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digestion, motility and absorption Flashcards

1
Q

What is the oral cavity made up of?

A
  • lips and cheeks → skeletal muscle embedded in elastic fibro CT
  • lined with stratified squamous epithelium (protection)
  • tongue body + root → skeletal muscle, both intrinsic (change shape) and extrinsic (allow movement)
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2
Q

Where does the oesophagus pierce the diaphragm and how is it innervated?

A
  • oesophageal hiatuse (T10)

- via vagus nerve

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3
Q

Describe the mucosa, submucosa and the types of muscle present in the oesophagus

A
  • mucosa: non-keratinised stratified squamous epithelium
  • submucosa: mucus secreting glands
  • skeletal muscle = upper 1/3 transitional muscle = middle
  • smooth muscle = lower 1/3
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4
Q

Describe the upper and lower oesophageal sphincter.

A
  • upper: hypopharyngeal sphincter
  • skeletal muscle fibres
  • lower: gastro-oesophageal sphincter
  • high pressure
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5
Q

In gustation, what are the 5 primary tastes and which taste buds can detect them?

A
  • sour (acid), salt (Na+), bitter (most sensitive), sweet (organic substance), umami (meat)
  • all taste buds can detect all tastes, although each most sensitive to 1 type
  • tip = sweet, sides of tip = salty, back = bitter, sides = sour
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6
Q

What are the papillae of tastebuds and where are the different types found?

A
  • papillae are where most taste buds are found on the epithelium of tongue
  • filiform papillae not involved with taste
  • fungiform papillae scattered on dorsal surface of tongue
  • foliate papillae on tip and sides of tongue
  • circumvallate at intersection of anterior/posterior tongue

(also receptor membranes bathed in saliva and dendrites of sensory nerves around gustatory cells)

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7
Q

Describe the process of taste.

A
  • substance dissolves in saliva
  • enters taste pore and attaches to chemoreceptor membrane
  • induces change in membrane permeability
  • depolarisation of taste cell (generator potential)
  • NT released to stimulate sensory neurone → neural pathway to brain (7th, 9th, 10th cranial)
  • impulses to tractus solitarius of medulla oblongata → thalamus → taste area of parietal cortex,
    hypothalamus, limbic system
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8
Q

What is aguestia?

A
  • loss of taste

- may result from medications or neuronal damage maybe drug-induced or metabolic or specific genetic deficiencies

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9
Q

Describe the secretions of saliva from the three major pairs of salivary glands.

A
  1. parotid (serous) = water and α-amylase
  2. submandibular (serous and mucous) = weak α-amylase and lysozyme
  3. sublingual (mucous) = thick, viscous secretion

(+ other glands scattered throughout mucosa)

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10
Q

What is the the composition of saliva?

A
  • > 99% water, <1% solids
  • ions (Na, K, Mg, HCO3-, supersaturated with Ca phosphates)
  • 50+ proteins including α-amylase, mucins
  • pH 6.2-8.0
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11
Q

What are the functions of saliva and what can lack of saliva cause?

A
  • lubrication for movement
  • taste sensation
  • digestion at optimum pH
  • protection
  • thirst (water intake)
  • speech, dentures
  • absorption of dissolved drugs
  • chemical balance (tooth enamel)
  • can make swallowing difficult, cause halotis (bad breath) problems, dental caries, gum disease, mucousal ulceration
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12
Q

Name some disorders of salivary gland and their causes.

A
  • mumps: infection of parotid gland by myxovirus - sterility in males
  • xerostomia: dry mouth
  • causes: autoimmune, diabetes, age-related atrophy, medication side-effect, Sjogrens syndrome (autoimmune disease)
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13
Q

What is mastication and how does it work?

A

(chewing)
• tooth shape adapted for different functions:
- incisors chisel-shaped for cutting
- canines for tearing
- molars for grinding
• movement controlled by touch, pressure and stretch receptors
- up-and-down movement of mandibles (biting by incisors)
- side-to-side movement of mandibles (crushing and breaking by molars)
- each assist mixing food with saliva, to lubricate + allow taste

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14
Q

How is chewing controlled?

