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Phase 1 Flashcards > Gastric physiology 1 > Flashcards

Gastric physiology 1 Flashcards

1
Q

What artery supplies the foregut? Organs included in the foregut?

A

The celiac artery

Pharynx, oesophagus, stomach and proximal half of duodenum and derivative (liver, biliary apparatus and pancreas)

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2
Q

What artery supplies the midgut? Organs included in midgut?

A

Superior mesenteric artery.

Distal half of duodenum, jejunum, ileum, caecum, appendix, ascending colon and right 2/3rds of transverse colon.

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3
Q

What artery supplies the hindgut? Organs included in hindgut?

A

Inferior mesenteric artery.

Left 1/3 of transverse colon, descending colon, sigmoid colon, rectum and anal canal.

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4
Q

What are mesenteries? Organ is known as what? What organs are intraperitoneal?

A

Parts of the gut tube suspended from the dorsal and ventral body walls by these.
Double layers of peritoneum that surround an organ and connect it to the body wall.
Intraperitoneal
Stomach, spleen, liver, small intestine, transverse and sigmoid colon

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5
Q

What is a retroperitoneal organ? Which organs? Mnemonic to remember?

A

When it sits on the posterior abdominal wall and is covered by peritoneum on its anterior surface only.
Suprarenal (adrenal gland,) aorta, duodenum, pancreas, ureters, colon (ascending and descending,) kidneys, oesophagus and rectum.
SADPUCKER

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6
Q

What are ligaments? Mesenteries and ligaments provide pathways for what?

A

Double layers of peritoneum which pass from one organ to another or one organ to the body wall.
Blood vessels, lymphatics and nerves to go to and come from the abdominal viscera.

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7
Q

When is swallowing initiated?

A

When pressure receptors in walls of the pharynx are stimulated by food or drink- forced into rear of mouth by tongue.

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8
Q

What is the first stage (voluntary) of swallowing?

A

Food is compressed against the roof of the mouth and pushed towards oropharynx by tongue.
Buccinator and supra hyoid muscles manipulate food during chewing and elevate hyoid bone and flatten floor of mouth.

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9
Q

What is the 2nd stage (involuntary) of swallowing?

A

Nasopharynx is closed off by soft palate- helps form bolus
Pharynx is shortened and widened using longitudinal muscles by elevation of hyoid bone
Impulses from swallowing centre inhibit respiration, raise larynx and close glottis
Epiglottis closed by food

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10
Q

What is stage 3 (involuntary) of swallowing?

A

Contraction of constrictor muscles followed by depression of hyoid bone and pharynx
Pharyngeal constrictor muscles contract from above down to drive bolus into oesophagus
Depression of hyoid bone and pharynx is by infra hyoid muscles

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11
Q

What muscle surrounds the oesophagus? Ring of skeletal muscle just below the pharynx? In last portion of oesophagus?

A

Skeletal surrounds upper third and smooth surround lower 2/3rds.
Upper oesophageal sphincter.
Lower oesophageal sphincter.

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12
Q

What are peristaltic waves? One wave takes how long to reach the stomach? What does the lower sphincter do during swallowing?

A

Food moves towards the stomach by progressive wave of muscle contractions along the oesophagus.
9 seconds
Relaxes

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13
Q

What is the gag reflux? Reflex arc between what nerves?

A

Irritation of the oropharynx (back of the tongue).

Glossopharyngeal and vagus nerve.

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14
Q

3 functions of saliva? Serous secretion? Mucous secretion?

A

1) Lubricant for mastication
2) Maintaining oral pH- about 7.4 due to bicarbonate/ carbonate buffer system
3) Release digestive enzymes- salivary alpha amylase from parotid gland
Alpha amylase
Mucins for lubrication of mucosal surfaces

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15
Q

Is parotid gland serous/ mucous? Submandibular gland? Sublingual glands? Minor glands?

A

Serous
Mucous and serous
Mucous and serous- mainly mucous
Mainly mucous but some serous

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16
Q

Factors affecting composition and amount of saliva?

A

Flow rate, circadian rhythm, type and size of gland, duration and type of stimulus causing saliva, diet, drugs, age, gender and time of day

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17
Q

4 defences of the oral cavity?

A

1) Mucosa- physical barrier
2) Saliva washes away food which bacteria/ viruses may use as metabolic support
3) Palatine tonsils= ‘surveillance’ for immune system
4) Salivary glands surrounded by lymphatic system- contain range of immune cells

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18
Q

Which glands are continuously active? Unstimulated components dominated by what? Which gland only becomes main source of saliva when stimulated?

A

Submandibular, sublingual and minor
Submandibular components
Parotid gland

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19
Q

How is salivary secretion stimulated? How is it inhibited?

A

Via parasympathetic NS.

Via sympathetic NS.

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20
Q

What is xerostomia? Salivary output below what %? May be consequence of what? Most common causes?

