Gastrointestinal Physiology Flashcards

1
Q

What are the 6 main functions of the liver?

A
  1. Maintain BSL (gluconeogenesis and glyconeogenesis)
  2. Protein metabolism (catabolism, ammonia conversion to urea)
  3. Fat metabolism (converts FFAs to ketones, formation/secretion of bile)
  4. Inactivation (chemical modification of steroids, makes things less lipophilic, toxins)
  5. Immunity (Kupffer cells)
  6. Other shit (plasma proteins, clotting factors, acute phase proteins)
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2
Q

Why do we find abnormally high blood ammonia levels in end stage hepatic failure?

A
  • porto-systemic shunting
  • reduced conversion from ammonia to urea
  • bacterial production of ammonia in the gut
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3
Q

How is ammonia formed? How much of it gets excreted by kidneys?

What is its relationship to Urea?

A

Ammonia formed by converting glutamine to glutamate (catalysed by glutaminase in renal tubular cells)

50% excreted by kidneys

Ammonia converted to urea in liver. Kidney does not produce urea but EXCRETES it.

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4
Q

Where is the space of disse?

A

Between basolateral membrane of hepatocytes and the sinusoids flowing towards the central vein.

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5
Q

Which structures compose the portal triad?

A

Portal vein
Hepatic Artery
Bile duct

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6
Q

What are the two phases of metabolism in the liver?

A

Phase 1: hydroxylation/oxidation via CYP450

Phase 2: esterification to allow for hydrophilic excretion

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7
Q

What makes up bile?

A

Bile salts: Na, K of bile acids cholic acid (50%), chenodeoxycholic acid (30%), deoxycholic acid (15%), lithocholic acid
Bile pigments: glucuronides, bilirubin, biliverdin
Other substances: cholesterol, FFA, lecithin, fat, inorganic salts

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8
Q

Describe the handling of bilirubin by hepatocytes

A

(fig 28-5 Ganong’s)

  • Albumin bound bilirubin enters space of disse
  • bilirubin selectively ransported into hepatocyte by OATP
  • UDGPG conjugates the bilirubin
  • Congugates secreted into bile by MRP2
  • some unconjugated and conjugated bili refluxes back into plasma
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9
Q

How much bilirubin in the small intestine re-circulates to liver in enterohepatic circulation?

How much bili is converted to urobilinogen?

How much urobilinogen is excreted in urine?

A

UNconjugated bilirubin is IMpermeable to intestinal mucosa

conjugated bilirubin passes and about 10% is re-circulated

50% of bili is converted into urobilinogen

5% urobilinogen excreted in urine, rest gets absorbed by intestinal mucosa, re-excreted by liver back into gut

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10
Q

How is uric acid formed? What is the usual plasma level of uric acid?

A

Breakdown of purines

0.2-0.4 mmol/L

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11
Q

What mechanisms cause true visceral pain? (4)

A

Ischaemia: due to acidic metabolites
Chemcial stimuli: eg. gastric juices and widespread damage
Spasm: widespread stimulation and diminished blood flow
Overdistension: overstretch collapsing blood vessels and causing ischaemic pain

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12
Q

What are the 3 key enzymes at the brush border of intestines for carbohydrate metabolism?

A

Maltase - > glucose
Sucrase - > glucose + fructose
Lactase - > glucose + galactose

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13
Q

Describe the ingestion to absorption pathway of vitamin B12

A
  • B12 found in red meats
  • source broken down by pepsin and acidic environment breaks it into B12 itself
  • B12 binds to transcobalamin and once it goes into duodenum, trypsin break down transcobalamin
  • Free B12 binds to intrinsic factor and absorbed in terminal ileum
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14
Q

Which amino acids are “conditionally essential”?

A

Arginine and histidine (histidine is only AA to have 3 nitrogen molecules)

required during times of rapid growth/recovery

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15
Q

How and where does glycine act as a neurotransmitter?

A

Hyperpolarises by affecting chloride channels in spinal cord and brain stem. Primarily inhibitory.

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16
Q

Where does amino acid digestion occur?

A
  • lumen: pancreatic enzymes
  • brush border: small peptidases
  • in cytoplasm of the cell: peptidases in the cell
17
Q

What is our caloric CARBOHYDRATE requirement daily for parenteral nutrition?

A

Patients require 25 kcal/kg/day. Aim BSL <12.5

18
Q

Which chemical messangers control contraction/relaxation of the lower oesophageal sphincter?

A

Tonically contracted, relaxes on swallowing (unlike rest of oesophagus)

Vagal release of ACETYLCHOLINE causes the intrinsic sphincter to contract

NO and VIP from interneurons innervated by other vagal fibres cause it to relax

PHRENIC contraction of the diaphragm contracts the extrinsic sphincter

19
Q

Which nerves mediate the afferent and efferent pathways for swallowing?
Where are these impulses integrated in the CNS?

A

AFFERENT

  • trigeminal
  • glossopharyngeal
  • vagus

EFFERENT

  • trigeminal
  • facial
  • hypoglossal nerves

nucleus tractus solitarius and nucleus ambiguus

20
Q

Which triggers when sensed in the duodenum inhibit gastric acid and pepsin secretion?

Which signalling messengers are most likely involved?

A

Fats
Carbohydrates
Acid

peptide YY, CCK and secretin

21
Q

What is the difference between the cellular composition of the antrum and the fundus?

A

Antrum: senses peptides via G cells or sense GRP which secrete gastrin

Fundus
Parietal cells secreting hydrochloric acid and intrinsic factor
Chief cells: secreting pepsinogen

22
Q

What are the three agonists of the parietal cell and how do they work?

A

GASTRIN and ACETYLCHOLINE: elevate cytosolic free calcium

HISTAMINE: increases cAMP

23
Q

What are the signals for the stomach to stop producing acid?

A
  • H+ ions sensed by D cells, which release somatostatin, inhibiting G cells
24
Q

How is pancreatic secretion controlled?

A

ACTIVATED

  • Secretin acts on ducts to increase pancreatic duct secretion and bile secretion
  • CCK acts on acinar cells to produce more zymogents
  • Acetylcholine: acts on acinar cells
25
Q

Where are D cells and what do they secrete?

A

somatostatin

stomach
duodenum
pancreatic islets

26
Q

What stimulates somatostatin release and what are its key functions?

A

Stimulated by acid in the lumen

inhibits

  • Gastrin
  • VIP
  • GIP
  • secretin
  • motilin