A
  • jaw movements voluntary, involve cerebral cortex and skeletal muscles
  • strength of bite controlled by sensory receptors in teeth, send signals to brain stem area to stop/reduce
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15
Q

What is deglutition (swallowing) and what are its 3 phases?

A
  • swallowing, initiated voluntarily, but becomes involuntary
    1. voluntary phase - tongue separates food into bolus + moves backwards/upwards
      1. pharyngeal phase - food into pharynx, pressure receptors in palate activated, impulses from trigem + glossophar nerves to swallowing centre in medulla → elevation of soft palate
  • impulses from swallowing centre inhibit respiration, raise larynx + close glottis
  • bolus tilts epiglottis over closed glottis and upper oesophageal sphincter opens to allow bolus then closes
  • glottis opens, breathing resumes
    3. oesophageal phase - peristalsis of food co-ordinated by vagus nerve influenced by swallowing centre
  • lower oesophageal sphincter relaxes to allow food to enter stomach + closes preventing acid reflux into oesophagus
  • increased gastrin increases tone of sphincter (when stomach filled)
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16
Q

Describe types of dysphagia (disorders of deglutination) and provide examples.

A

• dysphagia:
- damage to cranial nerves or to swallowing centre in medulla i.e. stroke
- degenerative diseases of skeletal muscle/transmission process
- defects in autonomic nerves/intrinsic nerves of oesophagus
• i.e.
- inactive swallowing reflex
- hiatus hernia
- diffuse oesophageal spasm → thickening of SM
- gastro-oesophageal reflux disease (GORD) → gastric contents into oesophagus (heartburn)

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17
Q

Describe control of salivary secretion and how it depends on the nervous system.

A
  • tastebuds + mechanoreceptors activated by food
  • sensory info sent to salivary nucleus in medulla
  • unconditional reflex activated by sensory input to brain
  • impulses via autonomic nerves (parasympathetic, cranial nerves 7 and 9) to salivary glands
  • increased secretion of fluids/enzymes/mucins and dilated vessels
  • composition depends on flow rate (low FR = low pH)
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18
Q

Name some gastric secretions and the cells which secrete them.

A
  • mucus: gel formed from glycoprotein w/ water - from surface epithelial + mucous neck cells
  • bicarbonate: protective against acid, trapped in mucus layer - surface epithelial cells
  • hydrochloric acid - parietal cells
  • intrinsic factor: protection of vit B12 - parietal cells
  • pepsinogens: protein digestion - chief cells
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19
Q

What are pepsins? Write out its structure.

A
  • endopeptidase enzymes which hydrolyse specific peptide bonds w/in protein chain
  • NH-CH₂-C(=O)- | -NH-CH₂-⬣(H)-C(=O) -NH-CH(R)- etc…
  • (| = cleavage point, exopeptidases hydrolyse terminal peptide bonds and generate free AAs)
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20
Q

State the five functions of gastric acid secretion.

A
  1. activates pepsinogens
  2. maintains pepsin activity
  3. bactericidal
  4. disrupts CT proteins
  5. dissolves particulate matter (from air) in food
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21
Q

On which on 3 factors does stimulation of gastrin secretion depend on?

A
  1. M1, acetylcholine: NT released from vagus nerve and local intrinsic nerves
  2. gastrin: hormone released from G-cells of antral mucousa by Ach, stretch, dietary proteins; circulates
    in bloodstream to parietal and other secretory cells
  3. H₂, Histamine: local hormone released from cells close to parietal cells by gastrin + Ach; acts alongside to give strong secretory response (= synergistic)
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22
Q

Describe the 3 phases of gastric secretion including their triggers and control.

