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Satia's MRCS copied decks > Gastro Physiology > Flashcards

Gastro Physiology Flashcards

1
Q

Enteric nervous system

A

Myenteric plexus / Auerbach’s
-Motor
-Runs bewtween circular and longitudinal muscle layers

Submucosal / Meissner’s
-Sensory
-Runs in submucosal layer

Parasympathetic: synapses with myenteric plexus

Sympathetic: synapses with myenteric and submucosal plexus

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2
Q

Saliva types

A

Parotid gland
-Watery
-No mucous
-IgA
-Amylase
-25%

Submandibular
-Mixed mucous/serous
-70%

Sublingual
-Contains mucoproteins
-Only 5% of saliva secretion

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3
Q

Ductal modifications of saliva

A

Glands secrete isotonic fluid

During duct movement
- K+ and HCO3- are added

-NA+ and Cl- are removed

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4
Q

Control of saliva production

A

Salivary nucleus in medulla

Parasympathetic supply from facial and glossopharnygeal nerve

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5
Q

Lower Oesophageal sphincter

A

Physiological not anatomical

Pressure ~ 15-25mmHg

Characteristics reducing reflux:
-Right crus of diaphragm presses on oesophagus as it passes through diaphragm
-Acute angle of oesophagus as it enters somach through diaphragm
-Mucosal folds in the lower oesophagus act as a valve

Closure of the sphincter is under vagal control

Hormone gastrin causes the sphincter to contract

Secretin, CCK and glucagon cause it to relax

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6
Q

Cells of the gastric mucosa

A

Two broad types:
Columnar epithelium: secrete protective mucus layer

Gastric galnds: secretory role
-Mucus cells: secrete mucus located at opening of gastric gland
-Peptic/chief cells: secrete pepsinogen and ar elocated at base of gastric gland
-Parietal cells: secrete HCl and IF
-Neuroendocrine cells: secrete a number of peptides that regulate GI motility and secretion, i.e. gastrin.

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7
Q

Gastric secretory cells

A

-Mucus cells: secrete mucus located at opening of gastric gland

-Peptic/chief cells: secrete pepsinogen and ar elocated at base of gastric gland

-Parietal cells: secrete HCl and IF

-Neuroendocrine cells: secrete a number of peptides that regulate GI motility and secretion, i.e. gastrin.

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8
Q

Cells found most at fundus and body of stomach

A

Parietal cells

Peptic cells

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9
Q

Cells found most at pylorus and antrum of stomach

A

Mucus cells

Neuroendocrine (secreting gastrin) cells

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10
Q

Cells of the cardia of the stomach

A

Mucus cells make up all of gastric gland

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11
Q

Factors that stimulate parietal cells acid production

A

Vagal innervation ACh

Gastrin secreted from G-cell

Histamine secreted from entero-chromaffin cells and mast cells

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12
Q

Factors that inhibit parietal cell acid production

A

Secretin produced by duodenal mucosa

CCK produced by duodenal mucosa

GIP produced by duodenal mucosa

Somatostatin producerd by D-cells

Nausea

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13
Q

Pepsinogen

A

Secreted by chief/peptic cells

Activated by HCl (and pepsin) to produce pepsin

Pepsin proteolytic enzyme that hydolyses peptide bonds in proteins

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14
Q

Factors protecting the epithelium of the gastric mucosa

A

Mucus is secreted from cells in the bottom of the gastric gland to coat the epithelium

Contains bicarbonate to off-set pH

Tight-epithelial junctions prevents gastric juices reaching deeper structures

Prostagland E increases thickness of mucus layer
-Stimulating HCO3 production
-Increasing blood flow in the mucosa (bringing nutrients to any damaged areas).

