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Physiology Flashcards

Lecture 1 - Intro to Structure, Function & control of alimentary canal Lecture 2 - Feeding & Satiety Lecture 3 - Digestion & absorption; small intestine and exocrine pancreas Lecture 4 - Digestion & absorption; Carbohydrates, protein Lecture 5 - digestion & absorption; Lipids, Ca, Fe and vitamins

1
Q

what is the alimentary canal?

A

= series of hollow organs running from mouth to anus (oral to aboral)

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2
Q

how are the structures in the alimentary canal separated?

A

= by sphincters which control movement

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3
Q

what does the mouth and oropharynx do?

A

= chops and lubricates food, = strating carbohydrate digestion
= propelling food to oesophagus

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4
Q

what does the oesophagus do?

A

= propels food too stomach

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5
Q

what does the stomach do?

A

= stores/churns food.
= continues carbohydrate digestion and initiates protein digestion.
= regulates delivery of chyme to duodenum

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6
Q

what does the small intestine consist of?

A

1) duodenum
2) jejunum
3) ileum

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7
Q

what tis the principle she of digestion and absorption of nutrients?

A

small intestine

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8
Q

what does the large intestine consist of?

A

1) caecum
2) appendix
3) colon

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9
Q

which part of the large intestine reabsorbs fluid and electrolytes, and stores faecel matter before delivery to rectum?

A

= colon

ascending, transverse, descending and sigmoidal components

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10
Q

what does the rectum and anus do?

A

= regulated expulsion of faeces

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11
Q

what are the 3 accessory structures?

A

1) salivary glands
2) pancreas
- note = only the exocrine pancreas is part of GI system
3) liver and gal bladder (hepatobiliary system)

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12
Q

what are 4 generalised structures of the digestive tract wall?

A

1) mucosa
2) sub-mucosa
3) muscularis externa
4) serosa

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13
Q

what 3 things does the mucosa contain?

A
  • mucous membrane (epithelial, exocrine & endocrine gland cells)
  • lamina propria
    (capillaries, enteric neurones, gut associated lymphoid tissue)
  • muscularis mucosa
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14
Q

what 4 things does the sub-mucosa consist of?

A
  • connective tissue
  • larger blood and lymph vessels
  • glands
  • sub-mucosa plexus (neurone network)
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15
Q

what does the muscularis externa consist of?

A
  • circular muscle layer
  • myenteric plexus (neurone network)
  • longitudinal muscle lauer
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16
Q

what does the serosa layer contain?

A

connective tissue

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17
Q

what are the 4 main functions of the alimentary canal?

+ describe each briefly

A

1) motility (movement)
= mostly involving smooth muscle, but skeletal at mouth, pharynx, upper oesophagus and external anal sphincter

2) secretion 
= into lumen of digestive tracts occurs from itself & accessory structures in response to presence of food, hormonal and neural signals. 
Required for; 
(i) digestion
(ii) lubrication
(iii) protection

3) digestion
= breakdown of foodstuff by enzymatic hydrolysis into absorbable (MONOSACARIDES) units

4) absorption
= transfer of absorbable products of digestion from digestive tract to blood/lymph
(mediated by numerous transport mechanism)

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18
Q

in GI motility, describe circular/longitudinal muscle contraction and muscularis mucosae contraction?
(smooth muscle)

A

circular muscle contraction
= lumen becomes narrower & longer

Longitudinal muscle contration
= intestine becomes shorter & fatter

Muscularis mucosae contraction
= change in absorptive & secretory area of mucosa (folding), mixing activity

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19
Q

how is smooth muscle in GI tract coupled?

A

= electrically coupled

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20
Q

how are adjacent smooth muscle cells coupled?

A

= by gap junctions

- electrical currents flow from cell two cell

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21
Q

how do the smooth muscles act?

A

= cells are depolarised & contract AT SAME TIME as a synchronous wave (single unit of smooth muscle)

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22
Q

how is spontaneous activity across coupled cells driven and how is it modulated?

A

= Driven by specialised pacemaker cells

Modulated by;

  • intrinsic (enteric) and extrinsic (autonomic) nerves
  • numerous hormones
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23
Q

in the stomach, how does spontaneous electrical activity in small and large intestine occur?

A

= SLOW WAVE

- rhythmic depolarisation & depolarisation that spreads from cell to cell via gap junctions

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24
Q

what does the slow wave electrical activity in the stomach determine?

A

= the frequency, direction and velocity of rhythmic contractions

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25
Q

how is the slow electrical activity of the stomach driven and what are they and where are they located?

A

by INTERSTITIAL CELLS OF CAJAL (ICCs)

= they are pacemaker cells located between circular & longitudinal muscle layers

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26
Q

what do the ICCs do?

and what do the slow waves in ICCs drive?

what do some ICCs from?

A

= form gap junctions with each other & smooth muscle cells electrically coupling them

= drive slow waves in smooth muscle cells coupled to them

= form a bridge between nerve endings and smooth muscle cells

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27
Q

Yes or No.

Does depolarising slow waves necessarily result in smooth muscle contraction?

A

no.
- Contraction in the intestines occurs only if the slow wave amplitude is sufficient to reach a threshold to trigger smooth muscle cell Ca action potentials

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28
Q

what is force related to?

A

number of action potentials discharged (driven in turn by duration of slow waves that is above threshold)

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29
Q

what are slow waves also known as?

and do slow wave vary along the GI tract?

A

= basic electrical rhythm (BER)

  • yes they do.
    along stomach, small intestine and colon.
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30
Q

what 3 things depend on whether or not slow waves reach threshold amplitude?

A

1) neuronal stimuli
2) hormonal stimuli
3) mechanical stimuli

= generally act to depolarise SMC rather than influence slow waves directly

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31
Q

what is the most important autonomic innervation of GI tract?

