Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

My Gastrointestinal > Physiology > Flashcards

Physiology Flashcards

1
Q

What do the words oral and aboral mean?

A

oral means moving towards the mouth

aboral means moving away from the mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the parts of the small intestine?

A

duodenum, jejunum and the ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the parts of the large intestine?

A

caecum, appendix and colon (ascending, descending, transverse and sigmoidal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the accessory organs of the digestive tract?

A
  • salivary glands
  • pancreas (makes digestive enzymes)
  • liver (makes bile)
  • gallbladder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the layers of the digestive tract wall?

A
  • mucosa
  • submucosa
  • muscularis externa
  • serosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does the mucosa consist of?

A
  • mucous membrane (epithelial, exocrine and endocrine gland cells)
  • lamina propria (capillaries, enteric neurones and gut-associated lymphoid tissue)
  • muscularis mucosae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does the submucosa consist of?

A

connective tissue, larger blood and lymph vessels, glands and submucous plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does the muscularis external consist of?

A

mostly smooth muscle consisting of circular muscle and longitudinal muscle and between is the myenteric plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does serosa consist of?

A

connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the four main functions of the alimentary canal?

A
  • Motility: mechanical
  • Secretion: required for digestion, protection and lubrication
  • Digestion: enzymatic hydrolysis of food
  • Absorption: transfer of products into blood or lymph
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What places use skeletal or smooth muscle?

A 
skeletal= mouth, pharynx, upper oesophagus and external anal sphincter
smooth= everywhere else
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What type of change does the circular muscle cause?

A

lumen becomes narrower and longer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What type of change does the longitudinal muscle cause?

A

intestine becomes shorter and fatter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What type of change does muscularis mucosae cause?

A

change in area for absorption and secretion and it causes a mixing motion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is smooth muscle made up of (cells and their connections)?

A

small cells connected by gap junctions making a low-resistance pathway so there is a single-unit sheet of smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is spontaneous contracting activity driven by in the GI tract and what is it modified by?

A

driven by pacemaker cells

modulated by intrinsic/extrinsic nerves and hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does slow wave electrical activity determine in the GI tract?

A

frequency, direction and velocity of rhythmic contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is slow wave activity driven by?

A

ICCs which are the pacemaker cells in the circular and longitudinal muscle layers which form gap junctions with themselves and smooth muscle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is required for the slow wave activity to cause a contraction?

A

the depolarising waves only cause a contraction in the wave amplitude reaches threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What determines the force of the slow-wave-induced contraction?

A

the longer the wave is above threshold, the more action potentials will be fired off
the starting potential of the cell also has an effect on how long the wave is above threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the starting electrical potential of a cell determined by?

A

neuronal, hormonal and mechanical stimuli causing depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the parasympathetic innervation of the GI tract?

A

preganglionic fibres that synapse with ganglion cells in ENS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What influences does the parasympathetic part of the GI tract have?

A

Excitatory influences: increased secretion, blood supply and mechanical activity
Inhibitory influences: relaxing of sphincters and stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the sympathetic innervation of the GI tract?

A

preganglionic synapse in the prevertebral ganglia and postganglionic fibres which innervate enteric neurons and others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What influences does the sympathetic innervation of the GI tract have?

A

Excitatory influences are increased sphincter tone

Inhibitor influences are decreased motility, secretion and blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What does the Enteric nervous system consist of?

A
  • Myenteric plexus- regulates motility and sphincters

- Submucous plexus- modulates epithelia and blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the three types of neurones in the ENS?

A
  • sensory (mechano-, chemo- or thermo-receptors)
  • interneurons (majority, for motor activity coordination)
  • effector neurons (execution)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the main features of peristalsis?

A
  • propulsive segment and ahead is receiving segment
  • stretch from sensory neurons so there is altered activity of interneurons then altered activity of motoneurons around the bolus
  • behind bolus, the circular muscle contracts and longitudinal relaxes
  • in front of the bolus, the circular muscle relaxes and longitudinal muscle contracts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does segmentation consist of?

