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GSSE pshysiology > GIT Phsiology > Flashcards

GIT Phsiology Flashcards

1
Q

What type of movements occur in the GI tract?

A

Propulsion and mixing.
Propulsive movements occur via peristalsis. The usual stimulus is distension but
also irritants and parasympathetic supply. Requires an active myenteric plexus.
It is directed towards the anus. Downstream gut typically relaxes to accommodate the bolus.
Mixing movements. Constricting type actions, produces mixing if against a
closed sphincter.

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2
Q

Name the layers of the bowel wall (outer to inner)

A

(1) Serosa (2) Longitudinal muscle layer (3) Circular muscle layer (4) Submucosa
(5) Mucosa

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3
Q

how many ml of endogenous secretions does the GIT make a day?

A

7000ml

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4
Q

what sets the basic electrical rhythm of the GIT?

A

• Basic electrical rhythm (BER) caused by interstitial cells of Cajal.
GI smooth muscle is excited intrinsically by slow waves and spikes.

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5
Q

how many spikes a min do each of these GIT organs have for peristalsis?
Stomach, duodenum, ileum, caecum, sigmoid.

A 
(stomach 4/min,
duodenum 12/min,
 ileum 8/min, 
caecum 2/min, 
sigmoid 8/min)
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6
Q

what factors make the GIT more excitable?

A

A number of factors make it more excitable (stretch, acetylcholine, parasympathetic supply and hormones)

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7
Q

which catecholamine always inhibits GIT activity?

A

NA

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8
Q

what are the names of the outer and inner plexi of the GIT? and what are they responsible for?

A

Outer, myenteric plexus (Auerbach’s plexus) which largely controls GI movement
– Inner, submucosal plexus (Meissner’s plexus) which largely controls secretion and local GI blood flow

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9
Q

which GI reflex go back to the sympathetic ganglia

A

To the prevertebral sympathetic ganglia (gastrocolic, enterogastric, colonoileal
reflexes)

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10
Q

where does the defecation reflex go to?

A

to the spnal cord or brain stem

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11
Q

what are the three basicmachanisms of adsorption?

A

– Active transport; energy is used to transport the substance
– Diffusion; a passive process via random movement
– Solvent drag; dissolved substances dragged across with a solvent

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12
Q

Name the functions of the liver

A

(a) Carbohydrate, protein and lipid metabolism
(b) Synthesis of plasma proteins
(c) Detoxification
(d) Immune modification

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13
Q

What is bile made of?

A

Water, bile salts (highest concentration after H2O), bilirubin, cholesterol, fatty
acids, lecithin and electrolytes (Na+, K+, Ca2+, Cl− and HCO3
−)

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14
Q

What is the function of bile?

A

Bile is needed for the absorption of fat as well as an excretory route for lipid
soluble waste products into the GIT

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15
Q

Name primary bile salts.

A

Primary bile salts are cholic acid and chenodeoxycholic acid

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16
Q

Where are bile salts absorbed?

A

94% are reabsorbed in the small intestine, largely in the terminal ileum

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17
Q

Name three causes of high blood ammonia.

A

High blood levels of ammonia can be due to liver dysfunction, portal hypertension with shunting or overproduction in the liver.

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18
Q

Name the exocrine enzymes released from the pancreas.

A

(a) Protein digestion: Trypsin (most abundant), chymotrypsin, elastase and
carboxypolypeptidases
(b) Fat: Pancreatic lipase, cholesterol esterase and phospholipase A
(c) Carbohydrate: Pancreatic amylase

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19
Q

what are the secondary bile salts which from in the GIT due to bacteria?

A

Secondary bile salts formed in colon due to bacteria

deoxycholic acid, lithocholic acid and ursodeoxycholic acid.

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20
Q

what is the role of bile salts in digestion?

A

– Emulsify large fat particles into minute particles

– Formation of micelles.

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21
Q

what percentage of bile salts are resorbed in the small intestine?

A

94%

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22
Q

what is bilirubin converted to in the gut?

A

urobilinogen

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23
Q

what is jaundice caused from?

A

Jaundice is due to an excess of bilirubin in the blood from excess production,
decreased uptake, impaired metabolism, or decreased secretion.

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24
Q

what does the liver convert ammonia to in the liver to be excreted in bowel and kidneys?

A

urea

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25
Q

what is the neural and hormonal stimulation of the pancreas?

A

naeual: achetylcholine
hormonal: CCK adn secretin

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26
Q

where are enzymes produced in the pacreas?

A

in the acini cells as zymogens

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27
Q

how are the pancreatic enzymes activiated?

A

Trypsinogen cleaved by enterokinase to trypsin in duodenum. Trypsin activates
other enzymes.

