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Physiology Flashcards

1
Q

What does the term motility mean?

A

Motility is mechanical activity mostly involving smooth muscle (skeletal at mouth, pharynx, upper oesophagus and external anal sphincter). It refers to the muscular contractions that mix and move food forward through the GI tract. It displays action potential bursts of movement as well as maintaining a low level of contraction called tone.

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2
Q

What type of chemical reaction allows digestion?

A

Hydrolysis

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3
Q

What four layers does the digestive tract wall have?

A
  1. Mucosa - lines the luminal surface of the digestive tract; is highly folded
  2. Submucosa - thick layer of connective tissue that provides the GI tract with its distensibility and elasticity
  3. Muscularis externa - major SM coat of the GI tract
  4. Serosa - outer connective tissue covering all of the GI tract, which secretes serous fluid, preventing friction between the surrounding organs and the digestive viscera
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4
Q

Describe the mucosa

A

The mucosa has three layers:

  1. Mucous membrane - the inner epithelial layer that serves as a protective surface
  2. The lamina propria - a thin middle layer of connective tissue on which the epithelium rests. It hosts gut associated lymphoid tissue (GALT) which is important in immunology
  3. Muscularis mucosa - a sparse layer of smooth muscle, at the outermost mucosal layer, lying adjacent to the submucosa
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5
Q

What are the two layers of the muscularis externa?

A
  1. Inner circular layer - contraction decreases the lumen

2. Outer longitudinal layer - shortens the tube

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6
Q

How is SM in the GI tract electrically coupled?

A

Like in self-excitable cardiac muscle cells, clusters of SM cells are pacemaker cells that display rhythmic, spontaneous variations in membrane potential.
Adjacent smooth muscle cells are coupled by gap junctions – allow spread of electrical currents from cell to cell forming a functional syncytium.
Hundreds of cells are depolarized and contract at the same time as a synchronous wave (i.e. single unit smooth muscle – as opposed to multiunit smooth muscle).

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7
Q

What is the character of electrical activity in the stomach, small and large intestine?
What are the interstitial cells that act as pacemakers to instigate cyclic slow wave activity called?

A

Spontaneous electrical activity occurs as slow waves - rhythmic patterns of membrane depolarization and repolarization that spread from cell to cell via gap junctions.
Interstitial cells of Cajal (ICC).

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8
Q

How does the AP occur in SM of the GI tract?

A

Contraction only occurs if the slow wave amplitude is sufficient to trigger SMC action potentials (upstroke mediated by voltage-activated Ca2+ channels, downstroke by voltage-activated K+ channels). Force is related to number of action potentials discharged.
NB not all slow waves trigger contraction.

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9
Q

Where are ICC cells located?

A

Between the longitudinal and circular muscle layers and in the submucosa

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10
Q

What plexuses form the enteric nervous system?

What do they mainly regulate?

A

Submucosal plexus - regulates epithelial and blood vessels

Myenteric plexus - regulates motility and sphincters

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11
Q

What is the basic electrical frequency (BEF) for:

(i) Stomach
(ii) Duodenum
(iii) Terminal ileum
(iv) Proximal colon
(v) Distal colon

A

(i) 3 slow waves per minute
(ii) 12 waves per minute
(iii) 8 waves per minute
(iv) 8 waves per minute
(v) 16 waves per minute

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12
Q

What is the parasympathetic innervation to the GI tract and what stimulates it?

A 
Preganglionic fibres (releasing ACh) synapse with ganglion cells (in essence post-ganglionic neurones) within the ENS
Excitatory influences - increased gastric, pancreatic and small intestinal secretion, blood flow and smooth muscle contraction
Inhibitory influences - relaxation of some sphincters, receptive relaxation of stomach
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13
Q

What is the sympathetic supply to the GI tract and what stimulates it?

A

Preganglionic fibres (releasing ACh) synapse in the prevertebral ganglia. Postganglionic fibres (releasing NA) innervate mainly enteric neurones, but also other structures
Excitatory influences – increased sphincter tone
Inhibitory influences – decreased motility, secretion & blood flow

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14
Q

What is segmentation?