A

parasympathetic.

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32
Q

in the parasympathetic division, what do the pre-ganglionic fibres (release ACh) synapse with and where do they do this?

A

synapse with ganglion cells within the enteric nervous system (ENS)

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33
Q

what 2 effects does parasympathetic division have on GI tract?

A

1) excitatory influences
- increased secretion (gastric, pancreatic and small intestinal)
- blood flow and smooth muscle contraction

2) inhibitory influences
- relaxation of some sphincters, receptive relaxation of stomach

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34
Q

in the sympathetic division, what do the pre-ganglionic fibres synapse in?
and what do the post-ganglionic fibres innervate?

A

= synapse ini pre-vertebral ganglia.

= innervate mainly enteric neurones, but also others

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35
Q

what 2 effects does sympathetic division have on GI tract?

A

1) excitatory influences
- increased sphincter tone

2) inhibitory influences
- decreased motility, secretion & blood flow

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36
Q

where are enteric nervous system cell bodies mostly located?

and how are they connected?

A

in ganglia

= located in ganglia connected by fibre tracts within;

  • myenteric plexus (regulates motility)
  • submucosa plexus (regulates epithelia and blood vessels)
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37
Q

why can the enteric nervous system cause reflex circuits that can operate independently?

A

because it has intrinsic controls.

- but also hormones and extrinsic nerves exert a strong regulatory infleucen

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38
Q

what does the enteric nervous system do and how does its do this?

A

= co-ordiantes muscular, secretive and absorptive activity via;

1) sensory neurones
2) inter-neurones
3) effector neurones

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39
Q

what are examples of local, short or long reflex?

A 
local = peristalsis 
short = intestine-intestinal inhibitory reflex
long = gastroileal reflex
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40
Q

what is peristalsis?

involved in motility patterns in GI tract

A

= wave of relaxation, followed by contraction that normally proceeds a short distance along gut in aboral direction
- triggered by distension of gut wall

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41
Q

what is segmentation
(mixing, or churning, movements)? and where dos it occur?
(involved in motility patterns of GI tract)

A

= rhythmic contractions of the circular muscle layer that mix and divide luminal contents

Occurs in;
= small intestine (in fed state) and large intestine (where its called haustration)

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42
Q

what is colonic mass movement?

A

= powerful sweeping contraction that forces faeces into the rectum – occurs a few times a day

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43
Q

what is migrating motor complex (MMC)?

A
  • powerful sweeping contraction from stomach to terminal ileum
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44
Q

what what are tonic contractions?

A

= sustained contractions

Low pressure - organs with a major storage function (e.g. stomach)
High pressure - sphincters

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45
Q

how many sphincters are there in the GI tract and what are they composed of?

A

= 6 in total

= composed of specialised circular, generally smooth muscle

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46
Q

how do sphincters act?

A

as one way valves by maintaining a positive resting pressure relative to two adjacent structures (e.g. oesophagus and stomach)

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47
Q

what causes opening and closing of sphincters?

A

stimuli (pressure) proximal and distal to a sphincter

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48
Q

give an example and describe what the upper oesophageal sphincter does?

A
  • relaxes to allow swallowing

- closes during inspiration

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49
Q

what does the lower oesophageal sphincter do?

A
  • relaxes to permit entry of food to stomach

- closes to prevent reflux of gastric contents too the oesophagus

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50
Q

what do the pyloric sphincter do?

A
  • regulates gastric emptying

- usually prevents duodenal gastric reflux

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51
Q

what do ileocaecal valve do?

A
  • regulates flow from ileum to caecum
    = distension of ileum opens
    = distension of proximal colon closes
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52
Q

what are internal (smooth muscle) and external (skeletal muscle) anal sphincters regulated by?

A

regulated by defaecation reflex

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53
Q

LECTURE 2

- feeding & safety

A

LECTURE 2

- feeding & safety

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54
Q

what is energy homeostasis?

and what does it promote?

A

= physiological process whereby energy intake is matched to energy expenditure over time

Promotes body fuel stability = energy primarily stored as fat

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55
Q

what causes obesity?

A

= small constant mismatch between energy intake and energy expenditure

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56
Q

what are factors that cause metabolic stress?

A
  • metabolic syndrome
  • central obesity
  • dyslipidemia
  • insulin resistance
  • type 2 diabetes
  • CV disease
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57
Q

what is obesity correlate with?

A

= increased body FAT

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58
Q

how do you measure BMI?

A

WEIGHT (kg)/SQUARE HIGHT (m)

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59
Q

what are the values of BMI that indicate thin/acceptable, overweight and obese and morbidity obese?

A

Thin/normal
- up to 25

Overweight
- up to 25-29.9

Obese
- 30-39.9

Morbidly obese
- >40

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60
Q

what are causes of obesity?

A

= consuming more calories than you expend.

  • high levels of activity
  • increased consumption of high fat foods
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61
Q

Yes or No.

Is obesity of singer disorder?

A

= NO

- its a heterogenous group of conditions with multiple causes.

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62
Q

what are the 2 major factors influencing obesity?

A

1) genetic
- susceptibility genes that increase your risk of developing disease

2) environmental
- these factors unmask latent tendencies to develop obesity
= dining out
= driving/public transport instead of active mode of transport
= static job

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63
Q

what 12 other diseases does obesity major contribute to?

A

1) type 2 diabetes
2) high BP
3) heart attack
4) certain cancers (colon, uterus, breast, prostate)
5) osteoarthritis
6) stroke (hypertension)

7) heart disease
= lipids, diabetes, hypertension

8) sleep apnoea
(resp disease)

9) gall bladder disease
10) dementia (Alzheimer’s)
11) NAFLD (fatty liver)
12) hyperuricaemia / gout

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64
Q

what does long term obesity drive?