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28
Q

Which areas of the stomach are HCl and gastrin released?

A

HCl is mostly released from the fundus and body. Gastrin is released from the
pylorus.

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29
Q

What is released from gastric parietal cells? Chief cells?

A

Parietal cells release HCl and intrinsic factor. Chief cells release pepsinogen and
gastric lipase.

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30
Q

Explain the mechanism of HCl release in the stomach.

A

HCl is released due to a variety of different stimuli ie vagal activity (which also stimulates chief and mucous cells), gastrin and histamine.
Histamine is secreted by enterochromaffin-like (ECL) cells. The rate of HCl production by parietal cells is directly proportional to the activity of ECL cells.
ECL cells are stimulated by gastrin production from the antral mucosa (Fig. 2.2).

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31
Q

What accounts for the largest increase in surface area of the small intestine?

A

argest increase in surface area of the small intestine?

The microvilli.

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32
Q

What are the functions of the large intestine?

A

Absorption of water and electrolytes, as well as storage of faeces.

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33
Q

Explain the handling of Na+, Cl−, HCO3

− in the large intestine?

A

Na+ is actively absorbed and with it, Cl− and water. The mucosa secrete HCO3
−,
helping to neutralise the acidic end products of bacterial action.

34
Q

what two things stimulate the parietal cell to make the HCL?

A

Histamine by the ECL cell (which needed stimulation from gastrin first)
and
Ach by the enteric neuron

35
Q

what hormone provides negative feedback to the parietal cell in response to HCL?

A

the somatostatin releasing cell D cells in pancreas

neg feedback to G cells , ECL cells and directly to parietal cells

36
Q

what can the stomach directly absorb?

A

some lipid soluable substances pass through

37
Q

what are the three phases of gastric digestion?

A

(a) Cephalic – secretion in response to sight, smell, taste or thought of food
(b) Gastric – secretion in response to stretching of the stomach and presence of
food in the stomach
(c) Intestinal – secretion in response to the presence of chyme in the duodenum

38
Q

which cells secrete pepsinogen and gastric lipase?

A

the chief cells.

39
Q

what activates chief cells?

A

Ach from vagus stimulation adn HCL in the stomach

40
Q

what activates pepsinogen?

A
  • activated when it comes in contact with HCl. The release is due
    to acetylcholine from the vagus nerve and acid in the stomach.
41
Q

where are the G cells located?

A

in the antrum of the stomach

42
Q

what do G cells secrete? and in response to what?

A

gastrin in response to neuro transmitters

43
Q

what do brunner glands secrete?

A

mucin and alkaline fluids

44
Q

what cells can be found in the Crypts of Lieberkuhn?

A

mucus goblet cells
paneth cells
enteroendocrine cells and
enterocytes

45
Q

what is the role of the enterocyte?

A

Enterocytes contain digestive enzymes that digest specific food substances while
they are being absorbed through the epithelium (e.g. peptidases, sucrose, maltase, isomaltase and lactase and intestinal lipase).

46
Q

in the large intesting what is secreted to meutralise the end products of bacterial fermentation?

A

HCO3

note K is also secreted

47
Q

What is gastrin released in response to?

A

Stomach contents and distension, vagal nerve discharge, amino acids, hypercalcaemia and tryptophan.

48
Q

Explain how gastrin causes HCl release?

A

Gastrin is transported in the bloodstream to the enterochromaffin-like (ECL)
cells in the fundus and body of the stomach. These cells release histamine which
acts on the parietal cells to cause HCl secretion.

49
Q

Why are patients who have proximal small bowel resections at risk of peptic
ulcer disease?

A

This is because gastrin, secreted by G cells in the stomach antrum, is primarily inactivated in the kidney and small intestine. After a proximal small bowel resection, there is more gastrin in the bloodstream to stimulate histamine secretion.
This, in turn, stimulates increased HCl secretion by parietal cells.

50
Q

What hormone is a powerful stimulant of pancreatic enzyme secretion?

A

Cholecystokinin, released by the enteroendocrine (I) cells of the small intestine.

51
Q

List the effects of cholecystokinin release.

A

(a) Acini secretion of enzyme rich pancreatic juice
(b) Gallbladder contraction and sphincter of Oddi relaxation
(c) Trophic effect on pancreas
(d) Stimulation of hepatic bile flow

52
Q

Which part of the pancreas does secretin act on?

A

This works on the pancreatic ducts to release HCO3

− rich secretions to help neutralise the acidic chyme as it enters the duodenum.

53
Q

what is secretin released from?

A

the S cells in the small intestine

54
Q

what stimulates secretin to be secreted?