A

Dry mouth, 50%
Cystic fibrosis/ Sjorgren’s syndrome
Medication and irradiation for head/ neck cancers

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21
Q

How are obstructions caused? Most common where?

A

Calcium and phosphate ions can form salivary calculi (stones)
In submandibular gland- block duct at bend around round mylohyoid/ at exit at sublingual papillae

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22
Q

What is inflammation caused by? Infections caused by what?

A

Infection secondary to obstruction

Mumps– fever, malaise, swelling of glands

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23
Q

Degeneration of glands caused by what?

A

Complication of radiotherapy to head and neck for cancer treatment
Sjorgen’s syndrome- affects lacrimal glands

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24
Q

Effects of salivary gland dysfunction?

A

Xerostomia
Low lubrication– oral function becomes difficult
Low natural oral hygiene- poor pH control– plaque build up, increases infection incidence, especially fungal e.g. candida- thrush

25
Q

9 functions of the stomach?

A

Store and mix food, dissolve and continue digestion, regulate emptying into duodenum, kill microbes, secrete protease, secrete intrinsic factor, activate proteases, lubrication and mucosal protection

26
Q

6 main cell types in stomach?

A

Mucous cells- mucous at entrance to gland
Parietal cells- gastric acid and intrinsic factor
Chief cells- pepsinogen
ECL cells- histamine
G cells- gastrin
D cels- somatostatin

27
Q

Epithelial layer of stomach invaginate into what and forms what? Glands in thin walled upper portions of body of stomach secrete what?

A

Mucosa- forms many tubular glands

Mucous, HCL from parietal cells and pepsinogen from chief cells

28
Q

Antrum in stomach has thicker layer of what? Secrete little what but secretes what?

A

Smooth muscle- mixes stomach contents

Little HCl but secrete gastrin

29
Q

From what cells does gastric acid secretion occur from? Volume secreted per day?
What is broken down in these cells?

A

Parietal cells
2 litres/ day
H2O into OH- and H+ ions

30
Q

CO2 and H2O from where is converted into H2CO3 via carbonic anhydrase? H2CO3 dissociates into what?

A

Respiration

HCO3- and H+

31
Q

H+ from H2CO3 can be used to do what? H+ ions from breakdown of H2) go where?

A

Reform H2O using OH- from breakdown of H2O

Pumped into stomach lumen via H+/ K+ ATPase pumps- require ATP

32
Q

K+ ions pumped into parietal cells go where?

Where does HCO3- from H2CO3 go? Cl- ions enter cells through what?

A

Diffuse back out into stomach via K+ channels on plasma membrane
Secreted into capillary for exchange of Cl- ions
Cl- channels in plasma membrane

33
Q

What things react to form HCl in the stomach? How is acid secretion increased?

A

H+ and Cl- ions
Migration of H+/ K+ ATPase protein in membranes of intracellular vesicles to plasma membrane by fusion with membrane- more H+ can be pumped in

34
Q

What is the cephalic phase of acid secretion? Via what NS? Initiated by what things? What thing is released? What does ACh act on?

A 
During a meal  
Parasympathetic 
Sight, smell, taste of food and chewing 
ACh
Acts indirectly on parietal cells- triggers released of gastrin from G cells in antrum and histamine from ECL cells
35
Q

How does gastrin and histamine increase acid secretion?

A

The number of H+/K+ ATPase pumps on plasma membrane of parietal cell are increased

36
Q

What is the gastric phase of acid production? Initiated by? What thing is released? Gastrin triggers release of what?

A

Once food has reached the stomach
Gastric distension- from volume of ingested material and presence of peptides and amino acids
Gastrin- acts directly on parietal cells
Histamine- also acts directly

37
Q

Why is histamine really important?

A

It mediates the effects of gastrin and acetylcholine- good therapeutic target for e.g. acid overproduction

38
Q

How does protein in the stomach increase acid production?

A

1) Direct stimulus for gastrin release
2) Act as buffer, reduce amount of H+ ions– decreased somatostatin secretion– more parietal cell activity– more acid production

39
Q

How does a low pH during gastric phase reduce acid secretion?

A

Directly inhibits gastrin secretion- indirectly inhibits histamine released
Stimulates somatostatin release- inhibits parietal cell activity

40
Q

What is the intestinal phase initiated by? Triggers release of enterogastrones such as what? What else is triggered?

A

Duodenal distension, low pH, hypertonic solutions, presence of amino acids and fatty acids.
Secretin(inhibits gastrin released and promotes somatostatin release) and cholecystokinin (CKK)
Short and long neural pathways- reduce ACh release

41
Q

What is an ulcer? Causes of peptic ulcer? Lives where? Secretes what substance which does what? Combines with H+ to form what?

A

Breach in a mucosal surface
Helicobacter pylori infection, NSAIDs, alcohol, bile salts
In gastric mucus
Urease splitting urea into CO2 and NH3
Ammonium- toxic to gastric mucosa resulting in less mucous

42
Q

What things can begin attacking the gastric epithelium further reducing mucous production? Results in what? Treatment for peptic ulcers?