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15
Q

Phases of gastric secretion

A

Cephalic
-Appeptite centre in thalamus
-30%
-Stimulation of parietal cells via G cells and from G-cells producing gastrin

Gastric
-60%
-Distension of the stomach and the chemical composition of food lead to acetylcholine release from the vagus

Intestinal
-5%
-Stimulation is the presence of food in the duodenum; this results in the release of gastrin from G-cells in the duodenal mucosa

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16
Q

Enterogastric reflex

A

Food entering duodenum causes release of secretin, CCK and GIP

All inhibit gastrin and parietal cell activity

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17
Q

Factors altering transit into duodenum through pylorus

A

Increased gastric volume leads to quicker emptying

Fats: CCK and GIP are released which cause contraction of pyloric sphincter

Proteins: stimulate gastrin secretion –> causes contraction of pylorus constriction

Low pH / Acid: causes vagus-mediated delay in passage + secretin release
Secretin
–> Inhibits contractions in gastric antrum
–> Contraction of pylorus
–>Increased production of bicarbonate release from pancreas to off-set acidic pH

Hypertonic chyme –> delays gastric emptying

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18
Q

Vomiting reflex

A

Coordinated by vomiting centre in the medulla

Impulses along
-CN V
-CV VII
-CV IX
-CN XII
-Intercostals
-Diaphragm
-Andominal muscles

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19
Q

Action of proton pump inhibitors

A

Inactive at neutral pH but is activated by the acidic conditions in the stomach

Irreversibly binds to sulphydryl groups on the proton pump

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20
Q

Gastric protection drugs

A

Sucralfate
-Polymerises at pH <4 and adheres to base of ulcer

Bismuth chelate
-Acts similar to sucralfate and ?eradicates H.Pylori

Misoprostol
-Prostaglandin E2 analogue
-Increases bicarb and blood flow

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21
Q

Complications post gastrectomy

A

Iron deficiency

B12 deficiency

Dumping syndrome

Diarrhoea

Billous vomiting
–> refluxed bile can also lead to gastritis –> recurrent ulcers

Gastric cancer from bile salt reflux gastritis

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22
Q

Early dumping syndrome

A

30–45 min after eating

Rapid gastric emptying of a hyperosmolar meal into the small bowel

Results in fluid moving into the small bowel by osmosis (third space loss) and rresults in dizziness, weakness and palpitations

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23
Q

Complications of a vagotomy

A

Reduced gastric acid secretion (therapeutic intent)

Delayed gastric emptying
–> failure of pylorus to relax

Reduced pancreatic secretions

Diarrhoea secondary to loss of vagal control of small bowel

Increased risk of large bowel cancer due to excess of bile salts reaching large bowel

24
Q

Components of small bowel crypts

A

Undifferentiated stem cell precursor

D-cell: somatostatin

S-sell: secretin

N-cell: neurotensin

Enterochromaffic cells: 5-hydroxytrptamine

25
Q

Activates pancreatic trypsinogen

A

Enterokinase

26
Q

Brunner’s gland

A

Present in duodenum only (not jejunum or ileum)

Secrete mucus-rich bicarbonate

27
Q

Glucose and galactose absorbtion

A

Secondary activae transport using NA-K ATPase

28
Q

Fructose absorbtion

A

Distinct Na-independent absorbtion

‘Facilitate’ diffusion

29
Q

Absorbtion of triglycerides

A

Absorbed into enterocytes
–>Smooth endoplasmic reticulum reforms triglycerides from the absorbed monoglycerides and FFAs

Reformed triglycerides are formed into chylomicrons, which are released from basal layer of the enterocyte to diffuse into the lacteals within the villi

From here they enter the lymphatic circulation and then into the venous circulation

30
Q

Fat-soluble vitamins

A

A, D, E and K

31
Q

Water-soluble vitamins

A

B and C

Vitamin C is absorbed by a Na+-dependent mechanism in the jejunum

Vitamin B12 is absorbed in the ileum after intrinsic factor (secreted in the stomach) binds to its specific receptor.

IF–vitamin B12 complex is then taken up into the cell

The remaining B vitamins diffuse freely across the enterocyte cell membrane.

