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growth, development, ageing, nutrition > gastrointestinal tract > Flashcards

gastrointestinal tract Flashcards

1
Q

What does the GI tract consist of?

A

Alimentary canal and accessory organs

Mucosa- epithelium, lamina propria, muscularis mucosae
Submucosa- glands
Muscularis- circular/longitudinal muscle layer
Serosa- c.tissue layer, peritoneum

+ ducts, lymph nodes, good blood supply, nervous tissue

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2
Q

What is the intramural plexus?

A

Myenteric plexus

Submucosal plexus

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3
Q

What does the GI tract do?

A

Breaks down ingested food into small molecules to be taken into body tissue by digestion (chemical/mechanical) and absorption

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4
Q

What are the normal transit times in the GI tract?

A 
Mouth- 1 min
Oesophagus- 10s
Stomach- ~2hrs
Small intestine- 3-6hrs
Large intestine- 1-2 days
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5
Q

What is swallowing?

A
  1. Oral phase (voluntary)
    Tongue compresses bolus against hard palate, respiration inhibited, retraction of tongue forces bolus into pharynx
  2. Pharyngeal phase (involuntary)
    Bolus pushed from pharynx into oesophagus, soft palate reflected backwards closing nasal pharynx
  3. Oesophageal phase (25cm by 2cm)
    Gravity + upper sphincter relaxes and bolus moved into oesophagus, vagus nerve triggers start primary peristaltic wave, enteric nervous system mediates secondary peristaltic wave, lower oesophageal sphincter relaxes (prevents reflux)
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6
Q

What is the stomach?

A

Two openings-
Oesophagus and duodenum

4 regions-
Fundus, cardia, body, pylorus

  1. Reservoir- stores food
  2. Prep chamber- begins mechanical digestion
  3. Emptying regulator- feedback response from duodenum, controls rate of release of calorie, H+ and particles into duodenum
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7
Q

What are the gastric functions?

A

Motility-
~gastric accom- temporary storage
~trituration- dissolve/mix/grind
~gastric emptying- controls delivery to small intestine

Digestion- initiates via gastric juice

Protection- from foreign invasion/mechanical abrasion/prevents autodigestion

Absorption- alcohol and fat soluble drugs

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8
Q

What is stomach lining composed of?

A 
Rugae (allowing stretch)
Lamina propria (ducts from gastric glands to pits on surface for gastric juice)
Muscularis mucosae
Submucosa
Muscularis externa
Peritoneum (serosa)
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9
Q

What is gastric juice?

A

Water ions
HCl-
~low pH, prevents bacterial growth, catalyses cleavage of pepsinogens to pepsin
Pepsinogens
Intrinsic factor (glycoproteins binds to Vit B12 to allow digestion in the ilium)
Mucus
Gastric (hormone produced from G cells, regulates acid secretion)

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10
Q

What are pepsinogens?

A

Proenzyme of pepsin

Breaks proteins into peptides

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11
Q

What are the gastric glands?

A

Cardiac glands- mucus/HCl
Oxyntic glands (acid secreting)- mucus/HCl/pepsinogens/intrinsic factor (aka parietal)
Pyloric glands- mucus/pepsinogens

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12
Q

What is the gastric secretory response?

A

Cephalic phase- sight/smell/thought of food triggers secretion and motility via vagus nerve (parasympathetic)

Gastric phase- physical presence of bolus triggers long (vagal) and short (myentric) reflexes causing peristalsis and gastrin release

Intestinal phase- intestinal gastrin release in response to distention of duodenum +/ products of protein digestion, hormones released to inhibit motility

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13
Q

What is the small intestine composed of?

A

Duodenum
Jejunum
Ilium

Highly coiled, folded and long
Most absorption takes place here

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14
Q

What are the three strata of folding?

A

Plicae- x5
Villi- x10 (light microscope)
Microvilli- x600 (electron microscope)

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15
Q

What does the large intestine consist of?

A

Chyme passes through (water/salt/sugar/vitamins)
~cecum
~ascending colon
~transverse colon
~descending colon
~sigmoid colon
Tenia coli- 3 bands of longitudinal muscle
Haustra- pockets undergoing segmentation (mixing of contents)
Sphincters- internal and external
Tightly packed mucosa- goblet cells- mucus
Peyers patches- local immune protection
Lots of bacteria- fermenting fibre and communicating w host cells

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16
Q

What are the control mechanisms?