A

mixing, churning by contractions of the circular muscle layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What does colonic mass movement consist of?

A

force of faeces into rectum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What does the migrating motor complex consist of?

A

powerful sweeping of the small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What do tonic contractions consist of?

A

low pressure (organs with major storage function) or high pressure (sphincter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the sphincters of the GI tract?

A
  • Upper oesophageal (skeletal): relaxes for swallowing and closes during inspiration
  • Lower oesophageal: entry of food into stomach and prevents reflux of gastric contents to oesophagus
  • Pyloric: gastric emptying and prevents reflux
  • Ileocaecal valve: flow from ileum to caecum
  • Internal and external anal: regulated by defecation reflex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is energy homeostasis?

A

physiological process whereby energy intake is matched to energy expenditure over time so there is body fuel stability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the table of classification for BMI?

A

BMI <25 = thin/normal/acceptable
BMI 25-30 = overweight
BMI 30-40 = obese
BMI > 40 = morbidly obese

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is fat used for?

A

energy storage, prevention of starvation and as an energy buffer during prolonged illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How does the CNS influence body weight?

A

behaviour (food and exercise), ANS activity (energy expenditure) and neuroendocrine system (hormone secretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How does the hypothalamus control food and how it is digested?

A

satiety signalling, adiposity negative feedback signalling and food reward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What do satiation, satiety and adiposity mean?

A

Satiation is the sensation of fullness
Satiety is the period of time between one meal ending and the start of the next
Adiposity is the state of being obese

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are some of the chemical satiation signals in the body?

A
  • Cholecystokinin
  • Peptide YY
  • Glucagon-like peptide 1
  • Oxyntomodulin
  • Obestatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What does Ghrelin do?

A

hunger signal and stimulates food intake, levels are raised by fasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the two hormones that are produced in peripheral tissue that act on hypothalamic neurones?

A
  • Leptin is made and released from fat cells

- Insulin is made and released from pancreatic cels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What do Leptin and Insulin do in terms of obesity?

A

both increase as more fat is stored and they inform the hypothalamus that the body should eat less and increase energy burn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the current treatment for obesity?

A
  • Orlistat which inhibits pancreatic lipase and reduces the efficiency of fat absorption in the small intestine
  • Bariatric surgery which is gastric by-pass surgery produces substantial weight loss and cures Type 2 Diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How can the stomach be mechanically divided?

A
  • orad (fundas and proximal body)

- caudad (distal body and antrum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the mechanical characteristics of the orad?

A
  • contractions are weak, maintained and tonic
  • storage area so there is no slow wave activity
  • minimal churning so there can be partial carbohydrate digestion
  • weak contractions propel the food occasionally to the caudad region
  • gastrin decreases the rate of contractions so there is little stomach emptying
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the mechanical characteristics of the caudad?

A
  • contractions are strong, phasic and intermittent
  • slow waves occur in the caudad region at a rate of 3 slow waves per minute
  • contents are propelled from the midstomach to the gastroduodenal junction towards the pylorus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How does the chyme leave the stomach?

A
  • waves reach threshold, they cause peristaltic contraction that moves towards pyloric sphincter so a small volume of chyme moves out of the stomach
  • slow wave reaches the pylorus before the peristalsis with the food so that the chyme bangs against the constricted sphincter which is retropulsion (mixes chyme)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the gastric factors that control stomach emptying?

A

Gastric: distension (increased stretch of smooth muscle, intrinsic nerve plexus stimulation and vagus nerve activity and gastrin release) and consistency of chyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the duodenal factors that control stomach emptying?

A

Duodenal:

  • duodenum delays emptying by neuronal (enterogastric reflex) and hormonal responses (release of enterogastrones eg CCK to inhibit stomach contraction)
  • fat presence (fatty acids and glycerol delay stomach emptying)
  • acid (must be neutralised for pancreatic enzymes to work) - hypertonicity (solution must not be hypertonic as water would be drawn out of the blood)
  • distension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How can the stomach be functionally divided in terms of secretions?