32
Q

Absorption of Vitamin C

A

Vitamin C is absorbed by a Na+-dependent mechanism in the jejunum

33
Q

Absorption of Iron

A

Absorbed in duodenum and jejunum

Ferrous Fe2+ form is absorbed (NOT ferric Fe3+)

Gastric acid converts iron to the ferrous form

Absorption transport protein transferrin
–> binds iron and links to a membrane-bound receptor, –> taken into the cell via endocytosis

34
Q

Absorption of Calcium

A

Absorption is dependent on a calcium-binding
protein in intestinal cells

These receptors can be increased by vitamin D

35
Q

Complications of duodenal resection

A

Ulceration
-Duodenum has Brunner’s glands to secrete mucus rich in HCO3-

Malabsorption
-Iron
-Calcium
-Phosphate
-Impaired fat emulsification

Dumping to uncontrolled passage of chyme

36
Q

Complications of ileal resection

A

Impaired bile salt reabsorption
–> Increased large bowel malignancy due to bile salts reaching colon
–> Gallstones: decrease in bile salt pool; this predisposes to cholesterol gallstones

B12 deficiency
–> Macrocytic anaemia
–> Subacute degeneration of cord

Impaired water reabsorption
–> Diarrhoea

37
Q

Pancreatic proteolytic enzymes

A

Secreted in inactive form = zymogen granules from pancreatic acinar cells

Activation of trypsinogen to trypsin –> activation of proteolytics

Activation of trypsinogen is by an enzyme secreted by the duodenum enterokinase and the alkaline environment

38
Q

Procarboxypeptidase

A

Cleaves peptides at C-terminus

Secreted by pancreas

39
Q

Chymotrypsin, trypsin and elastase

A

Cleave peptide bonds

Secreted by pancreas

40
Q

Splits α-1,4-glycosidic bonds

A

Amylase

41
Q

Amylase

A

Splits α-1,4-glycosidic bonds

Strach digestion resulting in oligosaccharides

42
Q

Phases of exocrine secretion from pancreas

A

Cephalic: vagal

Gastric: vagal

Intestinal: CCK and secretin.

43
Q

Complications of pancreatic resection

A

Malnutrition from malabsoption
-Inability to breakdown proteins
-Inability to breakdown fats
-Fat-soluble vitamin deficiency (ADEK)

Malabsorption: loss of alkaline pancreatic secretions
leads to failure to neutralise gastric chyme and leads
to Fe2+, Ca2+ and PO4
− malabsorption; this eventually leads to anaemia and osteoporosis

Diabetes mellitus: loss of the pancreas leads to an
absolute deficiency of insulin.

44
Q

Cholic acid and chendeoxycholic acid

A

Bile ACIDS

45
Q

Bile salts

A

Formed by linking glycine and taurine to bile acids

Cholic acid and chendeoxycholic acid = bile acids

46
Q

Transport of bilirubin circulation

A

Poorly soluble

Bound to albumin

After glucoronidation –> becomes water soluble

47
Q

25-hydroxycholecalciferol

A

Formed in liver by 25 - hydroxylation of Vit D3

48
Q

Clinically detectable Jaundice

A

> 40

49
Q

Complications of cholecystectomy

A

Inability to concentrate bile –> Increased flow of bile –> reflux and biliary gastritis

Formation of micelles during fat absorption is impaired
–> fat intolerance and malabsorption
–> abdominal pain and diarrhoea

50
Q

Enteroglucagon

A

Inhibits gastric and small bowel motility

Released by distal ileum and colon

Presence of glucose of fats in colon or distal ileum
–> enteroglucagon –> inhibits gastric and small bowel motility

51
Q

Essential amino acids

A

Cannot be synthesised

Isoleucine
Leucine
Lysine

Methionine
Phenylalanine
Threonine
Typtophan
Valine

52
Q

Essential fats

A

Linolenic
Linoleic
Arachidonic acid

53
Q

Selenium

A

Part of glutathioner peroxidase

AND

Responsible for convertign T4 –> T3 in liver microsomes

54
Q

Chromium

A

Facilitates action of insulin

55
Q

Copper

A

Required for synthesis of haemoglobin and is a component of coenzymes in the electron transport chain

56
Q

Hunger or feeding centre

A

Lateral hypothalamus

57
Q

Satiety centre

A

Ventromedial hypothalamus

Satia's MRCS copied decks (32 decks)

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