A
  1. cephalic phase (“head”)
    • triggered by thought, smell, sight, taste of food
    • controlled by nervous mechanisms (CNS impulses via vagus nerve), causing:
    - release of acid and pepsin
    - small release of gastrin from antral G-cells
  2. gastric phase (“stomach”)
    • triggered by:
    - distension (enlargement) of stomach by food
    - action of food components i.e. peptides, caffeine, alcohol, calcium
    • controlled by hormonal mechanisms:
    - gastrin release from G-cells of antrum, then circulating to glands in fundus/body
    - increases acid and pepsin secretion
  3. intestinal phase (“intestine”)
    • triggered by:
    - emptying of stomach contents into duodenum
    - low pH in gastric antrum
    • controlled by nerves + hormones:
    - release of hormones from duodenal mucousa which inhibit gastric secretion (secretin, CCK, gastric inhibitory peptide)
    - local and long CNS nervous reflexes which inhibit gastric secretion
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23
Q

What is peptic ulcer disease (PUD), its causes and treatment?

A
  • protective mechanisms in epithelium of stomach + upper small intestine fail
  • epithelial/sub-epithelial cells become inflamed + damaged by acid/pepsins
  • causes:
    • excess acid/pepsin/histamine
    • steroidal/nonsteroidal anti-inflammatory drugs
    • Helicobacter pylori infection
  • treatment:
    • antibiotics
    • change medication
    • block acid secretion using H⁺ pump inhibitors
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24
Q

What is Zollinger-Ellison syndrome and what effects does it have?

A
  • raised gastrin levels in secretory gastrinomas
  • effects: excess basal acid, stimulated acid + pepsin production, hypertrophy of gastric mucousa, ulceration, abnormal motility
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25
Q

Describe the motility patterns by which material is propelled and mixed whilst in GI tract.

A

SM cells in muscularis layer contract in 2 ways:
1. phasically; rapid contraction + relaxations i.e. peristalsis, segmentation of esophagus/small intestine/lower stomach
2. tonically; sustained contractions lasting mins/hours i.e. sphincters, upper stomach (fundus)
• different types of contraction allow different functions in different regions

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26
Q

What are contractions and how can they be modulated?

A
  • property of muscle cells
  • action of nerves, hormones, local factors by causing amplitude (phasic) or tone (tonic) of contractions to increase/decrease
  • SM cells arranged in sheets/bundles (effector units) to synchronously contract
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27
Q

Which properties allow GI SM cells to carry out their actions?

A
  • by gap junctions
  • in all directions
  • low electrical resistance between SM cells (gap junctions) → electrical activity spreads readily from cell to cell
  • level of polarisation varies regularly (basic electrical rhythm) set by specialised non-contractile pacemaker cells (cells of Cajal)
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28
Q

How do SM cells compare from their resting to stimulated to inhibited situation?

A 
• resting: 
- RMP in SM oscillates from -70mV 
- slight, ongoing contractions
• stimulated: 
- depolarised
- influenced by stretch, gastrin and Ach
- large contractions, ongoing under influence of stimulus
• inhibited: 
- hyperpolarised
- influenced by adrenaline, noradrenaline, CCK, secretin, GIP 
- very little muscular activity
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29
Q

Name and describe the 3 different types modulation of GI muscle.

A
  1. parasympathetic →increases gut muscle activity + relaxes sphincters
  2. sympathetic → inhibit gut movements + constricts sphincters
  3. hormones → either increase (motilin) or decrease activity (CCK + secretin)
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30
Q

Describe the modulation of membrane potential to get from slow waves and spikes to:

a) depolarisation
b) hyperpolarisation

A

a)
- stimulation by:
1. stretch
2. parasympathetics (Ach)
b) hyperpolarisation
1. sympathetics (noradrenaline)

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31
Q

What is peristalsis and which nerves control it?

A
  • when adjacent segments of intestine contract and relax to propel food (a bulbous) along
  • preceded by receptive relaxation, so low resistance area to move into
  • co-ordinated by intrinsic nerves (direction maintained)
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32
Q

What is segmentation and which nerves control it?