A
  • oxyntic (funds and most of body)

- pyloric gland area (distal dory and antrum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the secretions in the pyloric gland area of the stomach?

A

G cells (secrete gastrin) and D cells (secrete somatostatin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the secretions in the oxyntic area of the stomach?

A

parietal cells (HCl, intrinsic factor and gastroferin), chief cell (pepsinogen) and enterochromaffin-like cell (histamine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What substances promote HCl secretion in the stomach?

A

histamine

gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What does somatostatin do in the stomach?

A

inhibits HCl secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What do intrinsic factor and gastroferrin do in the stomach?

A

bind vitamin B12 and Fe2+ respectively to give absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How is HCl produced?

A

H+ actively pumped out by ATPase

Cl- leaves by CFTR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What three stimuli cause acid secretion from the parietal cell?

A

ACh
Gastrin
Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

At rest, where are the H+ pumps in the stomach?

A

H+ pumps are not inserted in the apical membrane of the parietal cell, they are in intracellular structures called tubular vesicles so are inactive
They secrete protons at the canalicular membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the three phases of gastric secretion?

A
  • cephalic phase: before the food reaches the stomach, the stomach is preparing
  • gastric phase: physical and chemical mechanisms when food is in the stomach
  • intestinal phase: chyme enters the upper small intestine causing weak stimulation of gastric secretion after food has left stomach via neuronal and hormonal mechanisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What happens in the cephalic phase of gastric secretion?

A
  • stimulation from food leads to vagal activation
  • enteric neurones are stimulated
  • increased GRP so G cells make gastrin
  • increased ACh to ECL cell makes histamine and D cell makes less somatostatin (leading to more gastrin)
  • these all lead to more HCl secretion form parietal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What happens in the gastric phase of gastric secretion?

A
  • distension is detected by sensory neurons (mechanoreceptors) so enteric neurons activates to increase ACh and activates G cells
  • protein digestion products activate G cell
  • so more acid from parietal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is involved in the process of inhibition of gastric secretion?

A
  • Cephalic phase: vagal nerve activity decreases stops acid secretion
  • Gastric phase: antral pH falls when food leaves, release of somatostatin from D cells and there is decreased gastrin secretion, also prostaglandin E2 is always secreted and reduces histamine and gastrin-caused HCl secretion
  • Intestinal phase: factors that reduce gastric motility also reduce gastric secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the ways and drugs that reduce acid secretion?

A
  • Inhibiting the proton-pump
    E.g omeprazole
  • Histamine H2 receptor antagonists block competitively so less histamine
    Eg ranitidine
  • NSAIDs block irreversibly cyclo-oxygenase so there is less PGE2 synthesised
    Eg aspirin
  • Muscarinic receptor antagonists block competitively so less ACh
    Eg pirenzepine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What helps protect the stomach mucosa?

A
  • mucous cells form gel layer
  • bicarbonate is secreted to make pH gradient
  • PGE2 and PGI2 reduce acid secretion, increase mucus and bicarbonate and increase mucosal blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What bacteria forms peptic ulcers and can this be treated?

A

H.pylori

reducing acid secretion, increasing mucosal resistance and eradicating H.pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What drug can cause peptic ulcers and how does it doe this?

A

NSAIDs reduce prostaglandin formation and trigger gastric ulceration and bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How can you prevent NSAIDs forming peptic ulcers?

A
  • stable PGE1 analogue called misoprostol

- inhibits basal and food-stimulated gastric acid formation and maintains secretion of mucus and bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the mechanisms of drugs that reduce acid secretion?

A
  • Irreversible inhibition of proton-pump
  • Competitive antagonism of histamine receptors
  • Competitive antagonism of M1 and M3 ACh receptors
  • Antagonism of gastrin receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are drugs that reduce acid secretion used to treat?

A

peptic ulcer, gastro-oesophageal reflux disease and acid hypersecretion diseases (Zollinger-Ellison syndrome or Cushing’s ulcer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What do proton-pump inhibitors do?