A

Secreted proteases, phospholipase and vacuolating cytotoxin A
Inflammatory response and less mucosal defence
Triple therapy- proton pump inhibitor (organism cannot live in alkaline) and antibiotics

43
Q

How do NSAIDs cause peptic ulcers?

A

They inhibit cyclo-oxygenase 1 which is needed prostaglandin synthesis.
Mucous secretion is stimulated by prostaglandins (also trigger inflammatory response in inflamed tissue.)

44
Q

Treatment for peptic ulcers from NSAIDs?

A

Use prostaglandin analogues- mimic effect of prostaglandins e.g. misoprostol and reduce acid secretion

45
Q

How do chemical irritants and duodenal-gastric reflux cause peptic ulcers? What are gastrinoma?

A

Wash away protective mucous lining- reduce mucosal defence
Rare tumours of parietal cells- excessive gastrin released= increase in gastric acid– increased attack on gastric mucosa

46
Q

Examples of proton pump inhibitors? What do H2 receptor agonists do? Examples?

A

Omeprazole, lansoprazole and esomeprazole

Block receptors for histamine thereby reducing acid secretion e.g. cimetidine, ranitidine

47
Q

Protective mechanisms of gastric mucosa? Tight junctions

A

Alkaline mucus on luminal surface, tight junctions between epithelial cells, stem cells at base of pits to produce new cells from damaged ones, feedback loops

48
Q

What is inactive form of pepsin? Produced by what cells? Mediated by input from what NS? What causes pepsin to be produced? What type of loop?

A

Pepsinogen
Chief cells
Enteric nervous system- via ACh (parasympathetic)
When pepsinogen goes into stomach and low pH from HCl
Positive feedback loop

49
Q

What released in the duodenum irreversibly inactivates pepsin? Stomach parietal cells produce what to enable vitamin B12 absorption in small intestine? Vitamin B12 helps with what? How?

A

HCO3-
Intrinsic factor
Protein digestion- breaks down collagen in meat- helps shred meat

50
Q

How can the volume of the stomach increase from 50ml to 1.5L with little increase in luminal pressure? Mediated by what nervous system? Coordination provided by what?

A

Smooth muscles in body and fungus receptive relaxation
Parasympathetic nervous system acting on enter nerve plexuses
Afferent input from stomach via vagus nerve and swallowing centre in brain

51
Q

What two substances released by the enteric nerves mediate relaxation in stomach muscles? Peristaltic waves in stomach starts where? Peristaltic contraction varies how?

A

Nitric oxide and serotonin
In body towards the antrum
In strength

52
Q

Power of contraction sin body compared to the antrum? What closes as peristaltic waves reaches it? This means what?

A

More powerful in antrum- enables better mixing
Pyloric sphincter
Little chyme enters the duodenum and astral contents forced back towards the body

53
Q

Frequency of peristaltic waves in stomach determined by what cells? They undergo slow what cycle types? Depolarisation waves are transmitted how?

A

Pacemaker cells= interstitial cells of Cajal in muscular proprietary (longitudinal muscle layer)
Slow-depolarisation-repolarisation cycles
Through gap junctions to adjacent smooth muscle cells

54
Q

How active are interstitial cells of Cajal? Action potential threshold for muscle contraction can be altered how?

A

Active all the time

Enteric nervous system

55
Q

What 2 things can increase strength of contractions? What 6 things can decrease contraction strength?

A

Gastrin and gastric distension (mediated by mechanoreceptors)

Duodenal distension, increase in duodenal fat, increase in duodenal osmolarity, decrease in duodenal pH, increase in sympathetic stimulation and decrease in parasympathetic stimulation

56
Q

Does the stomach/ duodenum have a greater capacity? Overfilling of duodenum results in what?

A

Stomach
Dumping syndrome- vomiting, bloating, cramps, diarrhoea, dizziness, fatigue, weakness, sweating and electrolyte imbalances

57
Q

Gastroparesis (delayed gastric emptying) caused by what? Can cause what?

A

Idiopathic(cause unknown,) autonomic neuropathies, abdominal surgery, Parkinsons disease, multiple sclerosis, scleroderma, amyloidosis, female generates
Matter in stomach can rot and smell

58
Q

Symptoms of delayed gastric emptying? Symptoms and causes of GORD?

A

Nausea, early satiety, vomiting undigested food, GORD

Pregnancy, hiatus hernia, obesity, smoking/ abdominal pain/ bloating, anorexia

59
Q

Drugs that can cause delayed gastric emptying?

A

H2 receptor antagonists, proton pump inhibitors, opioid analgesics, diphenhydramine, beta-adrenergic receptor agonists, calcium channel blockers and Levodopa

Phase 1 Flashcards (35 decks)

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