A
  • when non-adjacent segments of intestine phasically contract and relax moving food forward + backward so it mixes
  • coordinated by intrinsic nerves
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33
Q

Describe each stage of gastric motility:

a) empty stomach
b) filling
c) storage
d) mixing food with secretions
e) slow emptying of liquid chyme into duodenum at a controlled rate

A

a) contracts when blood glucose low due to activation of vagus nerve
b) expands from 50ml/L without pressure rising
c) not much activity in first 1⁄2 hour after feeding → gentle ripples of peristalsis
d) peristaltic contractions build up intensity during gastric phase after feeding → churning
e) small spurt with each peristaltic wave, most return to antrum

34
Q

Describe peristaltic waves in the stomach.

A
  • move toward pylorus
  • most vigorous peristalsis + mixing action occurs close to pylorus
  • pyloric end of stomach pumps chyme into duodenum, also forcing material back into
    stomach for further mixing
35
Q

Describe stimulation:

a) during gastric phase which leads to increased motility and emptying of stomach
b) during intestinal phase which leads to decreased motility and emptying of stomach

A

a) stretch of wall + presence of specific food components (proteins) → release of gastrin + activation of CNS and local reflexes
b) emptying of stomach contents into duodenum (fats, acid, stretch) → release of hormones to inhibit gastric motility (CCK, gastric inhibitory peptide) + activation of inhibitory nerve reflexes

36
Q

Describe the motility of the small intestine.

A
  • even w/o chyme, contractions move contents into colon and keep it clean
  • underlying migrating myoelectric complex used (slow wave which starts in duodenum as previous reaches terminal ileum)
  • as chyme enters SI, increase in segmentation contractions so thorough mixing of bile + pancreatic secretions
  • infrequent peristalsis and coordinated by extrinsic (gastro-ileal reflex) + intrinsic nerves/hormones
  • ileocecal sphincter controls rate of entry into large intestine → opened by peristaltic wave + gastrin
37
Q

What are the functions of the large intestine?

A
  • storage + release of faecal material
  • further absorption of fluid and electrolytes
  • absorption of nutrients (villi)
38
Q

Describe the motility of the large intestine.

A
  • mainly segmentation
  • strong peristalsis → movement of material into descending colon, sigmoid colon + rectum
  • defaecation as reflex response to sudden distention of rectum
  • associated with gastro colic reflex
39
Q

State the 3 stages of the defecation reflex.

A
  1. distension/stretch, of rectal walls caused by movement of faeces into rectum triggers depolarization of sensory fibers
  2. parasympathetic motor fibers stimulate contraction of rectal walls + relaxation of internal anal sphincter
  3. if convenient, voluntary signals stimulate relaxation of external anal sphincter; defecation may be temporarily delayed by conscious (cortical) controls, so voluntary constriction of external sphincter
40
Q

What is diarrhoea and why does it occur?

A
  • passage of watery faeces → results from increased colonic fluid volume
  • fluid accumulates in intestinal lumen due to:
    • defective ion transport (inhibited by bile salts, fat malabsorption + formation of inflammatory mediators)
    • osmosis
    • hypermotility of intestine (reduces ability to absorb H₂O)
    • active secretion (laxatives + bacterial toxins)
41
Q

What is constipation and which motility disorders can cause it?

A
  • difficulty in defaecation + delayed transit due to excessive dehydration of faeces
    Motility Disorders
  • damage to extrinsic nerves/intrinsic nerve plexuses
  • IBS
    → discomfort, pain, cramps, diarrhoea + constipation
    → hypermotility
42
Q

How can different drugs affect motility?

A
  • drugs which enhance motility of stomach and small intestine (dopamine antagonists)
  • drugs which enhance motility of intestines (stimulant laxatives)
  • drugs which reduce motility (morphine + other opiates)
43
Q

Digestion ‘costs’ energy but why is still done?

A
  • nutrients polymeric

- minimises likelihood of absorption of toxic molecules

44
Q

State the pancreatic secretions made in the body.

