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DEN203 > N- GI tract > Flashcards

N- GI tract Flashcards

1
Q

How long is the GI tract, oesophagus to rectum

A

8m

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2
Q

Function of GI tract?

A

Breaks down ingested food into small molecules which can be taken into body tissue. This is achieved by:

• Digestion

  • Chemical, secretion of enzymes
  • Mechanical, motility (mixing and grinding)

• Absorption
- Movement of small molecules across the gut wall and into the circulation

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3
Q

Small intest. transit time?

A

3-6 hours

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4
Q

Large intest. transit time?

A

1-2 days

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5
Q

What is deglutination

A

swallowing. Process by which food passes from mouth to stomach.

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6
Q

What are the 3 phases of deglutination?

A

1) Oral phase- voluntary
2) Pharyngeal phase- involuntary
3) 3- Oesophageal phase

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7
Q

What happens in the Oral phase

A

a. Tongue moves upwards- compress bolus against hard palate. Respiration inhibited
b. Retraction of tongue forces bolus into pharynx

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8
Q

What happens in the 2- Pharyngeal phase

A

c. Involuntary movement pushes bolus from pharynx into oesophagus
d. Soft palate reflected backward closing nasal pharynx

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9
Q

What happens in the 3- Oesophageal phase

A

e. Upper oesophageal sphincter relaxes and bolus moves into oesophagus
f. Start primary peristaltic wave (Vagal)
g. Secondary peristaltic wave (Enteric)
h. Lower oesophageal sphincter relaxes

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10
Q

What is the Oesophagus- muscular tube

A
  • 25cm in length
  • 2cm in diameter
  • Pharynx to stomach
  • Fast transport (10s)
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11
Q

Lower oesophageal sphincter function?

A

prevents reflux of material back into oesophagus

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12
Q

Stomach- J shaped organ
what are the openings?
What are the 4 regions?

A
  • 2 openings: Oesophagus and duodenum

* 4 regions: Fundus, Cardia, Body, Pylorus

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13
Q

Role of stomach?

A

store food and begin digestion (mechanical)

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14
Q

4 Stomach functions?

A
  1. Motility
    - Gastric accommodation- temporary storage reservoir
    - Trituration – Dissolve, mix and grind food particles
    - Gastric emptying - Control delivery to small intestine
  2. Digestion – initiate digestive process (proteins) via gastric juice
  3. Protection
    - Foreign invasion (acid/proteases)
    - Mechanical abrasion (mucus)
    - Prevents autodigestion (mucus)
  4. Absorption
    - Alcohol and fat soluble drugs (diffusion)
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15
Q

What is present in the Gastric juice?

A
  • Water and ions
  • HCl
  • Provides low pH (as low as 1 or 2!)
  • Prevents bacterial growth
  • Catalyses cleavage of pepsinogens to pepsin

• Pepsinogens

  • proenzyme of pepsin
  • Pepsin breaks down proteins into peptides

• Intrinsic factor

  • Glycoprotein
  • Binds to vitamin B12- allowing digestion in the ilium

• Mucus
- Protects gastric mucosa

• Gastrin

  • From ‘G cells’
  • Regulates acid secretion
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16
Q

Name the 3 gastric glands and what they release

A
  • Cardiac glands- Mucus and HCl
  • Oxyntic glands (acid secreting)- Mucus, HCl, Pepsinogen, Intrinsic factor
  • Pyloric glands- Mucus, pepsinogen
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17
Q

Name some cells of the stomach and what they produce/release

A

Mucus neck cells- mucus

Parietal cells- HCl and intrinsic factor

Chief cell- pepsinogen

Endocrine cells- G cells: gastrin to stimulate acid secretion and D cells: somatostatin to inhibit acid secretion

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18
Q

Gastric secretory response to a meal:

3 phases…

A
  • Cephalic phase 30%- sight, smell, thought of food triggers gastric secretion; instigated by vagal fibres
  • Gastric Phase 60%– food entering stomach stretches it (the stretch!); triggers secretion via long (vagal) and short (myenteric) reflexes.
  • Intestinal Phase 10%– intestinal gastrin release in response to distension of duodenum and/ or products of protein digestion
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19
Q

Small intestine, 3 regions:

A
  1. Duodenum
  2. Jejunum
  3. Ilium
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20
Q

Describe the SI

A
  • Highly coiled
  • 4-6 meters long
  • No definable junction
  • Highly folded- large SA
  • Most absorption takes place
  • Absorptive epithelium ( 3 orders/strata of folding increases the area available for absorption)
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21
Q

Large intestine, 5 regions:

A
  1. Cecum
  2. Ascending colon
  3. Transverse colon
  4. Descending colon
  5. Sigmoid colon
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22
Q

Describe the large intestine

A
  • 1.5m length
  • No nutrients in chyme (all have been absorbed?)
  • Removes water, salts, sugars and vitamins
  • Tightly packed mucosa- goblet cells for mucus secretion
  • Areas of lymphoid tissue- Peyers patches for local immune protection
  • Teeming with bacteria
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23
Q

Control mechanisms of the GI tract…

  • including long/ short reflexes,
  • peristalsis and motility,
  • secretion and absorption
A

There are three major control mechanisms: hormonal, paracrine, and neural.