A

Released in response to acidic gastric juice and amino acids in the duodenum

55
Q

what are the three functions of secretin?

A

Causes HCO3- rich pancreatic juice release from the pancreatic ducts
• Augments pancreatic secretion
• Inhibits gastric secretion and motility

56
Q

what secreted CCK?

A

the I cells in the small intestine

57
Q

what triggers CCK release?

A

fatty acids and amino acids in the small intestine

58
Q

what i the function of GIP?

A

to stimulate insulin release

59
Q

what is the function of VIP ?

A

increase electrolytes and water secretion in the GIT and relaxation of intestinal smooth muscle.

60
Q

Explain the way that glucose enters the enterocytes.

A

Glucose is absorbed via secondary active transport of Na+.
It occurs in two phases – active transport of Na+ ions through the basolateral
membrane encourages secondary active transport of glucose and Na+ through
the brush border by sodium-dependent glucose transport (SGLT, Na+ glucose
cotransporter). Once inside the cell, glucose transporter 2 (GLUT2) transports
glucose out of cell into the interstitium.

61
Q

What happens to fatty acids once they have been absorbed into the enterocytes?

A

This depends on the number of carbons in the fatty acid chain. The majority are
long chain FA (ie greater than 12C) and are taken up in the SER and reformed
into new triglycerides and these are then released as chylomicrons into the thoracic lymphatic duct (80–90%). Short and medium FA (ie less than 12C) can be
directly absorbed into the portal blood system.

62
Q

What are micelles?

A

These are small lipid molecules made up of 20–40 molecules of bile salts surrounding fatty acids and monoglycerides. They are used to ferry fatty acids and
monoglycerides to the enterocyte brush border. The fatty acids and monoglycerides can then diffuse across the cell membrane. The bile salts remain in the GI lumen.

63
Q

What is the protein requirement of adults?

A

Protein requirement is 1.2–1.5 g/kg/day

64
Q

What is the ideal pH for pepsin to work?

A

pH 2.0–3.0

65
Q

What percentage of protein is absorbed?

A

> 95%

66
Q

Why does gastric acid aid the absorption of non-haem iron?

A

This is because iron is absorbed in the proximal duodenum in its ferrous form
(Fe2+). The low pH oxides the Fe3+ to Fe2+

67
Q

How long do Vitamin B12 stores last for?

A

3–5 years.

68
Q

What biochemical abnormality is seen with a gastric outlet obstruction?

A

Hypochloraemic, hypokalaemic metabolic alkalosis. Loss of HCl and K+ from
the stomach.

69
Q

Why would a patient who has had their terminal ileum (TI) resected have issues
with steatorrhea?

A

They have fat maldigestion. This is due to bile salt malabsorption and failure of
the enterohepatic circulation, which occurs when more than 100 cm of TI has
been resected

70
Q

how many kcal/kg/day does a patient need?

A

Carbohydrates - patients require 25 kcal/kg/day.

71
Q

which brush border enzymes break down

oligosaccharide carbohydrates to monosaccharides?

A

sucrase, lactase, maltase and alpha-dextrinase

72
Q

what percentage of daily intake is from fats?

A

10–15% of daily calorie intake is from fats

73
Q

why does fat need to be emulsified before it can be absorbed?

A

In the small intestine, it needs to have been emulsified by bile salts and lecithin.
This is needed as the lipase enzymes are water soluble, therefore, can only act on
fat globules on their surface.

74
Q

how are triglycerides digested?

A

mainly TGs are mainly digested by pancreatic lipase, plus a small amount of enteric
lipase. Digested to fatty acid and 2-monoglycerides.

75
Q

what are micells and what do they do?

A

Then they form micelles – (3–6 nm) 20–40 molecules of bile salt with fatty acid
and monoglyceride center. Micelles ferry fatty acids and monoglycerides to the
brush border where they can be absorbed. At the brush border the monoglycerides and fatty acids diffuse immediately out of the micelles and into the interior of the enterocyte. This process leaves the bile salts in the chyme. In the absence
of bile salts only 50% of fat is absorbed.

76
Q

which of the pancreatic enzymes dugest protein?

A

The enzymes are

trypsin, chymotrypsin, carboxypolypeptidase and elastase.

77
Q

what form ae most proteins obsorbed like?

A

Most proteins are

absorbed as di- and tripeptides

78
Q

the brush border enzymes which breakdown protein are ?

A

Microvilli on enterocytes contain peptidases -

aminopolypeptidases and dipeptidases.

79
Q

which form does iron need to be in for absorption?

A

Fe2+

80
Q

what is the transporter which absorbs iron?

A

DMT1

GSSE pshysiology (5 decks)

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