A
  • endocrine (insulin + glucagon) and exocrine (acinar/epithelial → pancreatic juice)
  • alkaline fluid with enzymes needed for digestion of nutrients
  • mechanism of secretion similar to salivary secretion
45
Q

Describe control of secretin secretion from the pancreas.

A
  1. strongly acidic material enters duodenum as stomach empties
  2. this causes release of secretin from duodenal mucosa into bloodstream
  3. secretin causes pancreas to secrete bicarb-rich (alkaline) fluid into duodenum from pancreas
  4. acid neutralised by bicarbonate-rich secretion
    • secretin = 27 AA peptide
46
Q

Describe control of cholecystokinin (CCK) secretion from the pancreas.

A
  1. peptides + fats enter duodenum as stomach empties
  2. causes release of CCK from duodenal mucosa from bloodstream
  3. causes pancreas to secrete enzyme-rich fluid into duodenum
  4. peptides + fats digested
    - CCK also contracts gall bladder and relaxes sphincter of Oddi
    • CCK: 33 AA peptide
47
Q

The entry of peptides and fats cause release of CCK from duodenal mucosa, stimulating secretion of a fluid from pancreas. Describe its composition.

A
  • lipase
  • amylase
  • nucleases
  • proteolytic enzymes (inactive precursors)
  • endopeptidases i.e. trypsin(ogen), chymotrypsin(ogen)
  • exopeptidases i.e. pro(aminopeptidase), pro(carboxypeptidase)
48
Q

Where are proteolytic enzymes from the pancreas activated and what does this process involve?

A
  • in small intestine

- enterokinase: an enzyme from mucosa (intestinal brush border)

49
Q

Name some zymogens (inactive) and activated enzymes found in the small intestine.

A 
• zymogens:
- chymotrypsinogen  
- procarboxypeptidase
- procolipase
- prophospholipase
• activated enzymes:
- chymotrypsin
- carboxypeptidase
- colipase
- phospholipase

(normally ogen → active enzyme)

50
Q

Describe the therapeutic use of pancreatic enzymes and pancreatic enzyme inhibitors.

A

pancreatic enzymes:
• pancreatin (i.e. creon)
- orally-administered enzymes to compensate for deficiency in pancreatic secretions which may be given in enteric coating (CF, pancreatectomy, chronic pancreatitis)

pancreatic enzyme inhibitors:
• acarbose (i.e. glucobay) - α-glucosidase inhibitor which delays digestion + absorption of starches/sucrose (diabetes)
• orlistat (i.e. xenical) - lipase inhibitor which reduces digestion + absorption of fats (obesity)

51
Q

Describe bile and its composition.

A
  • formed by liver, stored and concentrated in gall bladder, released into small intestine by action of CCK to contract gall bladder
    • Functions:
  • excretory route for non-water soluble substances, especially pigment from Hb breakdown (bilirubin)
  • role in emulsification of fats before digestion
52
Q

What are bile salts and what are they made of?

A
  • cholesterol derivatives (non-polar)
  • cholic, deoxycholic + chenodeoxycholic acids conjugated to glycine/taurine (polar AAs)
  • amphipathic
53
Q

What is the function of the small intestine and its 3 sections?

A
  • digestion + absorption of nutrients
    1. duodenum - mixes stomach + exocrine secretions of pancreas and liver
    2. jejunum - chemical digestion + nutrient absorption
    3. ileum - ends at ileocecal valve which controls movement of intestinal contents into caecum
54
Q

For each small intestine cell state its location in the mucosa and function:

a) absorptive cells
b) goblet cells
c) paneth cells
d) G-cells
e) I-cells
f) K-cells
g) M-cells
f) S-cells

A

a) - epithelium/intestinal glands
- digestion + absorption of nutrients in chyme
b) - epithelium/intestinal glands
- secretion of mucus
c) - intestinal glands
- secretion of bacterial enzyme lysozyme; phagocytosis
d) - intestinal glands of duodenum
- secretion of hormone intestinal gastrin
e) - intestinal glands of duodenum
- secretion of hormone CCK, which stimulates release of pancreatic juices + bile
f) - intestinal glands
- secretion of hormone glucose-dependent insulinotropic peptide, which stimulates release of insulin
g) - intestinal glands of duodenum and jejunum
- secretion of motilin, which accelerates gastric emptying, stimulates intestinal peristalsis and production of pepsin
f) - intestinal glands
- secretin of hormone secretin

55
Q

Why is the small intestine well-adapted to its function?