  1. Autonomic nervous system
  2. Enteric nervous system
  3. Gut peptides
    • Paracrine
    • Hormonal
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24
Q

What is the ENS- Enteric nervous system?

A

Gut’s own NS.
2 nerve plexus in the gut wall.

  • 100 million neurons! As many as in the spinal cord
  • ‘senses luminal contents’ -controls muscle and glands
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25
Q

What is chyme?

A

Fluid that passes from the stomach to small intestine…

- Gastric juices + partly digested food

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26
Q

Long reflexes of the GI tract

A
  • External stimuli (i.e. sight and smell of food)
  • Involves CNS
  • Alters activity of ENS
  • Causes: changes in motility and secretion
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27
Q

Short reflexes of the GI tract

A
  • Internal stimuli (i.e. molecules in lumen)
  • ENS
  • Local neural circuits
  • Causes: changes in motility and secretion
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28
Q

what is Peristalsis and how is it controlled?

A
  • Movement through the GI tract - peristalsis

* Mediated by neurones in myenteric plexus…

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29
Q

What happens in peristalsis?

A

Distention by bolus of food (chyme) - stimulates peristalsis

  • Oral contraction
  • Aboral relaxation
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30
Q

What is Hirschprungs disease

A
  • Congenital disorder
  • All or part of colon has no innervation
  • 1:5000 children affected
  • Surgical removal of the colon
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31
Q

What are Enteroendocrine cells

A
  • Single cells scattered through the GI tract
  • Link between luminal contents and capillaries
  • Intestinal ‘taste’ cells
  • Densely packed with vesicles
  • Sense luminal contents and respond via release of peptide transmitters
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32
Q

Name some hormones secreted by Enteroendocrine cells in the mucosa

A
  • Gastrin
  • Secretin
  • Cholecystokinin
  • Glucagonlike
  • Somatostatin-like
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33
Q

Functions of the buccal cavity- Mastication

A
  • Teeth and tongue mechanically break down food and the addition of saliva results in a smooth soft bolus of food, lubricated and readily swallowed.
  • Muscles of mastication are- masseter, temporalis and the pterygoids-innervated by V3 of trigeminal (CNV).
  • Saliva contains alpha-amylase which begins breaking down starches in the bolus. Some people have more than other.
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34
Q

Stomach acts as:

3

A
  1. Reservoir- Store food
  2. Preparatory chamber – Breakdown injected materials
  3. Emptying regulator – Responds to feedback from duodenum. Controls rate of release of calorie, H+ and particles into the duodenum.
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35
Q

Stomach motility after a meal (4)

A
  1. Fasting state- quiescent
  2. Meal enters stomach
    o LOS relaxes- relaxation of fundus and body to allow accommodation
  3. Peristalsis begins
    o Begins in the middle- push towards the pylorus
    o Mixing occurs in antrum
  4. Retropulsion due to Antral systole
    o Peristaltic wave pushes contents back into body-
    o Some chyme into duodenum

Intestinal- arrival of chyme into first part of small intestine causes slowing down as it passes onto the next phase (feedback mechanism)

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36
Q

Rate of Gastric emptying for liquids, solids

A

Liquids- empty faster than solids – 2-3mins

Solids – lag due to time to reduce particle size (1 mm diam)

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37
Q

What are Gastric/ Peptic Ulcers

A

Break in mucosal barrier exposing underlying tissue to corrosive action (acid, proteases)

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38
Q

Symptoms of stomach ulcers

A

Abdominal pain
Bloating
Nausea/vomiting
Bleeding- haemorrhage and anaemia

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39
Q

Endogenous Factors of stomach ulcers

A 
> Anxiety 
	Parasympathetic output (Ach, Gastrin, acid
>Stress 
	Sympathetic output (Ad), HCO3/mucus
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40
Q

Exogenous Factors of stomach ulcers

A

> Diet
Alcohol - damages cells, stimulates parietal cell
Coffee – stimulates parietal cell