A
  1. Autonomic nervous system
  2. Enteric nervous system
  3. Gut peptides (paracrine and endocrine)

-long and short reflexes, peristalsis and motility, secretion and absorption

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17
Q

How does the ANS play a role?

A 
Stimulates digestion- parasympathetic nerves (vagus and pelvic)
Inhibits digestion- sympathetic nerves
Speeds up and slows down
Flight or flight via rest and digest
Controls some secretions
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18
Q

How does the ENS play a role?

A 
Myenteric plexus and submucosal plexus
Sense luminal contents
Controls muscle and glands
100 million neurons
Contains sensory/motor/interneurone/muscle/glands
Motility and secretion
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19
Q

What are long reflexes?

A

External stimuli
Involves CNS
Alters activity of ENS
Causes changes in motility and secretion

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20
Q

What are short reflexes?

A

Internal stimuli
ENS
Local neural circuits
Cause changes in motility and secretion

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21
Q

What is Hirschprungs disease?

A

Partly/unformed ENS
Congenital disorder
Must be surgically removed

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22
Q

How do hormones play a role?

A

22 hormones secreted by enteroendocrine cells in mucosa

S- stomach, D- duodenum, J- jejunum, I- ilium, C- colon

Gastrin- SDJ
Secretin- DJI
Cholecystokinin- DJI
Glucagon-like- SDJIC
Somatostatin-like- SDJIC

Stimulated by chemical, osmotic and pH
Negative feedback mechanisms

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23
Q

What are enteroendocrine cells?

A

Single cells scattered throughout
Link between luminal contents and capillaries
Densely packed w vesicles
Sense contents and respond via release of hormones into bloodstream

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24
Q

What is the stomach motility like after a meal?

A
  1. Fasting state- quiescent
  2. Meal enters, lower oesophageal sphincter relaxes- fungus + body relaxes=accommodation
  3. Peristalsis- waves push towards pylorus, mixing occurs in antrum
  4. Antral systole- retropulsion pushes some contents back into body and some chyme into duodenum, pyloric sphincter also regulates
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25
Q

What hormones are released to inhibit gastric motility and why?

A

Gastroinhibitory peptide
Cholecystokinin (CCK)
Secretin

Protects small intestine from being overloaded
Keeps food in stomach long enough to be broken down efficiently

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26
Q

What is the rate of gastric emptying?

A

Liquids- 2-3 mins, 80% in half an hour

Solids- lag due to time to reduce particle size (1mm diameter), ~few hours

27
Q

What are peptic ulcers?

A

Break in mucosal barrier to expose underlying tissue to corrosive action (acid, proteolytic enzymes)

Symptoms- abdominal pain, bloating, nausea, vomiting, bleeding (haemorrhage and anaemia)

28
Q

How are peptic ulcers formed?

A

Endogenous-
~anxiety (parasympathetic output [more Ach, Gastrin] so more acid)
~stress (sympathetic output [more Ad] so less HCO3/mucus]

Exogenous-
~diet (alcohol [damages cells, stimulate parietal cell] and coffee [stimulate parietal cell])

Non-steroidal anti-inflammatory drugs (NSAIDs) eg. Ibuprofen
~limits prostaglandin production so less inhibition of acid

Helicobacter pylori- bacteria producing proteases and endotoxins which break down tissue and produce inflammatory responses

29
Q

What secretions come from accessory organs into the duodenum?

A

Pancreas (exocrine gland 85% [acinar cells], endocrine gland 2%[Islets of Langerhans])
Acinus releases water/ions, HCO3 (bicarbonate) and enzymes
Islets release alpha cells (glucagon) and beta cells (insulin)

30
Q

What is the pancreas composed of?

A 
Acinar cells- polarised epithelial cells
Centroancinar cells- mainly HCO3
Islets of Langerhans
Intercellular canaliculi
Intercalated ducts
Intralobular duct
31
Q

What do acinar cells consist of?

A 
Nucleus
Mitochondria
RER
Golgi body
Zygomen granules (vesicles with enzymes)
32
Q

What enzymes do the zymogen granules contain?

A 
Proteins digested by-
~Trypsinogen- trypsin
~Chymotrypsinogen- chymotrypsin
~Proelastase- elastase
~Procarboxypeptidase- carboxypeptidase

Fats digested by-
Lipases and phospholipases

Nucleic acids digested by-
Nucleases

Carbohydrates digested by-
Alpha-amylase

33
Q

What duodenal feedback mechanisms exist?