A
  • large SA - due to length/folds/villi/microvilli/structured brush border
  • good blood supply/drainage
  • good lymphatic drainage
  • SM (villi contraction)
  • rapid division + turnover of cells
  • crypt cells secretory
  • specialised side and tip cells (produce enzymes + carriers)
  • highly-structured absorptive surface

(plicae circulares - permanent transverse folds of mucosa and submucosa)

56
Q

Describe the secretions of the small intestine.

A
  • alkaline fluid containing electrolytes, water, enzymes + mucus
  • fluid secretory cells are immature columnar epithelial cells in crypts of Lieberkuhn
  • fluid stimulated by substances which increase intracellular cAMP → hormones, cholera
  • protective enzymes such as lysozyme (paneth cells)
  • mucus
57
Q

What are the causes and effects of malabsorption diseases of the GI tract?

A
  • causes: bile salt deficiency, pancreatic enzyme deficiency, infections, brush border enzyme or carrier deficiency, coeliac disease, rapid transit
  • symptoms/effects: diarrhoea, steatorrhoea (excess fat in faeces), abdominal pain, vomiting, loss of appetite, weight loss, dehydration, oedema, anaemia
58
Q

Undigested carbohydrates move into the large intestine along with osmotic water load and may be fermented by bacteria into fatty acids, alcohols or gases. What are the two types of digestion and what do they mean?

A
  1. intermediate digestion: α-amylases hydrolyse α-1,4 glycosidic linkages in amylose, glycogen,
    amylopectin
  2. terminal digestion: disaccharidases in brush border PM of enterocytes located adjacent to hexose
    carriers (used for complete digestion of oligopeptides to AAs)
59
Q

How is the intestine a barrier to absorption of molecules from their lumen to the bloodstream?

A
  • unstirred layer (glycocalyx)
  • luminal PM
  • cell interior
  • basolateral PM
  • intercellular space
  • BM of capillary
  • PM of endothelial cell of capillary/lymph vessel
60
Q

What are the different routes and mechanisms of transport in the GI tract?

A
  1. paracellular absorption (between cells) -
    major route for fluid + small solute molecules, tight junctions can be regulated
  2. transcellular absorption (across cells) - simple for small molecules, carrier-mediated
  3. simple diffusion - depends on solubility of fluid/molecule
  4. carrier-mediated diffusion:
    - substrate binds to carrier, conformational change, releases substrate to cell interior
    - faster than simple diffusion
    - can be regulated by carrier proteins (saturable process)
  5. active transport: energy, against conc./electrochemical gradient, direct ATP hydrolysis (primary) or energy from indirect source (secondary)
    - may involve co-transport of molecules (symport/antiport)
61
Q

Describe the absorption of hexoses into an enterocyte.

A
  • fructose → GLUT5 transporter (no Na⁺ dependence)
  • (hexokinases) glucose + galactose → GLUT2 transporter (Na⁺ dependence)
  • move into circulation from enterocyte in basolateral membrane
  • secondary active transport, powered by Na⁺/K⁺ ATPase pump
  • SGLT1 carrier (Sodium-dependent GLucose Transporter 1)
  • across brush border luminal membrane

(see notes for diagram)

62
Q

Describe intermediate digestion.

A
  • denaturation via cooking, gastric acid
  • hydrolysis of peptide bonds by endopeptidases + exopeptidases → oligopeptides/AAs

(see notes for diagram)

63
Q

Describe absorption into enterocyte (absorptive cell of small intestine).