A

rhythmic contractions of the circular muscle layer that mix and divide luminal contents - occurs in the small intestine (in the fed state) and in the large intestine (where it is called haustration).

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15
Q

What is a colonic mass movement?

A

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

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16
Q

What are the three phases of deglution?

Describe each.

A
  1. Oral phase
  2. Pharyngeal phase
  3. Oesophageal phase
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17
Q

Describe the oral phase of deglution

A

Mouth closes, tongue moves to hard palate, mechanoreceptors are stimulated, stimulating afferent nerve impulses via CN IX and X, stimulating efferent nerve impulses via CN VII, X and XI to skeletal muscles of pharynx and larynx

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18
Q

Describe the pharyngeal phase of deglution

A

Inhibition of ventilation
Laryngeal muscles close and raise larynx
Contraction of superior and middle pharyngeal constrictors propels bolus into hypopharynx
Bolus forced epiglottis over larynx
Bolus enters oesophagus through open oesophageal sphincter
Glottis reopens, ventilation recommences

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19
Q

Describe the oesophgeal phase of deglution

A

Swallowing centre (pons and medulla) triggers closure of the upper oesophageal sphincter and a primary peristaltic wave (via vagus),
Wave mediated by skeletal muscle in upper oesophagus and smooth muscle in distal regions.
Peristalis (in smooth muscle) co-ordinated by the enteric nervous system.
Circular fibres behind bolus squeeze bolus down towards stomach - longitudinal fibres in front of bolus shorten distance of travel
Lower oesophageal sphincter opens within 2-3 s of the initiation of a swallow (closes after passage of bolus to prevent reflux)

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20
Q

What are the three major pairs of salivary glands?

A
  1. Parotid
  2. Submandibular
  3. Sublingual
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21
Q

Parotid salivary gland
Where is it located?
What duct is it associated with?
Where does saliva from this gland enter the mouth?

A

Anterior to ear, below zygomatic arch – duct (of Stensen) enters mouth opposite second maxillary molar teeth

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22
Q

Submandibular salivary gland
Where is it located?
What duct is it associated with?
Where does saliva from this gland enter the mouth?

A

Submandibular – medial to body of mandible – duct (of Wharton) enters mouth under tongue by lingual frenulum via sublingual caruncula

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23
Q

Sublingual salivary gland
Where is it located?
What duct is it associated with?
Where does saliva from this gland enter the mouth?

A

Medial to submandibular glands – ducts (of Rivinus and common Bartholin) connect with Wharton’s at the sublingual caruncula

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24
Q

What three things does a salivary gland consist of?

A
  1. An external capsule
  2. Septae separating lobes and lobules
  3. Lobules composed of salivons - the functional unit of the gland
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25
Q

What is an acinus?

What two types of cell make it up?

A

A lobe made up of pyramidal-shaped secretory acinar cells around a central lumen that are either:

  1. Serous cells producing a watery secretion rich in α-amylase; contain small, dense, secretory granules
  2. Mucous cells producing a thick mucus-rich secretion; contain relatively large, pale, secretory granules
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26
Q

Give 7 functions of saliva

A
  1. Begins digestion of carbohydrate in the mouth through salivary amylase
  2. Facilitates swallowing by moistening food particles and holding them together
  3. Exerts antibacterial activity, involving lysozyme, IgA, lactoferrin
  4. Solvent for molecules that stimulate the taste buds
  5. Aids speech by facilitating the movement of the lips and tongue
  6. Flushes away food residues, keeping the mouth clean
  7. Rich in bicarbonate buffers, which neutralize acids in food
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27
Q

What ions in saliva are present at higher volumes than in the plasma?

A

K+ and HCO3-

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28
Q

What are the two stages of saliva formation?

A
  1. Primary secretion by acinar cells

2. Secondary modification by duct cells

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29
Q

Give some facts about primary secretion of saliva

A

It is driven by the basolateral Na+/K+-ATPase which by secondary active transport

  • Drives inward movement of Cl- across the basolateral membrane via the Na+/K+/2Cl- (triple) transporter, raising [Cl-]I
  • Creates an electrochemical gradient driving Cl- efflux, by facilitated diffusion, through apical membrane Ca2+-activated Cl- channels
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30
Q

Give some facts about secondary secretion of saliva

A

Secondary modification by striated, intercalated and excretory ducts removes Na+ and Cl- from, and adds K+ and HCO3- to, the primary secretion. Influx of Na+ and Cl- exceeds efflux of K+ and HCO3- and since ducts are largely impermeable to H2O the overall effect is diluting
It is driven by the basolateral Na+/K+-ATPase

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31
Q

What are the two reflexes stimulating salivary production?