A

= chronic disease risk

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65
Q

why do you need fat?

A
  • energy storage
  • prevention of starvation
  • energy buffer during prolong illness
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66
Q

what feature is a survival adaptation to starvation and infection?

A

adipose tissue accumulation

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67
Q

what 3 ways does the CNS influence energy balance and body weight?

A

1) behaviour
- feeding
- physical activity

2) ANS activity
- regulates energy expenditure

3) neuro-endocrine system
- secretion of hormones

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68
Q

where is the site of integration of behaviour, ANS activity and neuroendocrine system of CNS system?

what neural centre is responsive?

A

Site of integration
= brain

Neural centre
= hypothalamus
- lesioning ventromedial hypothalamus = obesity
- lesioning lateral hypothalamus = leanness

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69
Q

what 3 concepts underlie the control system of energy intake & body weight?

A

1) satiety signalling
2) adiposity negative feedback signalling
3) food reward

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70
Q

what is satiation?

A

= sensation of fullness generated during a meal

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71
Q

what is satiety?

A

= period of time between termination of one meal & the invitation of end

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72
Q

what is adiposity?

A

= the state of being obese

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73
Q

what does satiation signal during meal to limit meal size?

A

= satiation signals to INCREASE during meals to limit meal size

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74
Q

what are 5 satiation signals?

A

1) cholecystokinin (CCK)
2) peptide YY (PYY3-36)
3) glucagon-like peptide 1 (GLP-1)
4) oxyntomodulin (OXM)
5) obestatin

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75
Q

where is cholecystokinin secreted from?

and why is it released?

what does it signal via?

A

= secreted from entero-endocrine cells in duodenum and jejunum

= release in proportion to lipids & proteinic meals

= signals via sensory nerves to hindbrain & stimulates hindbrain directly (nucleus of solitary tact NTS)

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76
Q

where is peptide YY secreted from?

when do levels increase?

what does it inhibit?

A

= secreted from endocrine mucosal L-cells of GI tract.

= increase rapidly post-prandially

= inhibits gastric motility, slows emptying and reduces food intake (hypo)

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77
Q

what is glucagon like peptide 1 a product of?

when is GLP-1 released?

and what does it inhibit?

A

= of pro-glucagon gene

= released from L cells in response to food ingestion

= inhibits gastric emptying and reduces food intake (hypo, NTS)

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78
Q

what is oxyntomodulin produced and released from?

what does it act to do?

A

produced from
= pro-glucagon gene

released from
= oxyntic cells and L-cells of small intestine after meals

= acts to suppress appetite

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79
Q

what is obestatin?

what produces obestatin?

what is obestatin suggested to reduce?

A

= peptide

= produced from genes that encode gherlin & released from cells lining stomach/small intestine

= to reduce food intake (may act to antagonise the actions of gherkin)

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80
Q

what is Gherlin?

A

= a hunger signal

  • Octanoylated peptide, produced and secreted by oxyntic cells in stomach
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81
Q

when do levels of gherlin increase and decrease and how are levels raised?

A

Increased
= before meals

Decreased
= after melas

Levels raised
= by fasting & hypoglycaemia

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82
Q

what does peripheral gherlin stimulate?

A

= stimulates food intake (hypo) & decreases fat utilisation

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83
Q

what do gherlin controlling neurones in hypothalamus do?

A

= help control fat metabolism, increase lipogenesis (liver & adipose)

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84
Q

true or false.

Weight is stable in humans over length periods of time?

A

True for lean and obese individuals

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85
Q

how is overall energy balance controlled?

A

by feedback loops which acts to maintain constance of Total body energy stores

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86
Q

describe signalling in the feedback loops?

A
  • signals produced in response tot body nutritional status
  • these are senses in hypothalamus
  • act to modulate food intake & energy expenditure
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87
Q

what are the controllers called?

A

central appetite controllers

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88
Q

what 3 things increase food intake when injected into hypothalamic centres - effecting modest/short lasting?

A

1) glutamate
2) gaba
3) opioids

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89
Q

what suppresses food intake?

A

= mono-amines

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90
Q

what is produced in peripheral tissues & acts on hypothalamus?

A

= 2 hormones

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91
Q

what are the signals called with communicate fat stores to brain?

A

= adiposity signals

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92
Q

what 2 hormones report fast status to brain and when are they made & release?

what is the function or hormones?

A

1) leptin
= made & released from fat cells

2) insulin
= made & released from pancreatic cells

  • inform brain (hypothalamus) to alter energy balance = eat less & increase energy burn
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93
Q

what does reduced leptin mimic?

A

= starvation causing un-restrained apettitte

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94
Q

what family does leptin belong to?

what does leptin circulate in proportion to?

what does intracerebroventricular (icv) leptin inhibit?

what does deletion of leptin receptor (Ob-Rb) result in?

A

= cytokine family 146aa long & secreted from adipocytes

= to body adiposity

= inhibits food intake and decreases body weight of rodents

= obesity

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95
Q

what is the biological role of leptin?

A

A PLEIOTROPIC HORMONE
1) Food intake/energy expenditure/fat deposition

2) Peripheral glucose homeostasis/insulin sensitivity
3) Maintenance of immune system
4) Maintenance of reproductive system
5) Angiogenesis
6) Tumourigenesis
7) Bone formation

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96
Q

what does insulin circulate in proportion to?

what does intracerebroventricular (icv) insulin inhibits?

what does neuron specific deletion of the insulin receptor results results in?

A

in proportion tot body adiposity

= food intake & decreases body weight of rodents

= in obesity

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97
Q

what is the hedonistic aspect of food linked to?

A

1) sugar

2) fatt

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98
Q

what are 4 areas implicated in substance abuse and drug addiction?

A

1) ventral tagmental area
2) nucleus accumbent
3) striatum
4) substantial nigra

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99
Q

what is a large proportion of obesity characterised by?

