Lecture 20 Flashcards

1
Q

What do we chew?

A

Mastification

  • Fruit and veg which have indigestible walls made of cellulose around the nutritious bits
  • Enzymes work on surface of food particles so smaller particles - larger SA:V
  • Finer particles of food prevent excoriation of the tract and increases the ease the food is emptied from the stomach
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2
Q

What are the steps of the chewing reflex?

A
  1. Presence of bolus in the mouth initiates reflex inhibition of the muscles of mastification - mandible drops
  2. This initiates the stretch reflex of the muscles of mastification that leads to rebound contraction and elevation of mandible and closure of the teeth
  3. This compresses the bolus against the lining of the mouth which inhibits the muscles of mastification once again allowing the mandible to drop and rebound another time
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3
Q

How much weight can incisors induce on food?

A

24kg

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4
Q

How much power does the molars have?

A

90kg

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5
Q

What can be noted about the reflex that causes chewing response in the mouth?

A

Almost impossible to reproduce artificially

Mandible produces circular movement

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6
Q

What is the reason why the jaw is powerful?

A

Masset’s muscle

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7
Q

What is the structure of the oesophagus?

A

20cm long
Upper third - skeletal muscle
Lower third - smooth muscle
Runs posterior to trachea, heart and lungs anterior to vertebrae and pierces the diaphram before entering the stomach

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8
Q

What is primary peristalsis?

A

Continuation of peristaltic wave that commences in oropharynx and spreads to oesophagus. Pharynx to stomach 8-10 seconds
Gravity assist: 5-8 seconds

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9
Q

What is secondary peristalsis?

A

Sweeps down any remaining food

Trigger is distension of oesophagus

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10
Q

What are the skeletal muscles of peristaltic waves controlled by?

A

Skeletal nerve impulses from CN IX and CNX

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11
Q

What is the smooth muscle for peristaltic waves controlled by?

A

CNX

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12
Q

What are diseases to oesophagus?

A

Barrett’s Oesophagus

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13
Q

What causes Barrett’s oesophagus?

A

Metaplasia (abnormal change) of cells lining the lower oesophagus

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14
Q

What can be seen in Barrett’s oesophagus?

A

Exposure to stomach acid in reflux oesophagitis
- Gastric acid (exposing oesophagus to HCl)
- damage genes
The normal stratified squamous epithelium is replaced by simple columnar epithelium with goblet cells (lower GIT cells)

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15
Q

What does Barrett’s oesophagus have a strong association with?

A

Oesophageal adenocarcinoma

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16
Q

What is oesophageal adenocarcinoma?

A

Virulent form of cancer
85% mortality rate
Barrett’s oesophagus is a premalignant condition
- younger people more affected by possibly due to junk food

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17
Q

What are symptoms of Barrett’s oesophagus?

A

None in themselves but in acid reflux

  • heartburn, dysphagia (inability to swallow properly)
  • Haemtemesis (vomiting blood), sub-sternal pain
  • Erosion of teeth due to acid exposure
  • -low pH exceeds solubility product of calcium phosphate
    • dissolves teeth
    • erosion (can be used to diagnose bulimia)
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18
Q

What can be used to managed Barrett’s oesophagus?

A

Proton pump inhibitor (prevents acid in oesophagus)
Endoscopic surveillance
Resection of the oesophagus

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19
Q

What does food do when it enters the stomach?

A

Forms concentric circles in the orad portion of the stomach

- old food by wall, newest food by opening of oesophagus

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20
Q

What is receptive relaxation?

A

Food stretches the stomach and a vagovagal reflex from the stomach to the brainstem and back to the stomach, reducing the muscular tone and allowing the stomach to bulge outwards and accommodate more food to a maximum of 0.8-1.5L

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21
Q

Where is gastric juice secreted from and where does it go?

A

Secreted by the gastric glands that cover almost the entire lumen of the stomach

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22
Q

What are G cells?

A

Enteroendocrine cells mostly found in base of gastric glands

23
Q

What do G cells secrete?

A

Gastrin

  • innervated by post-ganglionic fibers of the vagus nerve
  • releasing peptide during parasympathetic stimulation to stimulate secretion
    • start producing gastrin that is pushed into the stomach
24
Q

When does weak mixing waves churn the food and gastric secretions?

A

Beginning in mid/upper portion of the stomach. Reaching antrum in 15-20s

25
Q

Where are contractions most powerful?

A

Towards the pylorus

  • squeezing food out like a toothpaste tube
  • only few milimeters squirted out through pylorus into duodenum with each wave
26
Q

What are the steps of fluid moving from the stomach to the duodenum?

A
  1. Pylorus is slightly tonically contracted thus acting as a sphincter
  2. Open enough to allow fluids to pass directly into the duodenum
  3. But prevents food particles passing until they are well mixed and fluid-like
  4. Opening and closing of the pylorus is controlled by nervous and hormonal signals from the stomach and duodenum
27
Q

How is stomach emptying controlled?

A

Rate is never greater than the rate the chyme can be digested and absorbed in the small intestines

28
Q

Which part provides the most potent signals for stomach emptying?

A

Duodenum

29
Q

What are factors increasing rate of stomach emptying?

A

Increase food volume in the stomach - stretches the walls eliciting “myenteric reflexes”
Gastrin (hormone produced by G cells in the antral mucosa)
Mainly causes production of highly acidic gastric juice. Also mild stimulatory effects on motor activity of “pyloric pump”

30
Q

What are factors decreasing rate of stomach emptying?

A

Stretch of duodenal wall
- Directly inhibits pyloric pump via enteric nervous system in gut wall
- Via extrinsic nerves - prevertebral sympathetic ganglia - back to stomach via inhibitory sympathetic fibers
- Vagus nerves to the brainstem - Inhibit excitatory signals to the stomach through the vagi
(only a bit though…)

31
Q

What is the term to describe that increased volume of stomach caused by food DOES NOT cause increased pressure?

A

receptive relaxation

32
Q

What are peptic ulcers?

A

Damage to the wall of the stomach by stomach acid

33
Q

What are symptoms of peptic ulcers?

A

Gnawing, burning, upper abdominal pain. that worsens on eating (secreting more acid)
- can produce bleeding in the stomach or acute abdomen (stomach acid in all abdominal groups)
Indigestion “heartburn”, nausea,
Can affect duodenum and lower oesophagus

34
Q

What are causes of peptic ulcers?

A

Helicobacter pylori 60% of gastric acid and up to 50-75% of duodenal ulcers
Causes chronic inflammation in the antral mucosa
Acid secretion leads to erosion of the gastric wall
Non-steroidal anti-inflammatory drug such as ibuprofen or aspirin
- long time or at high doses

35
Q

What are treatments for peptic ulcers?

A
Proton pump inhibitor (PPI)
 - reduces acid to near zero allowing ulcer to heal naturally
"Triple therapy" if caused by H. pylori
 - amoxicillin, clarithromycin and PPI  - NOBEL ~~~
 - drank water containing H pylori
 - - stomach ulcers
 - - therapy
 - - heals
 - - repeat
36
Q

How does gastric cancer develop?

A

From lining of the stomach
Average age of diagnosis is 69 years old
Increasing in people in 20s

37
Q

What can be found in gastric cancer?

A

Can develop into linitus plasticus
Middle lining completely cancerous
Non-stretchy

38
Q

What are symptoms of gastric cancer?

A
Pain or burning sensation on swallowing
Food may stick in throat or chest
Weight loss
Upper abdominal pain
Persistent dyspepsia and burping
 - heartburn
Feeling full after even small amounts
 - due to cancerous cells taking part of stomach
Nausea and vomiting
Bleeding (dark stools), tiredness and breathlessness
39
Q

What is a limiting factor for absorption in the GI tract?

A

Surface area

40
Q

What are the Folds of Kerckring?

A

Folds that increase the absorptive surface are by three times
- well-developed in duodenum and jejunum protruding 8mm into lumen

41
Q

Where are the villi located?

A

Project from the very surface of the mucosa by 1mm

Numbers decrease toward distal end of the GI tract

42
Q

Where are the microvilli located?

A

Each epithelial cell has many 1000s of 1 micrometer extensions
Brush border
20 fold increase in surface area

43
Q

What is the increase in surface are overall?

A

1000-fold incresae

250m2 (in small intestines alone)

44
Q

How much fluid is ingested and how much fluid are gastro-secretions?

A

1.5L

7L - therefore 8-9L absorbed each day

45
Q

What happens in celiac disease?

A

Eating gluten induces immune response in celial disease which reduces microvilli

46
Q

What is the lacteal?

A

where fat is stored (has a milky appearance)

47
Q

How much can the small intestine absorb daily?

A
Several hundred grams of carbs
100g + fat
50-110 of amino acids
50-100g of ions
7-8L of water
Capable of several kilograms of carbs
500g fat
500-700g of protein
20L of water
48
Q

How is water transported?

A

Entirely by diffusion going from high to low concentrations
If chyme is dilute enough, water absorbed from mucous villi to blood entirely by osmosis
Can also go in other direction if chyme is hyperosmotic but within minutes chyme will be diluted to make it osmotic with plasma

49
Q

Where does water transportation mostly occur at?

A

Tight junctions between apical borders of epithelial cells (“paracellular route”) but also through cells (“Transcellular route”)
Osmotic movement of water creates flow of fluid into and through the paracellular spaces and into the blood of the villus

50
Q

How are ions transported?

A

Na is actively transported across the intestinal membrane

20-30g Na secreted in intestinal secretions per day

51
Q

How much ions do we ingest?

A

5-8g per day thus intestine must absorb 25-35g per day

52
Q

How much of Na is lost in feces?

A

Less than 0.5%

- rapidly absorbed through intestinal mucosa

53
Q

What happens when diarrhea occurs?

A

Na reserves can be depleted to lethal levels in hours

54
Q

How does water flow into the interstitial fluid since the chyme is hyperosmotic after a meal?

A

The protein transporters co-transport water. Glucose molecules are surrounded by water
Transported “uphill”!!