w apolipoproteins) with Cholesterol and triglyceride core

142
Q

What are 4 classification of causes for diarrhoea?

A

1) Hypermotility of intestine (inflammation)
- ↓absorption and transit time

2) Hyperosmolarity (osmotic diarrhoea)
- unabsorbed nutrients (eg. lactose intolerance)
→ malabsorption

3) Loss of absorptive capacity
- loss of villi and length
→ malabsorption

4) Enhanced secretion of water and electrolytes (secretory diarrhoea)
- enterotoxins, tumours, Cl- channels

143
Q

What is the definition of diarrhoea?

A

3 or more watery stools a day

144
Q

What are 10 functions of the liver?

A

Synthesis:
1) Serum protein synthesis
2) Cholesterol synthesis/homeostasis
3) Bile and bile salts synthesis

Metabolic:
4) Metabolic and heat production
5) Detoxification of lipophilic compounds
6) Excretion of lipophilic waste

Storage:
7) Nutrient storage and regulation (glucose buffer)
8) Vitamin, Fe and Copper storage
9) Blood Reservoir

Immunity:
10) Immune function (Kupffer cells)

145
Q

What are 3 key organs/tissues involved in nutrient/energy homeostasis?

A

1) Liver
2) Adipose Tissues
3) Skeletal muscles

146
Q

Describe how the liver contributes to a “glucose buffer”.

A

Fed state: First pass
- all nutrients absorbed (except FFA by lymphatics) → released into portal vein → drain into liver
1) Liver “mops up” excess blood glucose
2) Stores glucose as glycogen

Fasting:
- ensure continual supply of blood glucose
1) Liver glycogen stores → glucose
2) Gluconeogenesis

147
Q

Why do skeletal muscles lack glucose 6 phosphatase unlike that of hepatocytes?

A

So Glucose-6-phosphate is shunted into metabolic pathways for energy production rather than export into the bloodstream as in the liver

148
Q

What are the main precursors for gluconeogenesis?

A

Glucogenic amino acids (eg. alanine)

149
Q

Why is urea produced in the liver?

A

Amino group of amino acids→ ammonia → processed in urea cycle → urea

150
Q

The liver is able to _______ and _________ ribonucleotides and deoxyribonucleotides.

A

Synthesise and salvage

151
Q

What are 4 processes taht amino acids can partake in in the liver?

A

1) Deamination → detoxification
2) Interconversion
3) Biosynthesis (proteins)
4) Gluconeogenesis

152
Q

Describe the differences in fatty acid/cholesterol metabolism in a (i) fed and (ii) starved state.

A

i) Fed state:
- FA synthesis → Triacylglycerides → secreted as VLDL
- Cholesterol and bile salt synthesis

ii) Starved:
- FA from adipose tissue → liver → acetyl CoA → ketone bodies

153
Q

The liver detoxifies _____________ (eg. alcohol, drugs, food additives) and _________________ (eg. bilirubin) for excretion.

A

Xenobiotics

Endogenous compounds

154
Q

What is the Cori Cycle?

A

Liver and muscle/non-hepatic tissue to handle lactate

Muscles/RBC:
Glucose → glycolysis → pyruvate → lactate dehydrogenase → lactate → blood

Liver:
Lactate → pyruvate → gluconeogenesis → glucose → blood

155
Q

What is the glucose-alanine cycle?

A

Liver and muscle/non-hepatic tissue handle amino group on amino acids

Muscles:
Glucose → glycolysis → pyruvate → transamination → alanine → blood

Liver:
Alanine → NH4+ (detoxified to urea) + Pyruvate → gluconeogenesis → glucose → blood

156
Q

In transamination of pyruvate, pyruvate is converted to _______ as _________ is converted to __________.

A

Pyruvate → Alanine
α-amino acid → α-keto acid

157
Q

What are 6 chemicals measured in a liver function test?

A

1) Albumin
2) Coagulation tests (PTT, PT, INR)
3) Bilirubin
4) ALT (alanine aminotransferase)
5) AST (aspartate aminotransferase)
6) ALP (alkaline phosphatase)
7) GGT (ɣ-glutamyltransferase)

GIT (14 decks)

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