A
  1. Simple - occurs when chemoreceptors and pressure receptors in the oral cavity respond to the presence of food. It involves afferent nerve fibers and the salivary center, parasympathetic nerves and CN VII, I
  2. Conditioned - occurs without oral stimulation; just thinking, smelling or seeing the preparation of pleasant food stimulates this
32
Q

Give three functions of the stomach

A
  1. Secreted HCL and enzymes to begin protein digestion
  2. Stores ingested food before passing it into the duodenum as chyme
  3. Mixes the food with gastric secretions to produce chyme
33
Q

What regulates gastric emptying?

A
  1. Gastric factors e.g. the amount of chyme in the stomach; stomach distension; degree of fluidity of the chyme
  2. Duodenal factors e.g. presence of fat, acid, hypertonicity,or distension activates duodenal receptors, triggering either a neural or a hormonal response that puts the breaks on gastric motility by reducing the excitability of gastric SM
34
Q

What are the three phases of gastric secretion?

A
  1. Cephalic - before the food enters the stomach, vagus is activated, stimulating G cells, increasing secretion
  2. Gastric - when food is in the stomach
  3. Intestinal - as the stomach empties, the stimuli for secretion becomes less intense
35
Q

What are the two types of digestion that occur in the small intestine?

A

Luminal digestion - mediated by pancreatic enzymes secreted in the duodenum
Membrane digestion - mediated by enzymes situated at the brush border of epithelial cells

36
Q

What is the apical membrane?

A

The membrane facing into the lumen of the GI tract

Aka brush border

37
Q

Describe carbohydrate digestion

A

E.g. starch
Broken down in the mouth to an oligosaccharide by alpha amylase. Those which survive this are broken down in the small intestine by pancreatic amylase
Dextrokinase breaks oligosaccharides into the dissacharides sucrose, maltose and lactose.
Their associated enzymes break them down into monosaccharides that are then absorbed into the bloodstream

38
Q

What transporters are glucose, galactose and fructose associated with?

A

Glucose, galactose = SGLT1

Fructose = GLUT5

39
Q

How are amino acids absorbed from the lumen into the bloodstream?

A
  1. At the brush border - either by Na dependent co transporters (5 types) or Na independent co transporters (2 types)
  2. At the basolateral membrane - Na dependent (2 types) or Na independent (3 types
40
Q

Summary of protein digestion
Where is protein digested and what by?
How are AAs transported across the apical membrane?
How are oligopeptides transported across the apical membrane?
How are AAs transported across the basolateral membrane?

A

Protein is digested in the lumen to amino acids, or oligopeptides, by pepsin and the pancreatic proteases
Peptidases at the brush border further hydrolyse oligopeptides to amino acids
Amino acids are transported across the apical membrane via a variety of amino acid transporters, some of which are Na+-dependent and others Na+-independent
Oligopeptides are transported across the apical membrane by the H+/oligopeptide co-transporter, PepT1
Oligopeptides with the cytoplasm are hydrolysed to amino acids by peptidases within the enterocyte
Amino acids exit the enterocyte across the basolateral membrane by several, Na+-independent. transporters

41
Q

What role does bile play in fat digestion?

A

Bile salts secreted in bile from the gall bladder in response to CCK act as detergents to emulsify large lipid droplets to small droplets.
Bile salts increase surface area for attack by pancreatic lipase, but block access of the enzyme to the lipid with the hydrophobic core of the small droplets.
Problem solved by colipase, an amphipathic polypeptide secreted with lipase by the pancreas – binds to bile salts and lipase allowing access by the latter to tri- and di-glycerides.
Failure to secrete bile salts results in:
- Lipid malabsorption - steatorrhoea (fat in faeces)
- Secondary vitamin deficiency due to failure to absorb lipid vitamins

42
Q

How are mixed micelles transported across the apical membrane?