> Non-steroidal anti-inflammatory drugs (NSAIDs)
decreased prostaglandin production a and decreased inhibition of acid

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41
Q

Name the 3 accessory organs in the GI system

A

1- Liver: bile, exports to duodenum
2- Pancreas; makes pancreatic juices (digestive enzymes, bicarbonate ions)
3- Gallbladder; stores, concentrates and releases bile

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42
Q

Secretions into duodenum are from:

A
  • Gall bladder

- Pancreas (ducts)

43
Q

Pancreas is made up of 2 glands

A 
Exocrine gland (85%) – Acinus 
Endocrine gland (2%) – Islets of Langerhans
44
Q

What does the exo gland produce

A
  1. Water and ions
  2. Bicarbonate
  3. Enzymes –essential for normal digestion

Water, ions and bicarbonate neutralise duodenal contents to prevent damage and pH for enzymes.

45
Q

What does the endo gland produce

A
  • α cells – glucagon

* ß cells – insulin

46
Q

Pancreatic enzymes: Responsible for digestive function of pancreas. The major digestive step in the GI tract!

Those involved in Protein degradation:

A
  • Trypsinogen - trypsin
  • Chymotrypsinogen - chymotrypsin
  • Proelastase - elastase
  • Procarboxypeptidase – carboxypeptidase
47
Q

Some other pancreatic enzymes…

A

Other:
• Lipase and phospholipase- Fats
• Nucleases- Nucleic acids
• α-amylase- Carbohydrates

48
Q

How does the duodenum regulate this secretion from pancreas…

A
  • Nutrient levels in chyme

- HCl levels in chyme

49
Q

How does nutrient chyme affect feedback?

A

High protein and fat levels cause CKK release into blood stream.
- Pancreatic acinar cell secretion (produces enzyme rich fluid)

50
Q

How does HCl levels in chyme affect feedback?

A

If pH levels go below 5, Secretin released into bloodstream which causes
- Pancreatic ductal secretion

51
Q

Liver- functions? (metabolic and digestion!)

Name 5

A

Protein synthesis, particularly albumin and clotting factors (e.g. fibrinogen)

Storage
• triglycerides
• glycogen
• some vitamins (e.g. vitamin A)

Gluconeogenesis – conversion of lipids and amino acids to glucose

Toxins- changing the chemical structure
• Conjugation
• Breakdown

Bile - Synthesis and secretion of bile acids and bilirubin

52
Q

Bile secretion Production per day in ml?

A

250ml-1000ml per day!

Concentrated in the gall bladder for storage ( 15-60ml volume) …

53
Q

Main functions of bile (3)

A

1) Adequate pH
2) Facilitate fat digestion/ emulisification
3) Excretion of waste products (cholesterol)

54
Q

Composition of bile (5)

A
  1. Water and ions- alkali
  2. Bile acids- digestion and absorption of dietary fats (micelle formation) 70%
  3. Proteins- protect against infection
  4. Bile pigments- breakdown products of hemoglobin (bilirubin)
  5. Organic molecules
    • Cholesterol (4%)
    • Phospholipid- Lecithin (20%)
55
Q

Gallbladder function: Alters bile composition and delivery

A

Alters composition…

  • Absorption of Na, Cl, H2O
  • Secretion of H, mucin (neutralises)
  • Motor:
    o Interdigestive- storage of bile
    o Digestive- contraction, delivery of bile
56
Q

How is bile delivery controlled

A

Secretin: Stimulates secretion

CCK: Stimulates release of bile by:

  • Relaxing Sphincter of Oddi
  • Contracting gall bladder
57
Q

What are Gallstones

A

When the balance of components is disrupted- gallstones can form…
Calcified stones.
- Cholesterol, calcium, billirubin

58
Q

Symptoms of gallstones

A

Cause sharp pain,
infection
and inflammation (requires hospitalisation)

59
Q

Main causes of gallstones

A

1) Genetics
2) Body weight
3) Decreased mobility of gall bladder
4) Diet
5) Other diseases (cirrhosis, sickle cell(

60
Q

Describe the Small intestine

A
  • Highly coiled
  • 4-6 meters long
  • Highly folded- plicae
  • Large surface area – microvilli (brush border)
  • Key role in nutrient absorption
61
Q

What is the brush border of the SI

A
  • Large surface area
  • Glycocalyx (unstirred layer)

Brush border enzymes
• Additional surface for absorption
• Maltase, lactase, sucrase, dipeptidases
• Absorbed pancreatic enzymes

Final stages of CHO digestion

62
Q

Carbohydrate transport on SI membrane

A
  • Glucose/galactose carrier (Co transport, Na dependent… has a 2ndary AT protein)
  • Fructose- facilitated diffusion

Energy dependent!

-> CHO goes to capillaries by FD-> Hepatic portal vein

63
Q

Enzymes involved in Protein digestion

A

(stomach) Gastric pepsin
(duodenum) Pancreatic proteases
(brush border) peptidases

64
Q

Protein transport across SI brush border

A

Active transport into tissues
Carriers.
-> Facilitated diffusion into capillaries

65
Q

Enzymes involved in CHO digestion

A

• Brush border enzymes

  • Maltase, lactase, sucrase, dipeptidases
  • Absorbed pancreatic enzymes
66
Q

Lipid digestion enzyme

A

Lipase (pancreas)

67
Q

Break down of lipids ,.. products are:

A
  • Monoglycerides
  • Fatty acids
  • Glycerol
68
Q

How does lipid transport occur?

A

Fat transport occurs by membrane soluble diffusion
Membrane soluble diffusion

(Micelles - transport across unstirred layer)

69
Q

Malabsorbtion causes (3)

A
  • Absent or defective digestive enzymes
  • Defects in transporter proteins
  • Diseases or infections of small intestine
70
Q

Symptoms of malabsorption

A

– steatorrhea (frothy greasy stools),
diarrhoea,
weight loss

71
Q

Examples of diseases with malabsroption (3)

A
  • Lactase deficiency - lactose intolerance
  • Coeliac disease – abnormal immune response to gluten – loss of mucosal epithelium
  • Pernicious anaemia – malabsorption Vit B12 in ileum due to antibodies to intrinsic factor
72
Q

Main functions of large intestine…

A

High mucus secretion- goblet cell

No carrier mediated transport of nutrients (absorption by diffusion)

Efficient water reabsorption-Aided by Cl- absorption in exchange for HCO3-

HCO3- buffers acid produced by bacterial fermentation

73
Q

Bacteria in stomach

A

H pylori

74
Q

Bacteria in large intestine function=

A

Bacterial fermentation

  • Synthesise essential nutrients e.g. folic acid and vitamin K
  • Aid in absorption of vit. B12
75
Q

Dietary fibre function

A

Indigestible portion of plant food.

Motility
• Decrease gastric emptying-stomach
• Increase motility of colon- L. intestine

Adsorption
• Holds water
• Slows absorption of enzymes and nutrients

Colonic bacterial substrate (food!!)
• Prevention and treatment of constipation, hemorrhoids and diverticulosis
• Reduce risk of colon cancer?

76
Q

Source of Gastrointestinal gas

A

1-4 pints of gas/day

Sources:
• Swallowed air
• Result of neutralisation of acid or bacterial metabolism
• Diffusion from blood (small)

77
Q

What gases make up GI gas?

A

Hydrogen,
Methane

(ammonia, hydrogen sulphide, indole, skatole, volatile amines)

78
Q

Net absorption

- In the small intestine:

A

– 100% protein
– 100% digestible carbohydrate
– 95% fats
– Water, electrolyte (eg Na+, Cl-, Ca2+, Fe2+) vitamins (eg B12)

79
Q

Net absorption

- In the large intestine:

A

– Fermentation products, esp SCFA (eg butyrate)

– Water and electrolytes

80
Q

What is Excreted?

A 
indigestible fibre, 
bacteria, 
inorganic material, 
fat derivatives, 
desquamated cells, 
mucus
81
Q

What is diarrhoea?

A

• Increase stool volume or increased frequency of defecation

2 million die per year (e.g. cholera)

82
Q

What the 2 main diarrhoea mechanisms?

A
  • Osmotic

- Secretory

83
Q

What the 4 main diarrhoea mechanisms?

A
  • Osmotic
  • Secretory
  • Inflammatory/infectious
  • Deranged motility
84
Q

What is the osmotic diarrhoea mechanism?

A

Increased solutes in lumen causes less water reabsorption. This might be due to:
• Poorly absorbed substrate (i.e. sorbitol)
• Malabsorption disorder (lactose intolerance)

  • Can result in dehydration
  • Affects water balance
  • Main function of GI tract is to monitor water balance
85
Q

What is the Secretory diarrhoea mechanism?

A

Increased secretion of water into the lumen (secretion exceeds absorption).

  • Cholera Toxin- opening of Cl- channel, increase secretion of water
  • Laxatives, Hormones, Drugs (antidepressants), Caffeine
  • Bile acid malabsorption
86
Q

Cholera mechanism:

A
  • Binds to sugars
  • Enters
  • Binds to G protein
  • cAMP can activate lots of processes
  • Activates Chloride channel
  • Cl pumped out into gut
  • Movement of sodium ions into gut
  • Gradient
  • Water follows
  • Diarrhoea
87
Q

What is the inflammatory/infectious diarrhoea mechanism?

A

Pathogens breach and damage the absorptive epithelium

  • Clostridium difficile
  • Invasive parasites
88
Q

What is the deranged motility mechanism?

A

Altered transit time hence less time for water reabsorption

- Irritable bowel syndrome

89
Q

What are Segmented contractions?

A

99% of the time

  1. Retain material in the proximal colon: Fermentation, Water absorption
  2. Mixing contents
90
Q

What is the Gasto-colic response?

A

2-3 times per day

Mass movement of material into aboral end of colon- ready for defecation

91
Q

How is defecation controlled?

A

Faeces moved into the rectum, leading to distension. This activates stretch receptors- afferent signals to the spinal cord

92
Q

Nervous control of defecation:

A

If it is convenient to defecate, voluntary motor nerves are inhibited allowing the external anal sphincter to relax

Symp and Parasymp- Stimulate contraction of the rectum and relaxation of the internal anal sphincter

93
Q

Toxin Detectors= (3)

A
  1. Pre-ingestion
    Smell, sight, taste
  2. Pre-absorbtion
    Toxin detection in the lumen
94
Q

Emesis- protective mechanisms to prevent damage to GI tract and ingestion of contaminated/toxic substances (vomitting)

A

Pre-absorptive mechanisms in the gi tract provide for rapid elimination before the toxins enter the bloodstream.

95
Q

What is the 3. Post-absorption mechanism?

A

Chemoreceptive trigger zone - area postrema
Outside of blood brain barrier- samples toxins in the blood
Induces nausea to prevent further ingestion and activates vomiting centres.

Can be activated directly with drugs (emetics)

96
Q

Appropriate and inappropriate vomiting?

A

 Food poisoning
 Bowel obstruction
 Bowel disease

 Pregnancy
 Motion sickness
 Cancer therapy

97
Q

Features of nausea

A 
Vomiting preceded by nausea
•	Pallor
•	Sweating
•	Salivation
•	Irregular breathing
•	Increased heart rate 
•	Retching (several, increased force)

Way of body stopping you having any more food (of the bad type)

98
Q

GI motor actions that correlate with nausea :

A

GI motor events serve to return ingested material from the intestine to the stomach in preparation for expulsion.

The stomach relaxes and propulsive force comes from contraction of the diaphragm and abdominal muscles.

99
Q

Act of Vomiting- steps summary

A

1) GI smooth muscle - Relaxation of all areas from gastric body to upper oesophagus.
Violent contractions of gastric antrum

2) Respiratory system- Slow deep inspirations to decrease oesophageal pressure
3) Skeletal muscle- Contraction of abdominal muscle
4) Retching -Upper oesophageal sphincter remains closed
5) Vomiting-Upper oesophageal sphincter opened

100
Q

Origin of Sensory Triggers for vomiting

A

GI
• Distension (stomach and duodenum)
• Irritation of back of throat
• Chemical or toxin

Genitourinary system
• injury/infection

Hypothalamus/cerebellum
• stimulation or injury

Vestibular apparatus
• Motion sickness

Chemoreceptor trigger zone- 4th ventricle (brain)
•	Anaesthesia
•	Drugs
•	Radiation
•	Toxins
101
Q

Why does radiation therapy cause emesis?

A

Evidence for a GI trigger stems from both clinical and animal studies. radiation sickness due to cessation of mitosis shown by selective radiation of the abdomen. The inability of the mucosal cells to be replaced exposes the intestine to infection and inflammation which triggers vomiting

102
Q

Role of 5-HT in the emetic pathway?

5-HT3 on the chemoreceptor trigger zone

A

Radiation, injury, infection or toxins can stimulate the release of 5-HT from enterochromaffin cells in the gut, activating 5-HT3 receptors on Vagus nerve.

5HT also enters circulation and acts on chemoreceptor trigger zone.

Schematic showing mechanism of 5-HT in the emetic pathway.

103
Q

How do Anti-emetics work?

A

Work by blocking activation of the vomiting centre

• Chemoreceptor trigger zone – Ondanstron (5-HT3 antagonist)

5-HT3 receptor antagonists have revolutionized treatment of nausea and vomiting in cancer patients.

Chemoreceptor trigger zone contains 5HT3 receptors which respond to increased levels of circulating 5HT one of the causes being inflammation of the GI tract

DEN203 (11 decks)

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