A

= high leptin levels (correlating with high fat levels)

100
Q

what does diet-induced obesity (DIO) result in and what causes itt?

A
  • leptin resistance due to;
    1) deceptive leptin transport into brain
    2) altered signal transaction following leptin binding to its receptor
101
Q

give an example of an anti-obesity drug and how its acts?

what are some side effects of its?

A

= rimonabant
- acts on the endocannabinoid system - system targeted by marijuana active components - so stimulates appetite

  • also effective in assisting smokers to stop.
  • also might reduce addiction to drugs
  • improved Short term memory
  • anxiety
  • depression
  • increased risk of suicide
  • likely to promote development of neurodegenerative disease
102
Q

what is an over the counter drug for obesity?

what does it do?

what are side effects?

A

= Orlistat (Xenical or Alli)

Its function;
= Inhibits pancreatic lipase decreasing triglyceride absorption
= Reduces efficiency of fat absorption in small intestine

Side-effects;

  • cramping
  • severe diarrhoea

+ Need to take vitamin supplements

103
Q

what are 3 anti-obesity drugs in the pipeline?

and what do each of them do?

A

1) Lorcaserin:
- An agonist at 5-HT2c receptors – designed to target a different site to fenfluramine

2) Qsymia:
= Combination therapy – phentermine + topiramate (an anticonvulsant).

3) Contrave:
= Combination of bupropion (dopamine re-uptake inhibitor) + naltrexone (opioid antagonist).

104
Q

what is a new anti-obesity drug?

How does it work?

Side effects?

A

= Liraglutide (Saxenda)

how does it work?
Glucagon-like peptide 1 receptor agonist (GLP-1 - a satiety peptide)

Side effects;
Some concerns remain regarding thyroid and pancreatic cancer

105
Q

what is bariatric surgery?

what does its completely resolve?

and what does it do to calorie intake?

A

= gastric by-pass surgery producing substantial weight loss.

  • induces high levels of complete resolution of Type 2 diabetes
  • restricts calorie intake & induces mala-absoprtion of nutrients BUT
106
Q

what is adaptive thermogenesis?

A
  • Adults humans possess BAT (neck, clavicle, spinal cord)
  • BAT dissipates energy as heat
    = Inducible “browning” of WAT

Thermogenic adipocytes – increase energy expenditure uncoupling of oxidative metabolism from ATP production

  • Key function of uncoupling protein 1 (UCP1) – fatty acid
    activated protein – “short circuits” proton gradient in mitochondria – accelerates fuel oxidation – produce heat
107
Q

LECTURE 3 - physiology of digestion and absorption

= SMALL INTESTINE AND EXOCRINE PANCREAS

A

LECTURE 3 - physiology of digestion and absorption

= SMALL INTESTINE AND EXOCRINE PANCREAS

108
Q

what is the major sit for digestion and absorption?

describe the length and diameter of this structure.

A

small intestine

  • 6m long
  • 3.5cm diameter
109
Q

what are the 3 parts to the small intestine and describe their lengths?

A

1) duodenum - 30cm
2) jejunum - 3.5m
3) ileum - 2.5m

110
Q

what does the small intestine receive from;

(i) stomach
(ii) pancreas
(iii) gall bladder

A

(i) receives chyme from stomach
(via pyloric sphincter)

(ii) pancreatic juice from pancreas
(via sphincter of Oddi)

(iii) bile from gall bladder
(via sphincter of Oddi)

111
Q

what does the small intestine excrete and move?

A

Secretes = intestinal juice (success entericus)

Moves = remaining residues to lagre intestine via the ileocaecal valve

112
Q

wat does the leocaecl valve open in response to?

A

proximal pressure and in response to gastrin

113
Q

how is the surface area of small intestine increased (3)?

A

1) circular folds (of Kerckring)
= 3 folds

2) villi
= 30 folds

3) microvilli (bursh border)
= 600 folds

114
Q

what does the small intestine secrete, and where does it secrete from and into?

A

= secretes various peptide hormones

= FROM endocrine cells within mucosa

= IINTO the blood

115
Q

name 7 peptide hormones that the small intestine secretes?

A

1) gastrin
2) cholecystokinin (CKK)
3) secretin
4) moltin
5) glucagon like insulinotropic peptide (GIP) = aka gastric inhibitory peptide
6) glucagon-like peptide 1 (GLP-1)
7) Grelin

116
Q

where is gastrin and colecystokinin released from?

A

Gastrin
= from G cells of gastric antrum and duodenum

Cholecystokinin
= from I cells of duodenum and jejunum

117
Q

where is secretin and motilin released from?

A

Secretin
= from S cells of duodenum

Motlin
= from M cells of duodenum and jejunum

118
Q

where is glucagon-like insulinotropic peptide, glucagon-like peptide 1 and ghrelin released from?

A

Glucagon-like insulinotropic peptide
= an incretin from K cells of duodenum and jejunum

Glucagon-like peptide 1
= an incretin from L cells of gut

Ghrelin
= from Gr cells of gastric antrum, small intestine and elsewhere (e.g. pancreas)

NOTE - Incretins
= act on B cells of pancreas in feed forward manner stimulation release of insulin

119
Q

what do all the secretion of all intestine act on?

A

= on G-protein coupled receptors

120
Q

what is the juice of the small intestine called and how much of it is secreted per day?

A

= succus (juice) entericus (of intestine)
- approximately 2 litres secreted per day

= its composition varies throughout small intestine

121
Q

what are the control mechanisms involved in the secretions of small intestine?

A

1) distention/irritation
2) gastrin
3) CCK
4) secretin
5) parasympathetic nerve activity (enhances)
6) sympathetic nerve activity (decreases)

122
Q

what do the small intestine secretions contain and why?