A
  • AAs mainly co-transported w/ Na⁺
  • secondary active transport, powered by basolateral Na⁺/K⁺ pump
  • 5 carriers, depending on characteristics of L-AA
  • oligopeptides (2-3 AAs) transported with H⁺ by secondary active transport using basolateral Na⁺ pump and
    luminal H⁺/Na⁺ pump
  • transporter specific for oligopeptides of L-AAs (low affinity for larger peptides)
  • more rapid rate than individual AAs
  • absorbed into circulation by facilitated diffusion via 3 specific AA carriers in basolateral membrane
64
Q

Where may undigested proteins/oligopeptides be found and what are their consequences?

A
  • large proteins absorbed intact from maternal milk → antibody transfer gives infants passive immunity
    • unhydrolysed oligopeptides may pass into circulation → possible biological effects
65
Q

How is vitamin B12 absorbed by cells and what is caused by vitamin B12 deficiency?

A
  • water-soluble vitamins usually absorbed by mediated transport
  • major exception = Vit B12 as it contains cobalt
  • intestinal transporter for B12 found only in brush border of ileum which splits from IF
  • recognises B12 when vitamin is complexed with protein called intrinsic factor (IF) in stomach
  • pernicious anaemia
66
Q

How are iron and calcium absorbed by intestinal cells?

A

• iron
- mineral absorption by active transport regulated by iron (for both)
- availability of soluble Fe2+ for absorption factors can increase/decrease (i.e. Fe deficiency in anaemia – dietary or due to GI cancers)
• calcium
- substantial intake + loss via GI tract
- absorbed passively + actively (Ca2+ATPase or by Na+/Ca2+ antiporter)
- secondary active transport regulated by 1,25(OH)₂/vit D3

67
Q

Describe emulsification and the role of fats in digestion.

A
  • bile salts emulsify fats into colloidal form, due to amphipathic nature + detergent action
  • necessary to increase SA as enzymes can only work at water/lipid interface (cloudy)
  • in digestion, pancreatic lipase hydrolyses 1- and 3- bonds of triacylglycerols → monoglycerides + 2x FA chains (assisted by colipase)
  • pancreatic esterases digest cholesterol and vitamin esters
68
Q

Describe micelle formation by fats and lipids.

A
  • mixed micelles formed from substrates and products of fat digestion + phospholipids, vitamins etc…
  • stabilised by bile salts (clear suspension)
  • micelles can diffuse slowly across unstirred water layer to enterocyte membrane
  • present highly concentrated packets of fats to membrane
69
Q

Describe the absorption of fats into enterocytes from (mainly) the upper jejunum.

A
  • lipid-soluble contents of micelle cross membrane by passive diffusion
  • conc. gradient maintained by fats binding to proteins w/in cell
  • bile salts left outside cell (form more micelles)
70
Q

Describe the intracellular processing of fats and lipids.

A
  • short-chain ionised FAs (<10 C chains) pass directly into bloodstream
  • most FAs + monoglyceridesa → (re-esterified) triglycerides in SER
  • then coated with phospholipids and protein in golgi to form chylomicrons
  • surface negatively-charged thus repel each other
71
Q

Describe the absorption of fats and lipids into lymphatic circulation.

A
  • chylomicrons leave enterocyte via energy-dependent reverse pinocytosis → lacteals of lymph → bloodstream
  • triglycerides cleared from blood by lipase on capillary endothelium
  • triglycerides passively diffuse into cells e.g. adipocytes

(see notes for diagram)

72
Q

State the stages of the absorption of fats and lipids into lymphatic circulation.

A
  1. bile salts from liver coat fat droplets
  2. pancreatic lipase and colipase breakdown fats into monoglycerides and FAs stored in micelles
  3. monoglycerides and FAs move out of micelles and enter cells by diffusion; cholesterol is transported
    into cells
  4. absorbed fats combine w/ cholesterol and proteins in the intestinal cells to form chylomicrons
  5. chylomicrons are removed by lymphatic system
73
Q

What is the fate of bile salts once they have been used in the body.