A

Passive diffusion

43
Q

Define satiation, satiety and adiposity

A 
Satiation = sensation of fullness generated during a meal. 
Satiety = period of time between termination of one meal and the initiation of next. 
Adiposity = the state of being obese.
44
Q

What is the site of integration of CNS influences on energy balance and body weight?

A

Hypothalamus

45
Q

Name and briefly describe three satiation signals

A

CCK - secreted from endocrine cells in the duodenum and jejunum in proportion to lipids and protein in meal
Peptide YY - levels increase rapidly post prandially to inhibit gastric motility, slow emptying and reduce food intake
GLP-1 - same as peptide YY

46
Q

What is ghrelin?

A

A hunger signal - levels increase before meals and decrease after meals. Levels are raised by fasting and hypoglycaemia.

47
Q

What two hormones, produced in peripheral tissues, report fat levels to the brain?

A

Leptin - made & released from fat cells
Insulin - made & released from pancreatic cells
Reduced leptin mimics starvation, causing unrestrained appetite.

48
Q

What does Orlistat treat and how does it do this?

A

It treats obesity

  • Inhibits pancreatic lipase decreasing triglyceride absorption
  • Reduces efficiency of fat absorption (~30%) in small intestine
  • Side-effects include cramping and severe diarrhoea
  • Need to take vitamin supplements (fat soluble vitamins)
49
Q

Where does the major force of expulsion for vomiting come from?

A

The stomach, oesophagus, and associated sphincters are all relaxed during emesis.
The major force for expulsion comes from contraction of the respiratory muscles - mainly the diaphragm and the abdominal muscles.

50
Q

Why does pregnancy induced vomiting occur?

A

It is an adaptive change - encourages picky eating during a time of rapid foetal growth (CNS vulnerable to toxicosis)

51
Q

Define emesis

A

Forceful propulsion of gastric/intestinal contents out of the mouth
NB it is not due to stomach contraction

52
Q

What co-ordinates vomiting?

A

The vomiting center in the medulla oblongata of the brain stem

53
Q

Describe the events that occur during emesis

A
  1. Deep inspiration and closure of the glottis to prevent aspiration
  2. The contracting diaphragm descends downward on the stomach while simultaneous contraction of the abdominal mucles, increasing the abdominal pressure
  3. The stomach is compressed and gastric contents are forced up through the flaccid sphincters and oesophagus and out through the mouth
  4. This process may be repeated several times to completely empty the stomach
    When about to vomit, we salivate profusely in order to neutralise the stomach acid.
    Sweating and increased HR indicate use of the autonomic nervous system
54
Q

Describe the receptor and neural pathways in vomiting.

A

The presence of toxic materials in the gut lumen cause irritation of the mucosa of the GI tract.
Embedded in the mucosa are a population of cells - enterochromaffin cells, which are endocrine cells which store most of the body’s serotonin.
In response to the toxic stimulus, EC cells release 5-HT, which stimulates vagal afferent signals e.g. vagus nerve which connects to the CTZ and NTS, initiating vomiting

55
Q

What is the vomiting center?

A

A group of interconnected neurones within the medulla that are driven by a central pattern generator (CPG) that in turn receives input from the NTS

56
Q

How does efferent output from the vomiting center affect somatic and autonomic nervous systems?

A
  1. Parasympathetic system by vagus nerve – the longitudinal muscle of the oesophagus contracts, shortening the oesophagus; the stomach relaxes; the SI contracts.
  2. Somatic motor output – the stomach is compressed as a results of abdo muscle and diaphragm contraction
  3. Mixed A&S – in reased HR and force; increased salivation; vasoconstriction producing palor; sweating
57
Q

What two types of digestion occur in the small intestine?

A
  1. Luminal digestion - mediated by pancreatic enzymes secreted into the duodenum
  2. Membrane digestion - mediated by enzymes situated at the brush border of epithelial cells
58
Q

What is contained within a mixed micelle?

A

Free fatty acids
2-monoglycerides
Cholesterol
Other insignificant things e.g. phospholipids

59
Q

How does lipid absorption occur across the the apical membrane of the enterocytes?

