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Primary FRCA > GI Physiology > Flashcards

GI Physiology Flashcards

1
Q

How much saliva do the parotid, submandibular & sublingual glands produce in 24hrs?

A

500-1000ml

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2
Q

What are the constituents of saliva?

A

98% water
Electrolytes (Bicarb, Na < [serum], but K > [serum])
Proteins/enzymes (alpha-amylase, lipase, haptocorrin, mucin)
Bactericides (thiocyanate, lysozyme, lactoferrin, IgA)

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3
Q

How does salivary amylase work?

A

Structurally identical to pancreatic amylase.
Optimum pH 7 (i.e. saliva)
Catalyses complex carb breakdown.
Cleaves up to 75% of starch pre-stomach.

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4
Q

In which patient group is lingual lipase important?

A

Neonates.

Catalyses breakdown of triglycerides.
In neonates, pancreatic lipase is less effective, esp. on milk fats.

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5
Q

What is haptocorrin?

A

A binding protein for vitamin B12 - protects it from denaturing in the low pH of the stomach.

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6
Q

How is saliva produced?

A

Primary secretion is from the acinar cells, by active transport of electrolytes and passive diffusion of water. The resulting saliva is isotonic.

Secondary secretion occurs in the duct cells, where Na and Cl are reabsorbed, and K and HCO are secreted. The resulting saliva is hypertonic.

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7
Q

Does aldosterone affect the salivary glands?

A

Yes.

Same effect as kidney: increased Na reabsorption & K secretion.

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8
Q

What is the innervation of the salivary glands?

A

Sympathetic.

Parasympathetic:

  • Parotid = glossopharyngeal (CN IX) w/ pre-ganglionic fibres synapsing at the otic ganglion
  • Submandibular/sublingual = facial (CN VII) w/ pre-ganglionic fibres synapsing at the submandibular ganglion (post-ganglionic in lingual nerve)
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9
Q

What are the effects of sympathetic stimulation of the salivary glands?

A

Vasoconstriction & myoepithelial cell contraction.

Transient increase in secretion, then overall decrease.

More mucinous, amylase rich saliva.

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10
Q

What are the effects of parasympathetic stimulation of the salivary glands?

A

Vasodilation and myoepithelial cell contraction.

Serous, electrolyte rich saliva.

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11
Q

What are the phases of swallowing?

A

Oral.
Pharyngeal.
Oesophageal.

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12
Q

Describe the oral phase of swallowing.

A

Voluntary.

Chewing etc. -> sensation of food against the hard palate (efferent, glossopharyngeal CN IV -> medulla).

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13
Q

Describe the pharyngeal phase of swallowing.

A

Involuntary.
Afferent (from medulla).
1-2s apnoea.

  • Apposition of nasopharynx & soft palate (prevents passage of food up)
  • Adduction of the vocal cords & aryepiglottic folds via recurrent laryngeal nerves (prevents aspiration)
  • Elevation of hyoid/depression of epiglottis (prevents aspiration & propels food into oesophagus)
  • Contraction of superior and middle pharyngeal constrictors (move food downwards ~30cm/s)
  • Relaxation of cricopharyngeus (upper oesophageal sphincter)
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14
Q

Describe the oesophageal phase of swallowing.

A

Involuntary.

  • Contraction of cricopharyngeus (up to 100mmHg - prevents regurgitation)
  • Relaxation of lower oesophageal sphincter
  • Oesophageal peristalsis (3cm/s)

Peristalsis:

  • Primary = full length of oesophagus (medulla)
  • Secondary = local to bolus, triggered by wall stretch
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15
Q

What is intragastric pressure?

A

5-10mmHg

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16
Q

What is barrier pressure?

A

Difference between LOS and intragastric pressures.

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17
Q

What factors reduce barrier pressure?

A

Reduced LOS tone/pressure:

  • Swallowing
  • Pregnancy (due to progesterone)
  • Hiatus hernia
  • Drugs (EtOH, volatiles, propofol, thio, opioids, atropine, glyco)

Increased intra-abdo pressure:

  • Pregnancy
  • Obesity
  • Acute abdomen
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18
Q

Which drugs increase LOS tone?

A

Metoclopramide
Suxamethonium
Anticholinesterases

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19
Q

What is Mendelson’s syndrome?

A

Pneumonitis secondary to aspiration of gastric contents.

20
Q

Describe measures to avoid aspiration during anaesthesia.

A
  • Pre-op fasting
  • Semi-recumbent positioning
  • Pre-medication (PPI, H2R antagonist, sodium citrate)
  • Aspiration of NG
  • RSI w/ cricoid (debatable)
21
Q

What are the functions of the stomach?