A
  • inhibit active proton pump
  • form in an acidic environment
  • goes back to stomach (after systemic circulation) and enters parietal cells to enter canaliculus and irreversibly inhibits the proton pumps in the canalicular membrane
  • Eg omperazole
  • must be administered when proton pumps are active, one hour before breakfast, full effect is achieved after repeat dosing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What do histamine receptor antagonists do?

A
  • Eg ranitidine and cimetidine
  • Act as competitive antagonists of H2 receptors and completely block the histamine-mediated component of acid secretion and reduce secretion by gastrin and ACh
  • Used for peptic ulcer and reflux oesophagitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are examples of mucosal strengtheners and how do they work?

A
  • Sucralfate- requires an acid environment, binds to ulcer base, increases mucosal blood flow, mucus, bicarbonate and prostaglandin production
  • Bismuth chealate- mucosal strengthening action and is toxic to H. pylori so is used with antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What does the small intestine receive?

A
  • chyme
  • pancreatic juice form the pancreas
  • bile from the gallbladder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the forces that move chyme in small intestine?

A

segmentation, peristalsis and a migrating-motor complex

76
Q

What are the hormones secreted from the small intestine and what do they do?

A
  • Gastrin: acid secretion and growth of gastric mucosa
  • Secretin released in response to H+ and fatty acids in lumen: promotes secretion of pancreatic and biliary HCO3-
  • Cholecystokinin (CCK) released in response to nutrients: inhibits gastric emptying, causes secretion of pancreatic enzymes, relaxation of sphincter of Oddi and contraction of gallbladder so bile enters duodenum
  • Glucose-dependent insulinotropic peptide: stimulates release of insulin from pancreas and inhibits gastric emptying
  • Glucagon-like peptide-1: stimulates insulin secretion, inhibits glucagon secretion and decreases gastric emptying
  • Motilin: initiates the migrating motor complex
  • Ghrelin: stimulates appetite
77
Q

What do juices from the small intestine contain?

A
  • mucus from goblet cells

- aqueous salt from crypts of Lieberkuhn

78
Q

What is segmentation of the small intestine triggered by?

A

distension in the fed state but by gastrin from the stomach in the fasting state which is the gastroileal reflex

79
Q

What is the migrating motor complex?

A

a strong wave that passes slowly over entire small intestine, this is triggered by motilin and is suppressed by gastrin and CCK, inhibited by feeding

80
Q

What is in the pancreatic secretions?

A
  • Endocrine: insulin and glucagon into the blood

- Exocrine: digestive enzymes, aqueous NaHCO3- solution secreted to the duodenum collectively as pancreatic juice

81
Q

What does the pancreatic secretion act to do?

A

neutralises acidic chyme with bicarbonate to provide the best pH for pancreatic enzyme function and to protect mucosa from acid

82
Q

What are the main pancreatic enzymes?

A
  • proteases
  • amylases
  • lipases
83
Q

How is pancreatic secretion controlled?

A
  • Cephalic: mediated by vagal stimulation of acinar cells
  • Gastric: gastric distention causes vagovagal reflex so parasympathetic stimulation of acinar and duct cells
  • Intestinal: acid increases amount of secretin so increased aqueous NaHCO3, fat and protein increases CCK so increased secretion of digestive enzymes
84
Q

What are luminal and membrane digestion?

A
  • luminal is mediated by pancreatic enzymes secreted into the duodenum
  • membrane is mediated by enzymes situated at brush border of the epithelial cells
85
Q

What is absorption?

A

products of digestion crossing both the apical and basolateral membranes of the enterocytes in the intestinal epithelium

86
Q

How are carbohydrates broken down into a size that can be absorbed?

A
  • must be a monosaccharide to be absorbed
  • alpha ampfhylase breaks down into oligosaccharides in intraluminal hydrolysis
  • lactase, maltase and sucrase-isomaltase form the monosaccharides
87
Q

What type of enzyme is alpha amylase?

A
  • endoenzyme

- breaks down lineal alpha-1,4 linkages so no end bonds or branch bonds

88
Q

What does isomaltase break?

A

1,6 branching chain bonds

89
Q

What is lactase persistence?