A

1) mucus (from goblet cells)
= protection and lubrication

2) aqueous salts (from crypts of Leuberkuhn)
= for enzymatic digestion

123
Q

Yes or NO.

Does the small intestines secretions contain digestive enzymes?

A

NO

124
Q

what is the process of mixing and propulsion of chyme iii small intestine?

A

= segmentation

125
Q

how is the chyme moved back and forward?

A

= chopping moves chyme back and forward - vigorous after a meal by alternating contractions and relaxations of segments of circular muscle

126
Q

how are the alternating contractions & relaxation of segments of circular smooth muscle initiated by and what happens once they reach a threshold?

A

= small intestine pacemaker cells causing BER (continuously)
= at threshold, activates segmentation which in duodenum is primarily due to distension by entering chyme

127
Q

how is segmentation in the empty ileum triggered?

A

by gastrin from stomach (gastroileal reflex)

128
Q

out of the duodenum and ileum, which has more frequent segmentation?

A

Duodenum = frequent

Ileum = fewer

129
Q

how long does the movement of chyme take ad why is the time allowed?

A

= 3-5hours (Slow)

  • to allow for absorption
130
Q

how is strength of segmentation enhanced and decreased?

A

Enhanced
= parasympathetic

Decreased
= sympathetic

131
Q

what does peristalsis involve?

A

= few localised contractions

132
Q

what is the migraine motor complex (MMC) and when does it occur?

A

= strong peristaltic contractions passing length of intestine (stomach = ileocaecal valve)
= clearing small intestine of debris, mucus and sloughed epithelial cells between meals

Occurs;
= between meals every 90-120mins

133
Q

how is MMC inhibited, triggered and suppressed?

A

inhibited by

  • deeding
  • vagal activity

triggered by;
- motlin

suppressed by;

  • gastrin
  • CCK
134
Q

what are the 2 pancreatic secretions and what do they each secrete and where to??

A

1) endocrine
= insulin and glucagon
= to blood

2) exocrine
= digestive enzymes (acinar cells), aqueous NaHCO3- solution (duct cells)
= to duodenum as pancreatic juice

135
Q

how much secretion do the pancreatic duct cells secrete?

A

= 1-2litres of alkaline fluid into duodenum per day

136
Q

what is the function of the pancreatic duct cells and how does it do this function?

A

= neutralise acidic chyme entering the duodenum by;

(i) providing providing optimum pH for pancreatic enzyme function
(ii) protecting mucosa from erosion by acid

137
Q

Yes or No.

Can pancreatic enzymes completely digest food in absence of all other enzymes.

A

Yes.

138
Q

give 3 example of proteases and where are they formed?

A
  • trypsinogen
  • chymotrypsinogen
  • procarboxypeptidase A & B

= in acing cells

139
Q

give an example of an amylase and lipase and where are they formed?

A

Amylase
= pancreatic amylase

Lipases
= pancreatic lipase

= acinanr cells

140
Q

what are the 3 phases of control of pancreatic secretion and what happens in each?

A

1) cephalic
- mediated by vagal stimulation of mainly acing cells

2) gastric
- gastric distension evokes a vagovagal reflex resulting in parasympathetic stimulation of acinar and duct cells.

3) intestinal

141
Q

describe the process of neutralisation and digestion in intestinal phases of pancreatic secretion?

A

Neutralisation

  • increased secretion of aqueous NaHCO3 solution into duodenal lumen
  • pancreatic duct cells
  • increased secretion release from S cells
  • acid in duodenal lumen

Digestion

  • increased secretion of digesting enzymes into duodenal lumen
  • pancreatic acing cells
  • increased CCk release from I cells
  • fat and protein in duodenal lumen
142
Q

what are the 3 main constitutes of food and give examples of each?

A

1) carbohydrates (400g day)
- starch
- cellulose
- glycogen
- disaccharides

2) lipids (25-160g day)
- triacylglycerols
- phospholpids
- cholesterol & cholesterol esters
- free fatty acids
- lipid vitamins

3) proteins (70-100g dat ingested + 35-200g endogenous sources)

143
Q

what is digestion and absorption?

A

Digestion = enzymatic conversion of complex dietary substances to a form that can be absorbed

Absorption
= process by which the absorbable products of digestion are transferred across both apical and basolateal membranes of enterocytes (absorptive cells of intestinal epithelium)

144
Q

what do most digestive processes occur in small intestine as?

A

1) luminal digestion

2) membrane digestion

145
Q

how is luminal and membrane digestion mediated by?

A

Luminal
= pancreatic enzymes secreted into duodenum

Membrane
= enzymes situated at brush border of epithelial cells

146
Q

what is the process of digestion and absorption overall?

A

assimilaltion

147
Q

LECTURE 4 - physiology of digestion and absorption

= CARBOHYDRATES AND PROTEIN

A

LECTURE 4 - physiology of digestion and absorption

= CARBOHYDRATES AND PROTEIN

148
Q

what are 3 digestible carbohydrates?

A

1) polysaccharides
2) oligosaccharides
3) monosaccharides

149
Q

what are polysaccharides and provide examples of ?

A

= polymers of glucose

1) starch
- amylose (straight cain)
- amylopectin (branched chain)

2) Glycogen
- branched cain

150
Q

give examples of oligosaccharides and monosaccharides?

A

OLIGOSACCHHARIDES
1) sucrose
= glucose + fructose, alpha-1,2 linkages

2) lactose
= glucose + galactose, beta- 1,4 linkages

MONOSACCHARIDES

1) glucose
2) fructose

151
Q

what do all dietary carbohydrates need to be converted to for absorption?

A

= monosaccharides

152
Q

describe the sequence of absorption?