A
  • re-used for micelle formation
  • enterohepatic circulation of bile salts
  • 95% reabsorbed by active transport from terminal ileum: (recycled) → liver → gall bladder → intestine
  • bile salts not absorbed if terminal ileum damaged/resins given
74
Q

Describe the absorption of drug molecules into the GI tract and how they are classed.

A
  • some utilise carrier proteins (by structural resemblance to substrate for carrier)
  • most drugs → weak acids or bases in ionised (i) and non-ionised (n) form
  • i/n ratio depends on pK of compound and pH of environment (Henderson Hasselbalch)
  • n form absorbed by simple passive diffusion
75
Q

Describe fluid absorption into the GI tract.

A
  • small intestine and lesser colon function to reclaim fluid secreted into tract + replace excreted fluid
  • needed to maintain blood volume, BP, tissue perfusion, waste removal
  • in health, capacity for fluid absorption huge and H₂O crosses epithelial barrier by transcellular + paracellular routes
  • absorption capacity greatest where:
    • villi biggest
    • epithelium leakiest (usually duodenum and upper jejunum)
  • H₂O diffusion can occur in either direction, depending on osmotic gradient (net flux = absorption – secretion)
  • chyme in duodenum hypertonic, so net secretion of H₂O occurs until isotonic
  • in jejunum and ileum, net H₂O absorption arises from nutrient and Na⁺ absorption
    (crypts → secretory + tips of villi → absorptive)
76
Q

In which 3 ways can sodium be absorbed?

A
  • passively diffuse
  • be co-transported with glucose, amino acids (nutrient-dependent), small intestine and proximal colon
  • be transported by active transport mechanisms (nutrient-independent), distal colon

(H₂O follows, down osmotic gradient and Cl- follows, down electrochemical gradient)

77
Q

What is diarrhoea and its common causes?

A
  • loss of fluids and solutes from GI tract in excess of 500ml/day (20L/day = severe)
  • high volume reaching colon, by producing distension, activates defaecation reflex
  • common causes: drugs, toxins, infectious agents, foods, anxiety, IBS
78
Q

For which 3 reasons may fluid accumulate in the intestinal lumen?

A
  1. Osmotic factors
    - faulty nutrient digestion or absorption
    - intake of indigestible (cellulose) or unabsorbable (Mg) molecules
    - cause increase in osmotic pressure in lumen
    - provide osmotic gradient for water movement into lumen
    - bacteria in large intestine may ferment nutrients and contribute to diarrhoea
  2. Faulty water absorption
    - reduced ability of intestinal mucosa to absorb water from defective ion transport (bile acids in colon, inflammatory mediators, diabetes)
    - may result from increased intestinal motility (IBS)
  3. Active fluid secretion
    - response to stimulation (laxatives, bacterial toxins, bile salts)
    - fluid secretion from small intestine exceeds capacity of colon to absorb
    - V. cholera, E. coli toxins stimulate adenylate cyclase, increase cAMP levels, activate Cl- channels + stimulate Cl- secretion, Na⁺, H₂O in small intestine
    - cAMP inhibits active transport in small intestine + proximal colon
    - loss of fluids and electrolytes can be life-threatening
79
Q

How can acute diarrhoea and its symptoms be treated?

A
  • (self-limiting) maintain fluid/electrolyte input

- symptomatic relief: anti-motility drugs (opiates, antimuscarinics)

80
Q

What is oral rehydration therapy/solution and what is its composition?

A
  • oral rehydration solution (mmol/L): glucose = 111, Na⁺ = 90, K⁺ = 20, Cl- = 80, HCO₃- = 30
  • variations can be made commercially (sports drinks)
  • uses glucose and Na⁺ absorption in villi to pull H₂O into body from lumen
  • no specialised equipment required → made up + administered

N&E (6 decks)

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