A

being able to digest lactase

90
Q

What is lactose intolerance and what can it result from?

A

inability to digest lactose and can result from primary lactase deficiency, secondary lactase deficiency or congenital lactase deficiency

91
Q

What happens if a lactose intolerant patient consumes lactose?

A
  • short-chain fatty acids, hydrogen, carbon dioxide and methane are produced
  • these cause bloating, abdominal pain and flatulence
  • undigested lactose causes acidification of the colon and an increased osmotic load
92
Q

How are monosaccharides absorbed?

A
  • in duodenum and jejunum across two membranes
  • glucose and galactose are absorbed by secondary active transport mediated by SGLT1
  • fructose absorbed by facilitated diffusion by GLUT5
  • exit out of cells for all monosaccharides is by GLUT2
93
Q

How does SGLT1 work?

A
  • alternating access model

- glucose binds and unbinds depending on the binding of sodium ions

94
Q

How is protein digested in the stomach?

A

by pepsin which is an andopeptidase

95
Q

How is protein digested in the duodenum?

A 
- by endo and exo peptidases from pancreas:
= trypsin (endo)
= chymotrypsin (endo)
= elastase (endo)
= carboxypeptidase A (exo)
= carboxypeptidase B (exo)
96
Q

What are the other types of peptidases?

A
  • brush border can be endo or exo (amino or carboxypeptidases) and have affinity for larger oligopeptidases
  • cytoplasmic peptidases primarily hydrolyse di and tri peptides
97
Q

How do amino acids get absorbed in the small intestine?

A
  • transported with sodium into cell by secondary active transport
  • across basolateral membrane with sodium-potassium pump making the gradient
98
Q

How do larger peptides get absorbed in the small intestine?

A
  • moved by PepT1 with H+ by secondary active transport
  • hydrolysis in cell and amino acids are released as normal
  • sodium-hydrogen pump makes the gradient
99
Q

Where are bile salts released into?

A

into duodenum from gall bladder in response to CCK

100
Q

What does failure to secrete bile salts result in?

A

lipid malformation and secondary vitamin deficiency due to failure to absorb fat soluble vitamins

101
Q

What is the problem with bile salts emulsifying lipids and how is this overcome?

A

increase surface area but block enzyme access so colipase is needed to bind them together and allow lipase to access triglyceride

102
Q

What is colipase secreted as?

A

secreted as inactive procolipase which is activated by trypsin

103
Q

How are mixed micelles formed?

A
  • droplets of fat are stabilised by adding a coat of amphiphilic molecules
  • droplets become smaller to eventually form mixed micelle
104
Q

How does the stomach contribute to lipid digestion?

A

secretes gastric lipase in response to gastrin from chief cells (only important in pancreatic insufficiency and infants)

105
Q

What does pancreatic lipase do and require to work?

A
  • released from acing cells and stimulated bile flow

- full activity requires: colipase, alkaline pH, Ca2+, bile salts and fatty acids

106
Q

What does pancreatic lipase break down lipids to form?

A

2-monoacylglycerol and free fatty acids

107
Q

How is cholesterol absorbed?

A

mediated by NPC1L1 which binds it

108
Q

What does the drug Ezemtimibe do and what is it used to treat?

A

binds to NPC1L1 so there is no internalisation and absorption of cholesterol so is used with statins to treat hypercholesterolaemia

109
Q

How are chylomicrons formed?

A

long chain fatty acids and monoglycerides are resynthesises din the cells in the ER into triglycerides and are then made into chylomicrons

110
Q

How does the mixed micelle enter the cell?

A

makes contact with the apical membrane and diffuses across the membrane

  • short and medium fatty acids diffuse through enterocyte and then through basolateral and into capillaries
  • long chain are resynthesises to triglycerides in ER and are then made into chylomicrons
111
Q

What happens to the chylomicrons in the cells?

A

leave by exocytosis and enter the central lacteal

112
Q

How are calcium ions moved into the cells?

A
  • passive or active
  • calcium channels move in across apical
  • calciumbinds to ferine molecule and taken out by active transport of calcium or by calcium.sodium exchanger
113
Q

In what form is iron absorbed?