A

1) e.g. starch

2) oligosaccharide
(NOT ABSORBED)
e.g. lactose/sucrose from diet
alpha limit dextrin maltotriose, maltose

3) monosaccharides
- glucose, fructose, galactose

4) absorption

153
Q

how is the sequence of carbohydrate digestion accomplished?

A

by alpha-amylase (pancreatic & salivary)

154
Q

how is starch broken into oligosayccaides?

A

= intra-luminal hydrolysis by alpha-amylase

155
Q

how are oligosaccharides broken into monosaccharides?

A

= membrane digestion (fat brush border) by oligosaccharidases

156
Q

give 3 examples of oligisaccharidases used to membrane digest oligosaccharides to monosaccharides.

A

1) lactase
2) maltase
3) sucrase-isomaltase (2 enzymes bound together)

157
Q

what type of enzyme is alpha-amylase?

A

= endoenzyme

158
Q

what does alpha-amylase do?

A

= breaks down internal alpha, 1-4 linkages but not terminal alpha-1,4 linkages/
- hence no production of glucose

159
Q

Yes or NO.
can alpha-amylase cleave alpha-1,6 linkage at branch points (in amylopectin) or alpha-1,4 linkages adjacent to branch points?

A

NO.

160
Q

what are the 2 products of alpha amylase?

A

1) linear glucose oligomers (maltotriose, maltose)

2) alpha-limit dextrins

161
Q

what are oligosaccharidases?

A

= integral membrane proteins with a catalytic domain that faces the lumen of GI tract

162
Q

what is lactase only one substrate and what does it break it into?

A

breaks down lactose to glucose and galactose

163
Q

what do all other oligosaccharidases cleave?

A

= the terminal alpha-1,4 linkages of maltose, maltotriose and alpha limit dextrin (yielding glucose)

164
Q

what else can maltase degrade?

A

= the alpha-1,4 linkages in straight chain oligomers up to nine monomers in length

165
Q

what is sucrase specifically responsive for as an oligosaccharidase?

A

= hydrolysing sucrose to glucose and fuctose

166
Q

why is isomlatase unique as an oligosaccharidase?

A

= as its the only enzyme that can split the branching alpha 1,6 lungs of alpha-limit dextrin

167
Q

describe the rate of hydrolysis actions of maltase, sucrose and isomaltase compared to transport of released monomers?
and the rate of lactase hydrolysis?

A

Maltase, sucrose and isomaltase
= occurs at faster rate than subsequent transport of released monger

Lactase
= rate of hydrolysis is rate limiting in assimilation

168
Q

when might lactose intolerance arise?

A

= caused by impaired carbohydrate digestion

- due to inability to adequacy digest lactose; caused by lactase insufficiency

169
Q

what are 3 reasons why lactose intolerance could occur?

A

1) Primary lactase deficiency (primary hypolactasia)
= due to lack of the lactase persistence (LP) allele –

2) Secondary lactase deficiency
= caused by damage to/ infection of/ the proximal small intestine

3) Congenital lactase deficiency
= rare autosomal recessive disease – no ability to digest lactose from birth

170
Q

what is a non-disturbance consequence of lactase insufficiency?

when would this only cause disturbance?

A

= hypolactasia

  • unless you consume lactose-containing food & activity of remaining enzymes is overwhelmed
171
Q

if lactose is delivered to the colon from the ileum colonic, what would the microflora produce?

what would the by-products cause?

A

1) short chain fatty acids (which can be absorbed)

2) H+
(can be detected in breath of lactase deficient individuals)

3) CO2
4) methane

  • bloating
  • abdominal pain
  • flatulence
172
Q

what does undigested lactose cause?

A
  • acidification of colon
  • increased osmotic load
    = loos stools & diarrhoea
173
Q

where does the absorption of final products of carbohydrate digestion (glucose, galactose and fructose) occur?

A

= duodenum and jejunum

174
Q

describe the process of the absorption of the final products of carbohydrate digestion?

A

= 2 step process

- involving entry and exit from enterocytes via apical and basolateral membranes

175
Q

what are glucose & galactose absorbed by and what is fructose absorbed by?

A

glucose and galactose
= secondary active transport mediated by SGLT1

fructose
= by facilitated diffusion mediated by GLUT5

176
Q

how is exit of all monosaccharides mediated by?

A

= facilitated diffusion by GLUT2

177
Q

what are the 5 steps involved in the mode of operation of SGLT1 involved in glucose and galactose absorption?

A

1) 2 Na+ binds
2) Affinity for glucose increases, glucose binds
3) Na+ and glucose translocate from extracellular to intracellular
4) 2 Na+ dissociate, affinity for glucose falls
5) Glucose dissociates:

178
Q

what does protein need to be digested into?

A

be digested to oligopeptides and amino acids for efficient absorption

179
Q

how many pathways exist for protein digestion?

what is the basic step of protein digestion in all 4 pathways?

A

4 pathways

Protein 
Peptides 
Amino acids 
Amino acid in enterocytes
Amino Acid in blood.
180
Q

describe the most basic way protein can be converted into amino acids.

A

Protein to Peptides to Amino acids via conversion of luminal enzymes.

Amino acids - amino acid in enterocytes via conversion of apical membrane transporters

Amino acids in enterocytes to amino acid in blood via basolateral membrane

181
Q

describe the next level up from that step.

A

Protein to Peptides via conversion of luminal enzymes.

Peptides to Amino acids via conversion of brush border enzymes.

Amino acid to amino acids in enterocytes via apical membrane transporters

Amino acids in enterocytes to amino acid in blood via basolateral membrane

182
Q

describe an altogether different stepwise progression, 3rd step.

A

Protein to Peptides via conversion of luminal enzymes.

Peptides to peptides in enterocytes via conversion of apical membrane transporters .

peptide in enterocytes to amino acids in enterocytes via intracellular hydrolysis.