A
  • Storage/moderates release of food into duodenum
  • Mixing of food
  • Secretion of digestive enzymes, gastric acid, and IF
  • Endocrine (control of gastric emptying)
22
Q

List the substances secreted by the stomach.

A
  • HCl - parietal cells
  • Pepsinogen - chief cells (converted to pepsin at low pH)
  • Gastrin - G cells
  • Intrinsic Factor - parietal cells
  • Mucus - mucous cells
23
Q

Describe vitamin B12 absorption.

A
  • Derived from animal proteins during breakdown
  • Mouth -> stomach is bound by haptocorrin
  • Duodenum -> terminal ileum is bound by IF, as haptocorrin is broken down in duodenum by trypsin
  • Absorbed in terminal ileum as IF-B12 complex via IF receptors

NB. In pernicious anaemia, there is an IF deficiency due to autoimmune loss of parietal cells.

24
Q

What are the effects of gastrin?

A
  • increases HCl secretion directly and indirectly (via histamine release from enterochromaffin cells)
  • increases pepsinogen secretion from chief cells
  • increases gastric motility
25
Q

How is gastric acid produced?

A
  • CO2 diffuses into parietal cells from blood

CO2 + H2O —> H2CO3 —> HCO3- + H+

  • The HCO3- is exchanged out for Cl- at the basal membrane (HCO3-/Cl- ATPase)
  • The H+ is exchanged out for K+ at the apical membrane (into the secretory canaliculus) (H+/K+ ATPase - the ‘proton pump’)
  • Cl- diffuses into the secretory canaliculus via ion channels
  • In the secretory canaliculi H+ + Cl- —> HCl
26
Q

How do histamine, gastrin, and ACh increase acid secretion?

A

Histamine - cAMP

Gastrin - Ca2+

ACh - Ca2+

These second messenger systems increase synthesis of proton pumps and stimulate their exocytosis (the proton pump is stored within tubovesicular membranes that can fuse into the canalicular membrane).

27
Q

Name the phases of gastric secretion.

A

Cephalic - vagal response to anticipation of food triggers secretion of HCl, gastrin & pepsinogen

Gastric - gastric distension triggers secretion of gastrin, therefore indirectly HCl, pepsinogen & histamine

Intestinal - drop in duodenal pH at gastric emptying triggers secretion of secretin, which in turn inhibits gastrin release, and triggers secretion of HCO3- from pancreatic ductal cells.

28
Q

What factors slow the rate of gastric emptying?

A

Gastric:
- Consistency - solids

Duodenal:

  • Duodenal distension
  • Duodenal pH - low pH triggers secretin release, which inhibits gastrin, thereby reducing gastric motility
  • Fat content - triggers CCK release which increases pyloric tone
  • High osmolarity
  • Tryptophan

Other:

  • Sympathetic stimulation
  • Pain/trauma
  • Drugs e.g. opioids
  • Autonomic neuropathy
29
Q

Peri-op fasting guidance.

A

2hrs clear fluids (water, black tea/coffee, juice)

4hrs for breast milk

6hrs for food & formula or other milk

NB. Carb loading drinks only recommended for major abdo surgery

30
Q

Where is the vomiting centre?

A

In the medulla.

It is adjacent to:

  • the respiratory centre
  • the nucleus tractus solitarius
  • the chemoreceptor trigger zone (floor of 4th ventricle)
31
Q

What is special about the chemoreceptor trigger zone?

A

It is outside of the BBB.

This is of relevance, as it ensures a rapid repsonse to emetic compounds in blood, and a rapid response to antiemetic drugs in the circulation.

32
Q

What are stimulatory inputs to the vomiting centre?

A

CTZ:

  • Dopamine (D2)
  • Serotonin
  • ACh
  • Opioid
  • Substance P (NK-1)

CN VIII - afferent from vestibular system (e.g. motion sickness)

CN IX - afferent from pharynx (i.e. gag reflex)

Enteric nervous system & CN X - afferent from GI tract (e.g. infection)

Higher centres e.g. limbic - response to emotion

33
Q

Describe vomiting.

A

Pre-ejection phase:

  • nausea
  • decreased gastric motility
  • duodenal reverse peristalsis
  • salivation (parasympathetic)
  • sweating & tachycardia (sympathetic)

Retching:

  • deep inspiration then glottic closure
  • increase in intra-thoracic & intra-abdo pressures (muscle contraction)

Ejection:

  • pyloric contraction
  • relaxation of LOS
  • further increase in intra-abdo pressure
  • occlusion of nasopharynx by soft palate
34
Q

How are carbs absorbed?

A

Digestion by salivary amylase & pancreatic amylase.

Brush border enzymes (lactase, maltase, sucrase) break down the fragments into monosaccharides.