A

as ferrous (Fe2+) not ferric

114
Q

How are fat-soluble vitamins absorbed?

A

requires bile secretion as they are incorporated into micelles then into chylomicrons and into lymphatic system

115
Q

Why does there need to be a complex way to absorb B12?

A

it is only minutely in the diet but is necessary for life

116
Q

What is the structure of the longitudinal smooth muscle in the large intestine?

A

not continuous but is three stands called teniae coli but circles internal and external anal spincters at rectum

117
Q

What muscle forms the internal and external anal sphincters?

A

internal is smooth muscle

external is skeletal muscle

118
Q

What are haustra?

A

sac-like bulges in the large intestine which change shape in a living person

119
Q

What regulates the ileocaecal valve?

A

regulated by the gastroileal reflex and gastrin and CCK, permits movement into the caecum

120
Q

What affects the contraction and relaxation of the ileocaecal valve?

A
  • relaxes in response to distention of the duodenum
  • contracts in response to distention of the ascending colon
  • under control of vagus nerve, sympathetic nerves, enteric neurones and hormonal signals
121
Q

What connects the caecum and the appendix?

A

appendiceal orifice

122
Q

What does the colon absorb?

A

sodium
choloride
water
short chain fatty acids

123
Q

What does the colon secrete?

A

K+
HCO3-
mucus

124
Q

What is the function of the different parts of the colon?

A
  • ascending and transverse do fluid reabsorption and bacterial fermentation
  • descending and sigmoid colon do final drying and storage
125
Q

What is the more microscopic structure of the colon?

A

colonic folds, crypts, microvilli to increase surface area

126
Q

What do the cells of the colon do?

A
  • colonocytes mediate electrolyte absorption so drives absorption of water
  • crypt cells are involved in ion secretion
  • goblet cells are involved in mucus (contains glycosaminoglycans) secretion and trefoil proteins
127
Q

What enhances the absorption of sodium and secretion of potassium in the large intestine?

A

aldosterone

128
Q

What are the main patterns of motility in the large intestine?

A
  • haustration
  • peristaltic propulsive movement
  • defecation
129
Q

What does haustration involve?

A
  • non-propulsive movement

- haustra are caused by alternating contraction of circular muscle and slows movement of contents of large intestine

130
Q

What does peristaltic propulsive movement involve?

A
  • 1-3 times a day
  • triggered by a meal via gastrocolic response involving gastrin and extrinsic nerve plexuses
  • mass movement to rectum triggers the defecation reflex
131
Q

What does defecation involve?

A
  • rectum fills:
  • 1) rectum stretch receptors activated, activation of afferents to spinal cord and then parasympathetic efferents so contraction of smooth muscle of sigmoid and rectu, relaxing of internal anal sphincter then either relaxation or contraction of external anal sphnicter
  • 2) rectum stretch causes activation of afferents to brain then efferents to spinal cord giving same outcomes
132
Q

What is the function of the bacteria in the colon?

A
  • increase intestinal immunity
  • promote motility
  • synthesise vitamin K2 and free fatty acids
  • activate some drugs
133
Q

Where does gas in the GI tract come from?

A

swallowed air

bacteria in the colon which attack carbohydrates that are indigestible to humans

134
Q

What are the causes of constipation?

A
  • not defecating
  • decreased colonic motility
  • obstruction of faecal movement
  • paralytic ileum after abdominal surgery
  • impairments of motility/defaecation reflex sue to a lack of enteric nervous system (Hirschprung disease)
135
Q

What are the symptoms of constipation and what are they caused by?

A
  • malaise
  • abdominal pain
  • headache
  • loss of appetite
    all caused by prolonged colonic distention
136
Q

What is the difference between laxatives and purgatives?

A

laxatives are used to treat constipation but purgatives are used to cause a purging of the entire tract to clean the vowels before surgery or endoscopic procedure

137
Q

When are both laxative and purgatives completely contraindicated?

A

when there is a physical obstruction of the bowel

138
Q

What do laxatives do and when should they be used?