Amino acids in enterocytes to amino acid in blood via basolateral membrane

183
Q

what does the 4th variant involve?

A

= when the peptide is transported out of enterocyte without intervening intracellular hydrolysis by proteases.

184
Q

how much energy does protein assimilation account for?

A

10-15% of daily energy intake

185
Q

in digestion in stomach, what begins to denature protein?

A

HCL

186
Q

what cleaves proteins into peptides and describe it?

A

pepsin

  • has pH optimum of 1.8 to 3.5, inactivated at alkaline pH
  • an endopeptidase with preference for bonds between aromatic and larger neutral amino acids
  • NOT essential for protein digestion
187
Q

in digestion in duodenum, what are the 5 pancreatic proteases secreted as and where form and what are they converted into?

A

proenzymes from exocrine pancreas and converted to active form in the duodenum.

188
Q

what do the 5 pancreatic proteases function as either?

A

1) endopeptidases

2) exopeptiases

189
Q

what are 5 types of pancreatic proteases?

A

1) trypsin = endo
2) chymotrypsin = endo
3) elastase = endo
4) procarboxypeptidase A = exo
5) procarboxypeptidase B = exogenous

190
Q

how much protein does the pancreatic proteases convert to oligopeptides and free amino acids?

A

70% protein to oligopeptides

30% protein to free amino acids

191
Q

where are additional processes present?

A

1) at brush border

2) within cytoplasm of enterocyte

192
Q

describe brush border peptidases, in terms of number of them, affinity for oligopeptides, and whether or not they are endopeptidases or exopepttidases.

A
  • numerous
    = as enzymes attack a limited number of peptide bonds and oligopeptides to be digested are extremely varied in structure
  • have affinity for larger oligopeptides
  • either endopeptidases or exopeptidase
    = exopeptidase comprising both amino peptidases & carboxypeptidases
193
Q

describe cytoplasmic peptidases in terms of their numbers and their role.

A
  • less numerous than brush border peptidases

- primarily hydrolyse dipeptides or tripeptides

194
Q

describe 2 mechanisms used for protein absorption at the brush border.

A

1) 5 are Na+-dependent co-transporters mediating ‘uphill’ movement (secondary active transport)
= e.g. system B0AT1 (SLCA19) – mediates uptake of neutral amino acids (dysfunction results in Hartnup disease)

2) 2 are Na+ independent
= e.g. system b0+AT (SLC7A9/SCL3A1 dimer) – mediates uptake of cationic amino acids (dysfunction results in cystinuria)

195
Q

how many mechanisms are there for protein absorption in the basolateral membrane and describe what they do?

A

= at least 5 different mechanisms

  • 3 mediate efflux of amino acids and are Na+ independent
  • 2 mediate influx of amino acids and are Na+ dependent ( net movement bidirectional)
196
Q

how are di, tri and tetra peptides absorbed?

A

= via H+ dependent mechanisms (PepT1, SLC15A) at brush border (co-transport)

  • further hydrolysed to amino acids within the enterocyte
  • Na+-independent systems at the basolateral membrane (facilitated transport)
197
Q

LECTURE 5 - physiology of digestion and absorption

= Ca, Fe and vitamin absorption

A

LECTURE 5 - physiology of digestion and absorption

= Ca, Fe and vitamin absorption

198
Q

how much energy do ingested lipids provide?

A

55-60% of daily energy

199
Q

what do ingested lipids comprise?

A

1) fats/olis
- triaglycerols (TAGs)
= long chain fatty acyl esters of glycerol

2) phospholipids
= mostly glycerophospholipids e.g. phosphatidylcholine

3) cholesterol and cholesterol esters
4) fatty acids

200
Q

describe ingested lipids solubility status?

A
  • either insoluble (e.g. cholesterol esters, TAGS) or poorly soluble water thus causing a problem for digestion and absorption
201
Q

what must ingested lipids be converted from and into?

A

from solid fat and oil mass into an EMULSION of small oil droplets suspended in water

202
Q

how can emulsification occur?

A

1) mouth = chewing

2) stomach = gastric churning & squirting through narrow pylorus
- contents mixed with digestive enzymes from mouth and stomach

3) small intestine
= segmentation & peristalsis - mix luminal content with pancreatic and biliary secretion

203
Q

what do droplets produced by mechanical disruption provide?

A

an increase in surface area to volume ratio that increases the area of oil-water interface at which digestion buy lipase & other esterase’s can accomplish digestion

204
Q

how are the droplets stabilised?

A

by addition of a ‘coat’ of amphiphilic molecules that form a surface layer on droplets that include;
(i) certain products of lipid digestion itself (e.g. fatty acids, monoacylglycerols)
(ii) biliary phospholipids
cholesterol
(iii) bile salts (when the droplets have progressively been reduced to unilamellar and mixed micelles)

205
Q

what does digestion involve in terms of objects in human body and their phase name?

A

1) mouth
= lingual phase

2) stomach
= gastic phase
- by gastric lipase

206
Q

when is gastric lipase secreted?

A

= secreted in response to gastrin from chief cells

207
Q

describe the pH optimum of gastric lipase and when it is active and inactive.

A
  • pH optimum of 4 and is resistant to pepsin
  • inactive in duodenum due to digestion by pancreatic proteases and unfavourable pH
  • preferentially hydrolysis TAGs at position 3
208
Q

where are short and medium chain fatty acids absorbed?

A

= by stomach

- but long chain fatty acids are not.

209
Q

what does digestion by pancreatic lipase produce?

A

2-monacylglycerol and free fatty acids

210
Q

what is the phase called that occurs in the duodenum and what enzyme is involved?

A

intestinal phase

  • involving pancreatic (TAG) lipase
211
Q

where is pancreatic lipase secreted from and in response to what?