A

The mixed micelle collides with the apical membrane, causing exchange of the free fatty acids and 2-monoglycerides into the apical membrane of the enterocyte
The small and medium sized fatty acids go straight into the blood
The long chain fatty acids are re-synthesized into triglycerides and are eventually incorporated into chylomicrons

60
Q

How is Ca2+ absorbed?

A

Enters the luminal membrane of the small intestine epithelial cells down its EC gradient through a specialised channel.
It exits the basolateral membrane by two energy dependent mechanisms.
Vitamin D greatly enhanced all of these mechanisms

61
Q

Is water absorption active or passive?

What ion is the main driving force for this?

A

Passive

Na+ - provides an osmotic force for reabsorption of water

62
Q

Where are Na+/glucose and Na+/amino acid the major mechanisms of postprandial Na+ absorption?
What type of transport is this?

A

The jejunum

Secondary active

63
Q

What is an ENAC?

What does it do?

A

Epithelial Na+ channel

Mediates electogenic Na+ absorption in the distal colon

64
Q

The secretion of what ion is important in the development of secretory diarrhoea?
Where is this ion secreted from?

A

Chloride

Cells in the Crypts of Langerhan

65
Q

What does closed CFTR do to Cl- secretion?
What causes CFTR to be indirectly activated?
What is the overall effect?

A 
Secretion is very little
Bacterial endotoxins, e.g. Cholera, E.coli, C.difficile
Hormones e.g. 5-HT
Some laxatives
Secretory diarrhoea
66
Q

Causes of Diarrhoea

Name some causes of impaired absorption of NaCl

A

Congenital defects
Inflammation
Infection
Excess bile acid in colon

67
Q

Causes of Diarrhoea

Name one serious cause of excessive secretion of NaCl

A

Cholera - CFTR goes into overdrive, allowing massive efflux of chloride from the enterocyte

68
Q

Describe the liver lobule

A

Hexagonal on cross section
Has a branch of the hepatic vein at its centre
Has a portal triad at each corner, containing
- A branch of hepatic portal vein
- A branch of hepatic artery
- A bile duct
The flow of blood and bile are in opposite directions - blood moves centrally towards the central vein, bile moves outwardly to each of the six corners
Bile secreted by hepatocytes travels through the lobule in canaliculi to the bile duct

69
Q

What membrane of the hepatocytes faces the canaliculi?

What does the other mambrane face and what is this?

A

Apical membrane

Basolateral membrane faces a pericellular space called the space of Disse

70
Q

What are Kuppfer cells and where do they reside?

A

Macrophages resident in the sinusoidal vascular space - remove particulate matter e.g. bacteria

71
Q

Sinusoid
What is this?
What four things does this contain?

A

A location for mixing of the oxygen-rich blood from the hepatic artery and the nutrient-rich blood from the portal vein. Contains

  • Endothelial cells that form a fenestrated structure
  • Kuppfer cells
  • Stellate cells within the space of Disse - important in storage of VitA
  • Intrahepatic bile system
72
Q

Is bile constantly produced?
What happens when no immediately needed?
What stimulates the opening of the sphincter of Oddi?

A

Yes
Sphincter of Oddi at the distal and of the common bile duct is closed; bile is redirected into the cystic duct and stored & concentratd in the gall bladder
CCK - stimulates the gall bladder to contract - bile spurts into the duodenum via cystic and common bile ducts - mixed with bile from liver

73
Q

Aside from the liver hepatocytes, where else is bile produced?

A

Bile duct cells (25%)

74
Q

What does hepatic bile consist of?

A
  1. Primary bile acids, e.g. cholic and chenodeoxycholic acids
  2. Water and electrolytes
  3. Lipids and phospholipids
  4. Cholesterol
  5. IgA
  6. Bilirubin
75
Q

There is very little bile salt in the body.

How is this maintained?

A

Most of the bile salts which are secreted into the GI tract and biliary system are very effectively reabsorbed by active transport in the terminal ileum

76
Q

Morphine may be used for pain relief caused by gall stones. What is one adverse affect of this?

A

It constricts the sphincter of oddi

Gastrointestinal (16 decks)

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