A
  • increase peristalsis
  • soften faeces
  • stimulate enteric nervous system
  • overused can cause atonic colon
  • should be used when straining is painful or damaging, to purge bowel or to treat drug-induced constipation
139
Q

What are the four main types of laxatives and purgatives?

A
  • bulk laxatives
  • osmotic laxatives
  • stimulant purgatives
  • faecal softeners
140
Q

What do bulk laxatives do ?

A
  • indigestible carbohydrate
  • given orally
  • increase bulk
  • retain H2O
  • increase peristalsis
    eg methylcellulose
141
Q

What do osmotic laxatives do?

A
  • poorly absorbed solutes
  • slow acting if given orally compared to rapidly when given rectally
  • increase bulk, water and peristalsis
    eg magnesium sulphate/hydroxide orally or sodium citrate rectally
142
Q

What do stimulant purgatives do?

A
  • stimulates enteric nervous system to increase frequency and force of peristalsis
    eg bisacodyl orally/ suppository or sodium picosulphate
143
Q

What do faecal softeners do?

A

detergent-like action to lubricate stool

eg decussate sodium orally or arches oil in an enema

144
Q

What are IBS and IBD?

A
  • IBS is bouts of diarrhoea, constipation or abdominal pain

- IBD can affect entire gut (Chrohn’s) or just colon (ulcerative colitis)

145
Q

What is IBS treated with?

A

treatment is symptomatic with diet change, anti-diarrheals, antispasmodics or laxatives as required

146
Q

What is IBD treated with?

A
  • glucocorticoids for acute attack not long term eg prednisolone
  • aminosalicylates for maintenance eg -salazine
147
Q

How is water absorbed from the GI tract?

A
  • passive

- driven by the movement of solutes (especially Na+) from lumen to bloodstream

148
Q

What are the main ways in which sodium ions move in the GI tract to cause water movement?

A
  • sodium/glucose cotransport
  • sodium/amino acid cotransport
  • sodium/hydrogen exchange
  • epithelial sodium channels
  • parallel sodium/hydrogen and chloride/bicarbonate exchange
149
Q

What are the two mechanical ways that water can move into blood from GI tract?

A

transcellular

paracellular

150
Q

What is the mechanism of sodium/glucose and sodium/amino acid cotransport?

A
  • happens in the jejunum

- both are secondary active transport

151
Q

What is the mechanism of sodium/hdrogen ion exchange?

A
  • jejunum at both apical and basolateral membranes
  • NHE2 and NHE3 move Na+
  • exchange at apical end is stimulated by alkaline lumen
152
Q

What is the mechanism of parallel sodium/hydrogen and chloride/bicarbonate exchange?

A
  • occurs in interdigestive period
  • in ileum and proximal colon
  • absorption is electoneutral
  • regulated by cAMP, cGMP and Ca2+ which all reduce NaCl absorption
  • reduction in NaCl is a cause of diarrhoea
153
Q

What is the mechanism of epithelial Na+ channels?

A
  • ENaC mediate electrogenic Na+ absorption is the distal colon
  • important in Na+ conservation
  • increased by aldosterone which opens channels, puts more in membrane and increases synthesis of ENaC and sodium-potassium pump
154
Q

How does Cl- absorption occur?

A

passively

via transcellular or paracellular routes

155
Q

What is the driving force of Cl- movement in the small intestine?

A

lumen negative potential due to Na+ movement

156
Q

What is the driving force of Cl- movement in the large intestine?

A

lumen negative potential due to electrogenic movement through ENaC

157
Q

What are the other methods of chloride movement in the tract?

A
  • chloride/hydrogen carbonate exchange

- sodium/hydrogen and chloride/hydrogen carbonate parallel exchange

158
Q

Where does chloride secretion occur cellularly?

A

from cell in crypts not villi

159
Q

What are the three chloride movement processes in the basolateral membrane?

A
  • sodium/potassium pump
  • sodium/potassium/chloride co-transporter
  • potassium channels
160
Q

How does chloride move into the lumen?