A
  • secrete for acinar cells

- in response to CCK which also stimulates bile flow

212
Q

what does full activity of pancreatic lipase require?

A
  • collapse co-factor
  • alkaline pH
  • Ca2+
  • bile salts
  • fatty acids
213
Q

what does pancreatic lipase mainly hydrolyse?

A

TAGs at 1 and 3 position

214
Q

what are 2 additional lipase?

A

1) carboxyl esters hydrolase

2) phospholipase A2

215
Q

where are bile salts released into and from where?

A

released INTO = the duodenum in the bile

released FROM = the gall bladder in response to CCK

216
Q

what do bile salts act as?

A

= detergents to help emulsify large lipid droplets to small droplets

217
Q

are bile salts amphipathic, Yes or No?

A

YES>

218
Q

what does failure to secrete bile salts result in?

A

1) lipid malabsorption = steatorrhea (fat in faeces)

2) secondary vitamin deficiency duet to failure to absorb fat soluble vitamins (A, D, E and K)

219
Q

what do bile salts do the surface area and why?

A

increase surface area for;

  • attack by pancreatic lipase
  • but block access of enzyme to TAGs
220
Q

how is the problem of bile slats solved?

A

= colipase

221
Q

what is colipase?

what do they do?

A

= an amphipathic polypeptide secreted with lipase by the pancreas

  • they bind to bile salts & lipase allowing access by the latter to tri and di-acylglycerols
222
Q

what is colipase secreted as?

A

= inactive procolipase which is acivated by trypsin

223
Q

where are the final products of lipid digestion stored in and released from?

A

mixed micelles

224
Q

what are emulsion droplets replaced by when they are hydrolysed?

A

replaced by TAGs, within the core, decreasing droplet size until a mixed micelle results

225
Q

where do free fatty acids and monoacylglycerls transfer between?

A
  • between mixed micelles and apical membrane of enterocytes entering by the cell by passive diffusion and or membrane fatty acid translocates, fatty acid being protein ad fatty acid transport proteins
226
Q

where do short and long chain fatty acids diffuse through and exit through?

A

SHORT & MEDIUM chain

  • diffuse through enterocyte
  • exit through basolateral membrane and enter the villus capillaries

LONG chain
= res-synthesised to triglycerides in endoplasmic reticulum and are then incorporated into chylomicrons

227
Q

how does cholesterol absorption occur?

A

due to transport by endocytosis in clatherin coated pits by Riemann-Pick C10like 1 (NPC1l1) protein

228
Q

what binds to NPC1L1, preventing internalisation and thus cholesterol absorption?It is also used in conjunction with statins in hypercholesterolaemia

A

ezetimibe

229
Q

how is Ca2+ absorbed?

A

by passive (paracellular, whole length of small intestine) and active transports (transcellular, mainly duodenum and upper jejunum) transport

230
Q

when [Ca2+] in is chyme, how much of absorption is mainly active?

A

< 5mM

231
Q

how is active Ca2+ absorption regulated by?

A

= by 1,25-dihydroxyvitamin D3 (calcitriol) and parathyroid hormone (increases 1,25-dihydroxyvitaminD3 synthesis)

232
Q

what is iron an important constituent of?

A
  • haemoglobin
  • myoglobin
  • many haem containing enzymes
233
Q

what does iron deficiency and excess lead to?

A 
deficiency = anaemia 
excess = toxic
234
Q

how much is ingested daily, and what percent of that is absorbed by duodenum?

A

12-15mg

- 3-10% of that by duodenum

235
Q

what type of Fe is absorbable?

A
  • ferrous (Fe2+) but not ferric (Fe3+)
236
Q

how is Fe3+ reduced to Fe2+ by?

A
  • HCL
  • Vit C
  • brush border cytochorome b ferric reductase
237
Q

what is an example vitamin B12?

A

cobalamin

238
Q

describe the presence of Vit B12 in diet?

A

mine amounts, 5-15micrrograms

- daily requirement 6micrograms a day

239
Q

Why are vegans susceptible to deficiency?

A

as B12 is not present in vegetables

240
Q

describe what happens after Vit B12 has been ingested in food bound to proteins?

A

1) stomach acid releases B12 from protein
2) haptocorin, secreted in saliva, binds vit B12 released in stomach
3) stomach parietal cells release intrinsic factor
4) pancreatic proteases digest hepatocorin in small intestine, Vit B12 released
5) Vit B12 binds to intrinsic factors in small intestine
6) vit B12 intrinsic factor complex is absorbed in terminal ileum by endocytosis

241
Q

what are examples of fat soluble vitamins?

A
  • A, D, E and K
242
Q

what does absorption of fat soluble vitamins require?

A

adequate bile secretion and intact intestinal mucosa

243
Q

what happens once fat soluble vitamins are absorbed?

A

= incorporated into mixed micelles, passively transported into enterocytes.
= incorporated into chylomicrons, or VLDLs
= distributed by intestinal lymphatics

244
Q

what are examples of water soluble vitamins?

A
  • B complex vitamin, NOT B12

- C, H vitamins

245
Q

what are transport process in apical membrane after absorption of vitamins similar to?

A

= those described for monosaccharides, amino acids and di and tri peptides.
- either Na+ dependant o independent

246
Q

how is vit B12, vit C and Vit H transporte?

A

1) Vitamin B9 (folic acid)
= Na+-independent proton-coupled folate transporter 1; FOLT – aka SLC19A1) – driven by pH gradient?

2) Vitamin C (ascorbate)
= the Na+-dependent vitamin C transporters (SVCT1 and 2, aka SLC23A1 and SLC23A2) – couples inward movement of 2 Na+ to 1 ascorbate

3) Vitamin H (biotin)
= Na+-dependent multivitamin transporter (SMVT, aka SLC5A6) – couples inward movement of 2 Na+ to one biotin

GI (43 decks)

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