Monosaccharides are absorbed into enterocytes:

  • Glucose via SGLT1 (Na/Glu co-transporter)
  • Fructose via facilitated diffusion
  • Pentose via passive diffusion

Monosaccharides then pass into capillaries via GLUT-2 (facilitated diffusion)

35
Q

How are proteins absorbed?

A

Digested in stomach by pepsin, and in the duodenum by trypsin and chymotrypsin, down to tri- and di-peptides.

At brush border these are broken down by peptidases into AAs.

Absorbed into enterocytes by Na-linked co-transporters (like Glucose)

Pass into capillaries by facilitated diffusion.

36
Q

How are lipids absorbed?

A

Emulsification by bile acids in the duodenum.

Hydrolysis to free fatty acids by pancreatic lipase.

Micelle formation (monoglycerides, fatty acids, bile salts).

Absorbed into enterocytes by diffusion.

In the ER of the enterocyte, monoglycerides and fatty acids are recombined to form triglyceride, which is combined with cholesterol, phospholipid, and apolipoprotein to form chlyomicrons.

Chylomicrons pass into the lacteal of the villus, and into the lymphatic system.

37
Q

Endocrine pancreas.

A

Islets of Langerhans.
1-2% of pancreatic mass.

α-cells - glucagon
β-cells - insulin
δ-cells - somatostatin
PP-cells - pancreatic polypeptide

38
Q

Exocrine pancreas.

A

1.5L secretions per day.

Acinar cells:

  • Proenzymes trypsinogen & chymotrypsinogen.
  • α-amylase
  • Lipase

Duct cells:

  • H2O
  • HCO3-
39
Q

How is HCO3- secreted by the pancreas?

A

CO2 into ductal cell from capillaries.

CO2 + H2O —> H2CO3 —> H+ + HCO3-

H+ out across basal membrane via Na/H+ exchanger.

HCO3- out into duct lumen via HCO3-/Cl- exchanger.

Water follows HCO3-

NB. Cl- is recycled back out into the duct lumen predominantly along Cl- channel CFTR (which is dysfunctional in cystic fibrosis, reducing HCO3- transport, drying out pancreatic secretions)

40
Q

How is the secretion of pancreatic fluid controlled?

A

Neural:
Vagal activity in response to sight/smell of food results in increased acinar cell activity

Humoral:

  • Gastrin stimulates acinar cells
  • Cholecystokinin stimulates acinar cells
  • Secretin stimulates duct cells
41
Q

What is the electro-mechanical activity of the small intestine during fasting?

A

The migrating motor complex (MMC).

Occurs at intervals of 90mins, and is a co-ordinated peristalsis from stomach to ileum.

Four phases:

1) Quiescence
2) Increasing AP frequency, therefore contractility
3) Peak contractility (just a few minutes)
4) Declining AP frequency

42
Q

What is the intrinsic electrical activity of the small intestine?

A

Slow waves - fluctuations in membrane potential (20-30x/min)

Usually below depolarisation threshold, unless additional neurohumeral input.

They help coordinate peristalsis.

43
Q

Describe small intestinal motility.

A

Propulsive and non-propulsive contractions.

Non-propulsive/segmental contractions compartmentalise a portion of bowel and allow for mixing of the food in the lumen.

Propulsive contractions occur behind a food bolus and propel it caudally.

Contractility is mediated by gut hormones (endocrine & paracrine), and neural inputs, which may be triggered distantly or locally.

44
Q

Which hormones influence small intestinal motility?

A

Motilin - released from duodenal mucosa every 90 mins, stimulating the MMC. (Erythromycin is a motilin agonist)

Vasoactive intestinal peptide - increases motility, but also secretion of water & electrolytes. (VIPoma - pancreatic cholera)

45
Q

What is the innervation of the enteric nervous system?

A

It is a complete reflex circuit i.e. has features not requiring CNS input (although does communicate with brain stem and spinal cord)

Sensory afferents to medulla.

Parasympathetic motor efferents via CN X - increased motility & secretions

Sympathetic motor efferents via sympathetic chain - reduced motility & secretions.

46
Q

List the regulatory mechanisms of hepatic blood flow.

A

Intrinsic:

  • Autoregulation of hepatic arterial pressure
  • The hepatic arterial buffer response

Extrinsic (sympathetic innervation):

  • Vasoconstriction of hepatic arteries
  • Vasoconstriction of portal and splanchnic capacitance vessels
47
Q

Describe the hepatic arterial buffer response.

A

Semi-reciprocal relationship between hepatic arterial and portal venous flow.

Simply, changes in portal flow influence hepatic arterial flow (but not vice versa).

Theory is that adenosine sits in the spaces of Mall, and is washed out at a rate determined by portal flow. For example, at low portal flow rates, [adenosine] increases, and this has a vasodilatory effect on the hepatic arteries, compensating for the low portal flow.

Primary FRCA (4 decks)

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