A

Cholecystokinin release into bloodstream in response to proteins and fat= pancreatic acinar cell secretion

Secretin release into bloodstream in response to pH<5= pancreatic centroacinar cell secretion (HCO3)

34
Q

Why is the liver important?

A

Protein synthesis- esp. albumin and clotting factors
Storage- triglycerides, glycogen and some vitamins
Gluconeogenesis- lipids/AAs into glucose
Toxins- conjugation and breakdown
Bile synthesis and secretion of bile acids and bilirubin

35
Q

What is bile composed of?

A

Water/ions- alkaline
Bile acids- digestion/absorption of fats and micelles formation
Proteins- antibacterial, protect against infection
Bile pigments- breakdown products of Hg (bilirubin)
Organic molecules- cholesterol, phospholipids etc

36
Q

What does the gall bladder do?

A

Reservoir, regulates delivery and alters bile composition

Absorption- concentrates bile (Na+, Cl-, H2O)
Secretion- neutralises and protects (H+, mucin)
Motor- expand to accommodate and contract to deliver bile, regulated by-
Ach (cephalic phase) 20%
CCK (intestinal phase) 80%

37
Q

How is bile delivery regulated?

A

Secretin- stimulates secretion

CCK- releases by relaxing sphincter of Oddi and contracting gall bladder

38
Q

What are gallstones?

A

Disruption of balance
Calcified stones of cholesterol, bilirubin and calcium
Cause sharp pain, infection and inflammation

Causes- genetics, body weight, decreased mobility of gall bladder, diet and other diseases such as liver cirrhosis or sickle cell anaemia

39
Q

What is the microvilli brush border?

A

Large surface area
Glycocalyx (unstirred layer) contains enzymes-
Maltase, lactase, sucrase, dipeptidases
Absorbed pancreatic enzymes

40
Q

How are carbs transported across the border?

A

Glucose/galactose carrier
~co transport- Na+ dependent via SGLT1
~energy required to maintain Na+ gradient

Fructose
~facilitated diffusion via GLUT2

Lead to capillaries to hepatic portal vein

41
Q

How are proteins digested?

A

Stomach- gastric pepsin turns it into polypeptides and small peptides

Duodenum- pancreatic proteases turns it into polypeptides, small peptides and AAs

Jejunum (brush border)- peptidases turns large peptides into small peptides and AAs

42
Q

How are proteins transported across the border?

A

Peptidase in border breaks down any large peptides
Carrier proteins take small peptides and AAs across via active transport
Intracellular proteases break down small peptides into AAs
The AAs enter capillaries via facilitated diffusion

43
Q

How are lipids digested?

A

Pancreatic lipase generate monoglycerides, fatty acids and glycerol
Bile salts emulsify fats
Micelles transported across glycocalyx

44
Q

How are fats transported across the border?

A

Intracellularly products are reconstituted and packaged into chylomicrons
These are exocytosed into the lateral space
These are diffused into lacteals which return to system circulation via thoracic lymph duct

45
Q

Why might malabsorption occur?

A

Absent or defective enzymes
Defects in transported proteins
Diseases/infections of small intestine

Symptoms- steatorrhea (frothy/greasy stool), diarrhoea, weight loss

Lactase deficiency- lactose intolerant
Coeliac disease- abnormal immune response to gluten, loss of mucosal epithelium
Pernicious anaemia- malabsorption of Vit B12 in ileum due to production of antibodies to intrinsic factors

46
Q

What are the main functions of the large intestine?

A

High mucus secretion to help passage of stool
Water reabsorption aided by Cl- absorption in exchange for HCO3- (osmotic gradient)
HCO3- buffers acid produced by bacterial fermentation

47
Q

What is the GI tract flora?

A

ORAL
Commensalism bacteria, pathogens eg. Porphyromonas gingivalis

STOMACH
Helicobacter pylori

GUT/LARGE INTESTINE 
10^14 microorganisms 
Primes gut immune system 
Fibre fermentation
Symbiosis between host and bacteria
Synthesis of essential nutrients- folic acid, Vit K
Aids absorption of Vit B12
48
Q

Why is dietary fibre important?

A

Regulates motility
~slows gastric emptying
~increase motility of colon-intestine

Absorption
~holds water
~slows absorption of nutrients

Colonic bacterial substrate

Prevents/treats constipation, haemorrhoids and diverticulosis

49
Q

What is gastrointestinal gas?

A

1-4 pints a day
Via swallowed air, neutralised acid or bacterial metabolism, diffusion from blood

Esp. Beans (stachyose), onions, cabbage, prunes and nuts

Components-
Hydrogen, methane (ammonia, hydrogen, sulphide, indole, skatole, volatile amines)

50
Q

What is excreted?