A

CFTR channels on apical membrane

161
Q

How is CFTR activated?

A
  • bacterial enterotoxins
  • hormones
  • immune cells
  • laxatives
162
Q

What does activation of CFTR cause?

A
  • generation of second messengers including cAMP, cGMP and Ca2+ (causes secretory diarrhoea)
163
Q

What are the causes of diarrhoea?

A
  • Impaired absorption of NaCl: congenital, inflammation, infection or excess bile acid in colcon
  • Non-absorbable solutes in intestinal lumen (eg lactase deficiency)
  • Excessive secretion eg cholera
  • Hypermotility
  • Other causes include: infectious agents, chronic disease, toxins, drugs and psychological factors
164
Q

What can diarrhoea result in?

A

can involve small or large intestine, can result in dehydration, metabolic acidosis and hypokalaemia and may be fatal

165
Q

What is the treatment of sever diarrhoea?

A

maintenance of fluid and electrolytes, use of anti-infective agents and use of non-anti-microbial antidiarrheal agents

166
Q

What does rehydration therapy for diarrhoea exploit?

167
Q

What are the anti-motility agents used in diarrhoea and how do they act?

A
  • codeine, diphenoxylate and loperamide
  • inhibit enteric neurons, decrease peristalsis, increase fluid absorption, constrict sphincters and increase the tone of the large intestine
168
Q

What are the main functions of the liver?

A
  • metabolism of carbohydrate, fat and protein
  • deactivation or inactivation of hormones
  • storage
  • synthesis of proteins
  • protection
  • detoxification
169
Q

How does the liver help with metabolism?

A
  • Carbohydrate- convert different glucose units
    • Fat- processing chylomicron remnants, synthesize lipoproteins and ketogenesis
  • Protein- plasma protein synthesis, transamination and deamination of amino acids and conversion of ammonia to urea
170
Q

How does the liver contribute to the deactivation of hormones?

A

Deactivated: insulin, glucagon, ADH or steroid
Activated: thyroid and vit D

171
Q

How does the liver contribute to storage?

A

fat and water soluble vitamins, iron, copper and glycogen

172
Q

What proteins does the liver produce?

A

coagulation factors, albumin, complement, apolipoproteins and carrier proteins

173
Q

How does the liver act to protect?

A

Kupffer cells and production of immune factors

174
Q

What does the liver produce to help with detoxification?

A

Endogenous and exogenous substances

175
Q

What is in primary juice?

A

primary bile acids, electrolytes, lipids, IgA and bilirubin

176
Q

What is cholelithiasis and the treatment for it?

A

gallbladder stones forming which can be treated with laparoscopic cholecystectomy, ursodeoxycholic acid (dissolves small stones)

177
Q

What is biliary colic treated with?

A 
pain meds
(not morphine as it constricts sphincter)
178
Q

What is bilary spasm treated with?

A

atropine or GTN

179
Q

What happens with bile before during and after a meal?

A
  • Between meals: bile is stored and concentrates in the gall bladder
  • During a meal: chyme makes gall bladder smooth muscle contract and bile goes into duodenum
180
Q

What does bile do?

A

assists in micelle formation, neutralisation of chyme, pH adjustment and protection of the mucosa

181
Q

How is bile reabsorbed?

A
  • reabsorbed by active transport in the terminal ileum and undergoes enterohepatic recycling
  • primary bile acid form secondary bile acids which are returned to the liver
182
Q

What are resins?

A

act by binding to bile acids do they aren’t reabsorbed, converts cholesterol to bile acids and increases LDL receptor expression

183
Q

What are resins used to treat and what are the side effects?

A
  • used in hyperlipidaemia, cholestatic jaundice and bile acid diarrhoea
  • can cause diarrhoea
184
Q

When does hepatic encephalopathy occur?

A

detoxification of ammonia to urea fails so it becomes toxic

185
Q

What is the treatment for hepatic encephalopathy?

A
  • lactulose which acidifies the stool so ammonium is made

- antibiotics which suppress flora and inhibit ammonia generation

My Gastrointestinal (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions