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Semester 3 > GI 1-6 > Flashcards

GI 1-6 Flashcards

1
Q

What changes does digestion make to food?

A

Sterile

Neutral

Isotonic

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2
Q

What state does digestion change food to?

A

Solution of small sugars, amino acids, lipids in very small peptides and other small molecules

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3
Q

What does the body excrete?

A

Residues from food

Debris from the gut

Materials specifically excreted via liver to gut

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4
Q

How does the body break down food?

A

Physically to release large molecules

Chemically to release small molecules

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5
Q

Define chyme.

A

The semifluid mass of partly digested food expelled (slowly so as not to overwhelm) by the stomach into the duodenum. Generally sterile due to stomach acid.

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6
Q

Why must chyme be diluted?

A

Very hypotonic and acidic so must be made isotonic and neutral so as not to damage the rest of the GI tract.

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7
Q

What is mastication?

A

Chewing.

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8
Q

What is the purpose of saliva?

A

Protects mouth

Lubricates food for astication and swallowing - wet, mucus

Starts digestion - enzymes (esp. sugars)

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9
Q

How does saliva protect the mouth?

A

Wet

Bacteriostatic

Alkaline

High calcium

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10
Q

Why is the formation of a bolus important?

A

streamlined allowing for rapid, easy transport from mouth to stomach for storage.

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11
Q

How does the stomach accomodate storage and digestion?

A

Relaxes to accomodate food - receptive relaxation

Contracts rhymically and periodically to mix and disrupt - exposes chyme to secretions

Secretes acid and proteolytic enzymes to break down tissues and disinfect

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12
Q

What processes occur in the duodenum/jejunum?

A

Dilution and neutralisation - makes it safe to pass through the rest of the system

Osmotically draws water in from ECF to make it isotonic

Pancreas and liver secrete alkali (HCO3) to neutralise the acid

enzymes and bile salts to complete digestion

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13
Q

What are some of the products of digestion?

A

Amino acids from polypeptides

Monosaccharides from polypeptides

Break down and reform lipids

Break down nucleic acids

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14
Q

How is the surface area of hte intestine increased?

A

Brush border - villi

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15
Q

How are molecules absorbed in the small intestine?

A

Actively/passively

Often coupled to Na absorption

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16
Q

Where are absorbed molecules from the small intestine transported to?

A

Liver by hepatic portal vein

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17
Q

What is absorbed in the large intestine?

A

Water and some electrolytes

Very slow process

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18
Q

Where in the large intestine do faeces accumulate?

A

Descending and sigmoid colon

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19
Q

What are the 3 main processes of the GI system?

A

Secretion

Motility

Absorption

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20
Q

Why is it important to maintain a balance between secretion and absorption?

A

Imbalance will cause considerable loss of water and electrolytes - dehydration and electrolyte disturbance. Mostly from body fluids rather than ingested food adn water.

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21
Q

What are the 3 methods of control of the body for motility and secretion?

A

Neural

Paracrine

Endocrine

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22
Q

What is the neural control of the gut?

A

Somatic motor system for ingestion and excretion

Autonomic nervous system the rest - mostly parasympathetic. Coordinates both secretion and motility. Range of neurotransmitters. Gut is full of nerve cell bodies in the walls - plexuses

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23
Q

What is paracrine control? Give some examples in the gut.

A

Chemical messengers diffusing locally - NOT through blood

Histamine in stomach

Vaso-active substances to alter blood flow

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24
Q

How are hormones used in GI?

A

Secretion of stomach acid

Alali secretion from liver and pancreas

Enzyme secretion

All peptides in structurally related families

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25
Q

What does the mouth do?

A

Way into the GI tract - preliminary disruption of food (mastication), formation of bolus, swallowing

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26
Q

How is the mouth protected?

A

Teeth and oral mucosa

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27
Q

What do the different teeth do?

A

Incisors cut

Molars crush

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28
Q

What is the muscle of mastication?

A

Masseter. Innervated by branch of the trigeminal nerve

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29
Q

What is the function of saliva?

A

Lubricates and wets food

Starts digestion of carbs

Protects oral environment

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30
Q

How does saliva protect the oral environment?

A

Keeps mucosa moist

Washes teeth

Maintains alkaline environment - neutralises acid produced by bacteria

High calcium content

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31
Q

What are the consequences of poor saliva production?

A

Zerostomia (dry mouth)

Can still eat food provided it is moist but teeth and mucosa degrade very quickly

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32
Q

What are the constituents of saliva?

A

Water (hypertonic)

Electrolytes - Na and Cl in lower conc than plasma, Ca, K and I ususally at higher conc than plasma

Alkali - HCO3 in higher conc than plasma

Bacteriostats

Mucous - mixture of mucopolysaccharides

Enzymes - salivary amylase

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33
Q

What type of glands are salivary glands?

A

Ducted exocrine

3 paired glands - parotid, sub maxillary and sub-lingual

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34
Q

Describe exocrine glands

A

Blind ended tubes

Acini lined with acinar cells

Connected system of ducts lined by duct cells

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35
Q

Describe the secretion of the parotid gland

A

Watery, rich in enaymes but little mucus. Serous saliva

25% of total saliva

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36
Q

Describe the secretions of the sub-lingual glands

A

Viscous

No enzymes

Lots of mucus

(Mucous saliva)

5% of total saliva

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37
Q

Describe the secretions of the sub-maxillary glands.

A

All components of saliva - mixed serous and mucous

Gland is made up of mixture of serous and mucous acini leading to common ducts

70% of total saliva

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38
Q

How is a hypotonic saliva created?

A

Made from more concentrated extra-cellular fluid

No cellular mechanism for secretion of water so a more concentrated solution is secreted and then solute taken out

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39
Q

What determines the volume adn composition of saliva?

A

Volume - acinar secretion

Composition - ductal secretion. Has a max rate of modification except for HCO3

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40
Q

Describe resting saliva

A

Low volume

Very hypotonic

Neutral or slightly acid

Few enzymes

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41
Q

Describe stimulated saliva.

A

High volume

Less hypotonic than resting

More alkaline than resting

Lots of enzymes

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42
Q

What is the mechanism of acinar secretion?

A

Not ultra-filtration

Active secretion of ions - Cl

Water and other ions follow passively

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43
Q

How is salivary secretion controlled?

A

Largely nervous

ANS - sympathetic, superior cervical ganglion and parasympathetic, Glossopharyngeal (9th) and Otic ganglion

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44
Q

Where is the afferent informatino of the parasympathetic outflow to the salivary glands from?

A

Moth and tongue - taste receptors, especially acidic

Nose

Conditioned reflexes - pavlov’s dogs

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45
Q

What are the affects of parasympathetic outflow on saliva?

A

Releases acetyl choline

Acts on acinar cells to promote formation of primary secretion

Acts on duct cells to promote HCO3 secretion

Muscarinic receptors - blocked by atropine like drugs

Co-transmitters stimulate extra blood flow

Sympathetic stimulation reduces blood flow - dry mouth

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46
Q

What stimulate swallowing?

A

Bolus moving to pharynx

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47
Q

What are the phases of swallowing?

A

Voluntary phase

Pharyngeal phase

Osophageal phase

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48
Q

What happens in the voluntary phase of swallowing?

A

Separation of the bolus and it moves to the pharynx

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49
Q

What happens in the pharyngeal phase of swallowing?

A

Pressure receptors in the palate and anterior pharynx which are afferent to the brain stem swallowing centre which:

Inhibits respiration

Raises the larynx

Closes the glottis

Opens the upper oesophageal sphincter

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50
Q

Describe the oesophageal phase of swallowing

A

Upper third is voluntary

Lower two thirds is smooth muscle

Rapid peristaltic wave coordinated by extrinsic nerves

Transit time to stomach about 9 seconds, lower osophageal sphincter opens

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51
Q

What might cause dysphagia?

A

(problems swallowing)

Motility problems - achalasia

Obstruction or compression of the oesphagus - tumours

Swallowing is absent in brain death and must be checked after head injury/surgery

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52
Q

Why are the abdominal muscles (Rectus abdominous) not one long muscle?

A

Short muscles more efficient

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53
Q

Where is mcburneys point?

A

2/3rds of teh distance between the umbilicus and ant sup iliac spine

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54
Q

Define referred pain

A

Pain perceived at a site distant from the site causing the pain

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55
Q

What is somatic referred pain?

A

Pain caused by a noxious stimulus to the proximal part of a somatic nerve that is perceived in the distal dermatome of the nerve

56
Q

Why does visceral referred pain occur?

A

In the thorax and abdomen, visceral afferent pain fibres follow sympathetic fibres back to the same spinal cord segments that give rise to preganglionic sympathetic fibres. The CNS preceives visceral pain as coming from the somatic portion of the body supplied by the relevant spinal cord segment(s).

57
Q

What causes visceral pain?

A

Not superficially sensitive eg. Touch, burning, cutting, crushing

Ischaemia, abnormally strong muscle contraction, inflammation adn stretch does.

58
Q

Where does midgut pain refer to?

A

Umbilicus

59
Q

What is a hernia?

A

A protrusion of the abdominal contents through the abdominal wall

60
Q

Why is the transversalis fascia so important?

A

Stops us getting a direct hernia

61
Q

What are the common types of hernia?

A

Femoral

Inguinal

epigastric

Umbilical

Richters

Spiliegan

incisional

62
Q

What are risk factors for hernias?

A

Age

Male

Smoker

63
Q

What is Hesselback’s triangle?

A

Area where direct hernias are common in between the abdominal muscle, inguinal ligament and inferior epigastric artery

64
Q

Where do indirect hernias occur?

A

Deep inguinal ring within the diverging arms of the transversalis fascial sling

65
Q

Where do femoral hernias occur?

A

Below the inguinal ligament

66
Q

What is the most common hernia in women?

A

Indirect inguinal but femoral is more common in women than men

67
Q

What is a divaricatioin of recti?

A

separation of the rectis abdominis muscle

68
Q

What is a Richter’s hernia?

A

part of the bowel strangulates through the hernia so no obstruction but painful

69
Q

What is a spigelian hernia?

A

hernia at the junction where the internal/external obliques meet the rectis muscle and the posterior sheath stops

70
Q

Why are hernias operated on?

A

Painful

worrying - cosmetic

bowel obstruction

risk of strangulation (1%) - mortality over 15%

71
Q

How are hernias repaired?

A

Try and obtain primary closure

Tension free

Laproscopic reinforcement

Mesh

72
Q

What is the purpose of the stomach and why is it necessary?

A

Stores food as we ingest food faster than we can digest it

Disinfects food to prevent disease

Breaks food down into chyme

73
Q

Why does the stomach need protection and how is this provided?

A

It is designed to destroy biological material but it is itself biological material so protects itself with mucus and alkali

74
Q

What does the stomach secrete?

A

Attack - Hydrochloric acid and proteolytic enzymes

Defence - Mucus and HCO3-

75
Q

Where do stomach secretions come from?

A

Gastric pits:

Chief cells - enzymes

Parietal/oxyntic cells - acid

Neck cells - mucus

Endocrine cells - gastrin

76
Q

Describe the mechanism of secretion of acid in the stomach

A

Made from slightly alkaline solution. 1 mol of alkali must be produced for every mol of acid- acid into stomach, alkali into blood

Cells split water into H+ and OH- ions.

OH- combines with CO2 to produce HCO3-

H+ produced by mitochondria

77
Q

How are parietal cells adapted for acid production?

A

Have lots of mitochondira which produce H+ at high rate. H+ cannot accumulate in the cells so the sells have canaliculi - invaginations in the cell wall which have proton pumps - expel H+ against high conc grad.

This requires lots of energy

78
Q

What happens to blood pH when we eat?

A

Increases because alkali is made in the stomach at same rate as acid

79
Q

What factors can act on the parietal cell to stimulate acid secretion?

A

Gastrin

Histamine

Acetyl Choline

80
Q

Describe gastrin and explain how it acts in the stomach.

A

Hormone secreted by G-cells in the stomach

Polypeptide, main form 17 aa long

Bind to surface receptor on parietal cell

Stimulates acid and intrinsic factor secretion via second messenger pathway

81
Q

How does histamine act in ithe stomach?

A

Released from mast cells

Binds to H2 surface receptor on parietal cell

Stimulates acid secretion via c-amp

82
Q

Describe the action of acetyl chomine on the stomach

A

Released from post ganglionic parasympathetic neurones

Acts on muscarinic receptors on parietal cell

Stimulates acid secretion by second messenger pathway

83
Q

What affects gastrin secretion?

A

Stimulated by:

Peptides

Acetyl choline from intrinsic neurones

Inhibited by:

Low pH in stomach - feedback control

84
Q

What stimulates mast cells?

A

Gastrin

Acetyl choline

Causes it to secrete histamine. This is therefore an amplifier action.

85
Q

What causes the release of acetyl choline to parietal cells?

A

Distension of the stomach

CNS

86
Q

What are the phases of control in the stomach?

A

Cephalic phase

Gastric phase

Intestinal phase

87
Q

What is the cephalic phase and how does the control work?

A

Detecting and ingesting food

Autonomic stimulation - Ach stimulates parietal cells directly and via histamine

88
Q

What is the gastric phase of control?

A

Food reaches stomcha - buffers stomach acid so pH rises (disinhibits gastrin)

Stomach distends - stimulates intrinsic nerves (release Ach)

Initial digestion releases peptides - stimulates gastrin release

Histamine release stimulated by gastrin and Ach

89
Q

What is the intestinal phase of control?

A

Stomach begins to empty

Chyme stimulates release from intestines of hormones which antagonise gastrin

Accumulation of acid in empty stomach inhibits gastrin secretion

Stomach pH low betwen meals - can aggravate ulcers and cause night pain

90
Q

How are the stomachs defence mechanisms controlled?

A

Mucus and alkali secretion stimulated by prostaglandins

Promoted by most factors stimulating acid secretion

Defences match the attack

91
Q

How might the stomachs defences be breached?

A

Alcohol dissolves the mucus

H. Pylori

NSAIDS - inhibit prostaglandins therefore reduce defences. Some, like aspirin, converted into non-ionised form by stomach acid, pass into cells and then re-ionise

Breaching results in peptic ulcers

92
Q

How is acid secretion reduced?

A

Histamine receptor antagonists - H2 - cimetidine

Proton pump inhibitors - Omeprazole

Also treat ulcers by eliminating H. Pylori with antibiotics

93
Q

Describe the stomachs motility.

A

Relaxes to accomodate food

Contracts rhythmically to break down large particles

Delivers chyme slowly to the duodenum

94
Q

How does receptive relaxation occur?

A

Neural reflex

Triggered by swallowing

Efferent pathway via vagus

Tension in resting stomach wall is ‘actively’ relaxed

Pressure in stomach does not increase as it fills - limits reflux

So can consume large meals (but not if vagus nerve damaged

95
Q

How deos rhythmic contraction occur?

A

Stomach has longitudinl and circular muscle

Driven by pacemaker in cardiac region

Fires about 3 times a miute

Wave of peristalsis spreads towards antrum accelerating as it goes

This initially drives all stomach contents ahead of it. Chyme overtakes larger lumps as it accelerates and the lumps are driven back to the fundus

Small squirt ejected then wave reaches the pylorus and shuts it. Rest of chyme returns to stomach

96
Q

How is gastric emptying controlled?

A

Volume of each squirt affected by rate of acceleration of peristaltic wave wiche is affected by hormones from intestine

Gastric emptying slowed by fat in duodenum, low pH in duodenum and hypertonicity in duodenum

Rate of stomach emptying matched to rate of digestion

97
Q
A
98
Q

What are complications of gastric/duodenal ulceration?

A

Bleeding

Perforation

Gastric obstruction

99
Q

What is gastritis?

A

Histological inflammation of the stomach

100
Q

What is a gastric ulcer?

A

Broken down the mucous bicarbonate and epithelial barrier

101
Q

What is the cause of gastritis?

A

Helicobacter pylori - produces inflammatory response

Motile, microaerophilic, urease producing bacteia

Adheres to gastric mucosa and produces cytotoxins

Always associated with ulcers

Transmission by oral-oral route/feacal-oral route

102
Q

What does the upper 2/3 of the stomach secrete?

A

HCL and pepsinogen

103
Q

What does the lower 1/3 of the stomach secrete?

A

Mucus and gastrin

104
Q

What is dyspepsia and what is the difference between functional and non-functional dyspepsia?

A

indigestion - impaired digestion. Pain in the upper abdomen and premature fullness. Ofen associated with bloating, belching, nausea and heartburn. May be caused by gastritis or gastroesophageal reflux disease.

Functional dyspepsia is not associated with ulcers.

105
Q

What enhances acid secretion in the stomach?

A

TNF, IL1 IF stimulate gastrin secretion

TNF decreases antral D cells which are responsible for shutting off acid secretion

106
Q

What increases mucus secretion?

A

Cytokines

107
Q

What effect does vitamin C have on gastric cancer cells?

A

Inhibits their growth

108
Q

What are the causes/risk factors of ucers?

A

Acid

Diest

Smoking

Alcohol

Stres

ZE syndrome

Helicobacter pylori

NSAIDs

109
Q

What is ZE syndrome?

A

Caused by a non-beta islet cell, gastrin secreting tumour of the pancreas that stimulates the acid secreting cells of the stomach to maximum activity with consequent gastrointestinal mucosal ulceration

110
Q

How does a bacterium that only colonises gastric mucosa cause duodenal ulceration?

A

Antral helico pylori colonisation causes and increase in gastrin production which then increases the parietal cell acid production. The duodenal cap is damaged and gastric metaplasia gastric mucosa. Helicobater colonise the gastric mucosa of the duodenum and the immune response causes duodenitis which can lead to ulceration

111
Q

What need to be considered pharmacologically when looking to manage ulceration?

A

Bacterial niche

Antibiotic resistance

Compliance

Testing for eradication

Treatment in the elderly

PPI-Hp-stomach interations

112
Q

Describe the stages of mucoal change leading to cancer of the stomach from gastritis.

A

H. pylori chronic active non-arophic gastritis -> multifocal atrophy -> intestinal metaplasia -> dysplasia -> carcinoma

113
Q

How is chyme “conditioned?

A

Acidtity corrected by HCO3- secreted from the pancreas, liver and duodenal mucosa

Hypertonicity corrected by osmotic movement of water across the duodenal wall

Digestion is completed by enzymes from the pancreas and small intestinal mucosa and bile acid from the liver

114
Q

What does the exocrine pancreas secrete?

A

Alkaline juice

Enzymes :

  • Proteases
  • Amylases
  • Lipases
115
Q

What proteases are released from the exocrine pancreas?

A

Trypsin

Chymotrypsin

Elastase

Carboxypeptidase

116
Q

What is teh exocrine pancreas made up of?

A

Acini and ducts:

Acini secrete enzymes, ducts secrete alkaline juice

117
Q

Describe acinar secretion.

A
  • Enzymes synthesised on ribosomes - mostly as inactive precursors
  • Packaged into condensing vacuoles by Golgi comples
  • Form zymogen granules secreted by exocytosis
  • Activated in intestine by enzymatic cleavage
  • If pancreas is damaged (eg. pancreatitis) enzymes (amylase - easy to assay) appear in blood
118
Q

How is acinar secretion stimulated?

A

Hormone. Cholecystokinin (CCK) released from duodenal APUD cells. Sensitive to Hypertonoicity and fats -> release CCK (intestinal phase)

Same receptors also stimulated by Gastrin

Vagus nerve also stimulates by release of acetyl choline (cephalic phase)

119
Q

Describe ductal secretion from the pancreas.

A

Secrete HCO3-

Present in blood at elevated concentration because of gastric secretion of acid

Celliular mechanism loke other HCO3- secretion (Na-K-ATPase coupled, transported as H2O and CO2)

120
Q

What stimulates duct secretion?

A

Secretin released from jejunal cells in reponse to low pH. Action of secretin facilitated by CCK

121
Q

What is the function(s) of the liver?

A

Blood:

  • Energy metabolism
  • Detoxification
  • Plasma proteins

Gut:

  • Secretion of bile - 0.25-1l/d. - bile acids and alkaline juice for digestion, excretion of bile pigments - prevents damage of kidneys
122
Q

Describe the blood supply to the liver

A

Portal blood supply- In through hepatic portal vein from gut to central vein through sinusoids surroundsd by hepatocytes which fulfill the blood facing function

Also has an arterial supply of oxygenated blood

123
Q

Describe the structure of the liver in relation to its function for the gut.

A

Bile is secreted into blind ended canaliculi by hepatocytes (bile acid dependent) and duct cells (bile acid independent) and flows to the bile duct.

124
Q

What is the difference between bile acid dependent and independent secretions in the liver?

A

Dependent - from hepatocytes, contains bile acids and pigments

Independent - Secreted by duct cells, contains alkaline juice like that from pancreatic duct cells

125
Q

How are bile acids related to cholesterol?

A

Cholic acid

Chenodeoxycholic acid

Travel in bile as micelles - bile acid + cholesterol + phosphlipids

126
Q

Why is lipid digestion complicated and how does bile acid help with this?

A

Hydrophobic nature:

  • Tend to for mlarge globules as stomach acid breaks down natural emulsions
  • Low surface area for enzymes to act

Bile acids emulsify fat into much smaller globules

  • increase surface area for lipase to cleave fatty acids and glycerol
  • Colipase links bile acids and lipase to spread them over surface
127
Q

How do released fatty acids form micelles?

A
  • Polar groups of bile acids on outside
  • Hydrophobic fatty acids within
  • 4-6nm in diameter (20 lipid molecules)
  • Need bile acids to be above a critical concentration to form
  • Also sequestre cholesterol, fat soluble vitamins and phospholipids
128
Q

What are micelles?

A

Vehicle to carry hydrophobic molecules through aqueous luminal contents into unstirred layer next to epithelial cells. Released slowly and enter cells by diffusion

129
Q
A

Fatty acids etc used to re-synthesise lipids in epithelial cells

Exported to lymphatics as chylomicrons (lipid with polar protein and phospholipid coat)

130
Q

Describe the route of bile acids through the body

A

Enterohepatic circulation

  • Released into the gut lumen after fatty acids etc absorbed
  • continue to terminal ileum
  • Absorbed actively by epithelium of terminal ileum
  • Return in hepatic portal blood to hepatic sinusoids
  • Hepatocyts take up actively and resecrete into canaliculi
131
Q

Why might bile acids not return to the liver?

A

Some are unconjugated by bacterial action in the gut and lost

132
Q

What are the problems with the recovery of bile salts and how are they overcome?

A
  • Bile acids return to the liver in beteen meals
  • Secreted by canalicular cells well before needed next (cannot be stored in liver)
  • Stored in the gall bladder
  • Volume stored reduced by concentration - transport of salt and water across gall bladder epithelium
  • Concentration process increases risks of precipitation - gall stonesW
133
Q

How is bile removed from storage?

A

Cholecystokinin secreted by duodenum in response to gastric emptying -> Stimulates contraction of gall bladder muscle, ejecting concentrated bile acids together with enzymes from pancreas and alkali from pancreas and liver in response to secretin

134
Q

What is steatorrhoea?

A

Bile acids or pancreatic enzymes are not secreted in adequate amounts (malabsorption of fat) -> fat appears in faeces (pale, floating, foul smell)

135
Q

What is caused if bilirubin accumulates in the blood?

A

Jaundice

136
Q

What is the excretery route of bilirubin?

A

Breakdown product of haemoglobin conjugated in liver, secreted into bile and excreted in faeces

137
Q

What are the common causes of jaundice?

A
  • Pre-hepatic jaundice occurs when a condition or infection speeds up the breakdown of red blood cells. This results in an increase in bilirubin levels in the blood and triggers the symptoms of jaundice.
  • Intra-hepatic jaundice occurs when damage to the liver, either as the result of infection or exposure to a harmful substance, such as alcohol, disrupts the liver’s ability to process bilirubin.
  • Post-hepatic jaundice is triggered when the bile duct system is damaged, inflamed or obstructed, which results in the gallbladder being unable to move bile into the digestive system.

Semester 3 (19 decks)

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