A 
Indigestible fibre
Bacteria
Inorganic material
Fat derivatives 
Desquamated cells
Mucus
51
Q

What is the normal balance between absorption and secretion like?

A

Volume moving from blood to gut lumen is less than lumen to blood
So absorption is greater than secretion

52
Q

What are the reasons for diarrhoea?

A
  1. Osmotic
    ~increased solutes in lumen- less water reabsorption
    ~poorly absorbed substrate
    ~malabsorption disorder eg. Lactose intolerance
2. Secretory
~increased secretion of water into lumen
~eg. cholera toxin- opens Cl- channel
~laxatives, hormones, drugs (antidepressants), caffeine
~bile acid malabsorption
  1. Inflammatory/infectious
    ~damages absorptive epithelium
    ~clostridium difficile
    ~invasive parasites
  2. Deranged motility
    ~altered transit time so less time for water reabsorption
    ~irritable bowel syndrome
53
Q

What is colon motility like?

A

The haustra form pockets that contract contents into the next pockets where mixing occurs
It can be pushed forwards and backwards

Fermentation and water absorption occurs

2-3 times a day a gastro-colic response happens-
~mass movement of matter into aboral end of colon for defecation

54
Q

How is defecation/emptying regulated?

A

Faeces in rectum cause distension
Stretch receptors are activated and afferent signals are sent to the spinal cord

Voluntary somatic motor nerves are inhibited allowing external anal sphincter to relax

Autonomic symp/para symp stimulate contraction of rectum and relaxation of internal anal sphincter

55
Q

What is continence, incontinence and defecation failure?

A

Continence- storage- rectal accommodation and sphincter contraction

Incontinence- pelvic floor damage, pudental nerve damage

Defecation failure- spinal injury, outlet obstruction (eg tumours)

56
Q

What is emesis?

A

Protective mechanisms to prevent damage to GI tract and ingestion of contaminated/toxic substances

Vomiting

57
Q

How are toxins detected?

A
  1. Pre ingestion- smell, sight, taste
  2. Pre absorption- toxin detection in lumen, mechanoreceptors and chemoreceptors trigger expulsion (vomiting)

Rapid before ends up in bloodstream

  1. Post absorption- chemoreceptive trigger zone, in postrema (in medulla oblongata) and outside blood brain barrier which samples blood toxins
    ~induces nausea to prevent further ingestion
    ~activates vomit centres
    —can be activated w emetic drugs
58
Q

What are some appropriate and inappropriate vomiting?

A

Food poisoning
Bowel obstruction
Bowel disease

Pregnancy
Motion sickness
Cancer therapy

59
Q

What is nausea?

A 
Pallor
Sweating
Salivation
Irregular breathing
Increased heart rate
Several increased force of retching
60
Q

How is nausea conducted in the GI tract?

A

Retrograde giant contractions into stomach
Proximal stomach relaxes to allow
Antral motility inhibited to prevent emptying
Saliva protects oral cavity/oesophagus
Deep inspiration
Glottis closure to protect airways
Air/saliva drawn into oesophagus- decrease oesophageal pressure
Soft palate elevated to prevent entry into nasopharynx
Expiration and diaphragm/abdominal contraction- increase intra abdominal pressure
Lower oesophageal sphincter relaxes
Contents pass into oesophagus
Upper oesophageal sphincter relaxes

61
Q

What is the vomiting centre?

A

Chemoreceptor trigger zone or direct nerve impulses

Inputs may be-
Higher CNS- pain, injury, sight, smell, fear, memory
Vestibular system- motion sickness

Via cranial nerve IX and X

Irradiance of abdomen- highly emetogenic, indicating that trigger lies within

62
Q

What are enterochromaffin cells?

A

Releases 5-HT (serotonin) in gut which activates 5-HT3 receptors on vagus nerve
This triggers emesis and also enters circulation and acts on chemoreceptor trigger zone

63
Q

How does anti cancer chemotherapy involve vomiting?

A

Anticipatory- conditioned
Acute- enterochromaffin cells release 5HT
Delayed- damage to epithelial/cell breakdown products evoke mediator release (5HT again)

64
Q

What are anti-emetics?

A

Block activation of vomiting centre
Ondanstron- 5HT3 antagonist- competes w 5HT

For motion sickness- antihistamines eg. hyoscine

growth, development, ageing, nutrition (40 decks)

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