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PSL301 > Digestion 5 & 6: Control, Disorders, and Diseases > Flashcards

Digestion 5 & 6: Control, Disorders, and Diseases Flashcards

1
Q

3 phases of GI activity. The name of the phase tells you…

A

1) cephalic phase
2) gastric phase
3) intestinal phase

where the activity begins

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2
Q

Cephalic phase: excitatory // inhibitory?

A

excitatory; promote movement and digestion of material

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3
Q

Gastric phase: excitatory // inhibitory?

A

excitatory; promote movement and digestion of material

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4
Q

Intestinal phase: excitatory // inhibitory?

A

inhibitory: slows digestion → stops digestion

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5
Q

Cephalic phase is activated when…

A

seeing, smelling, tasting, thinking about food

  • activates salivary reflex
  • short duration: ends when bolus enters esophagus
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6
Q

when does the cephalic phase end?

A

when bolus enters esophagus

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7
Q

process of swallowing (CNS)

A

food in mouth → CN IX, X → swallowing center (medulla) → CN V, VII, IX, X, XII → swallowing

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8
Q

CN =

A

cranial nerve

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9
Q

effect of cephalic phase on stomach

A
  • Swallowing activates CN X
  • X stimulate submucosal plexus
    → mucous cells → mucus
    → chief cells → pepsinogen
    → Parietal cells → HCl
    → G cells → gastrin
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10
Q

Effect of cephalic phase on small intestines

A

Very small influence;

1) Vagus nerve → G cells in stomach → gastrin → ancinar cells of pancreas → enzyme secretion
2) Vagus nerve → duct cells → bicarb secretion

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11
Q

GERD

A

gastroesophageal reflux disease

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12
Q

Long-term risks of GERD

A

Barrett’s esophagus: potential precursor to esophageal cancer

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13
Q

Barrett’s esophagus

A

causes the metaplasia of cells in the distal esophagus

  • epithelial cells become goblet cells
  • may lead to esophageal cancer due to abnormal behaviour of cells
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14
Q

GERD is caused by…

A

acidic chyme splashing back into the esophagus

  • relaxed lower esophageal sphincter
  • damage cells in lower esophagus
  • become goblet cells to protect themselves
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15
Q

GERD can happen because…

A
  • full stomach
  • lying down
  • breathe in: esophagus passes through thorax and will suck up some chyme (*think: syringe)
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16
Q

Symptoms of GERD

A
  • burning sensation in lower chest that spreads towards neck
  • chronic, reoccurring heart burn
  • worst symptoms after eating, but symptoms are constantly present
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17
Q

Treatment for GERD

A

Drugs: antacid (reduce acid secretion), enhance stomach emptying

Lifestyle: smaller meals, lose weight, eat earlier, stop smoking

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18
Q

diagnosis for GERD

A

use pH monitoring catheter at lower esophagus for 24h

  • normal individuals will have only a few instances where pH < 5 (after meals)
  • GERD: many instances where pH <5, constant low pH during night (lying down)
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19
Q

Foods that enhances effects of GERD

A
  • fatty meal (stops stomach emptying)
  • alcohol & caffeine (more gastrin→HCl secretion)
  • chocolate
  • peppermint
    → increased relaxation of lower esophageal sphincter
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20
Q

Why does smoking make GERD worse?

A

Smoking causes:

  • weakens LES muscle permanently
  • reduce salivation (less protection for esophagus)
  • deep breathing when smoking (suck up chyme)
  • smoker’s cough: pressure on abs push stomach inward (similar to emesis)
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21
Q

Cephalic phase is a ___ reflex

A

long

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22
Q

Gastric phase is a ___ reflex

A

short

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23
Q

Stimuli for gastric phase

A

1) Distension of stomach (mechanoreceptors) → submucosal and myenteric plexuses of ENS
2) elevated pH (chemoreceptors): food entering stomach will make stomach less acidic → activate ENS → peristalsis & secretions
3) partially digested peptides → G cells → gastrin → more HCl and pepsinogen secretion & peristalsis

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24
Q

Regulation of stomach secretions (process) during gastric phase

A
  1. food initiates gastric secretions & activate ENS
  2. ENS → G cells → gastrin → ECL cell & parietal cells → more HCl
  3. acid → chief cells → pepsinogen → pepsin
  4. increased stomach acidity → D cells → somatostatin → stop HCl & pepsinogen secretion (neg feedback: takes 3h)
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25
Q

If you are vegan, will the gastric phase still stimulate secretions for protein digestion in the stomach? Why?

A

Yes;

  • gastric phase builds upon cephalic phase
  • protein still present in stomach (enzymes, cell lining)
  • less secretion will happen, but it will still happen
  • most of enzymes & dead epithelial cells will be recycled
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26
Q

in the ____, there will be correct enzyme secretion based on what was in the diet because…

A

duodenum;

absorption of nutrients allow body to know what is needed

27
Q

___ enzyme secretion is affected by diet

A

pancreatic

28
Q

symptoms of gastric ulcer

A
  • nausea after meals
  • burning sensation in stomach that gets worse a few hours after meal & at night
  • poor appetite
  • weak
29
Q

Contributions of Dr. Marshall & Dr. Warren to ulcer discovery

A

Warren: biopsy of patients with stomach ulcers have bacteria → bac’t shouldn’t be able to exist in stomach

Marshall: took culture of bacteria and experimented on himself → got acute gastritis (precursor to ulcer) with epithelial damage → cured by antiboitics
(ONLY INFLAMMATION, NO ULCER DEVELOPMENT)

30
Q

Caues of peptic ulcers

A

Primary: H. pylori

Secondary: drugs, excess acid, stress ulcers, others

31
Q

example of a drug that causes ulcers

A

NSAIDs: decrease secretion of prostaglandins (responsible for secretion of mucus & bicarb in the stomach)

32
Q

which disease may cause peptic ulcers?

A
  • ZE syndrome

- pseudo ZE syndrom

33
Q

ZE syndrome vs. pseudo ZE syndrome

A

ZE: increased gastrin secretion due to pancreatic tumour

pseudo ZE: increased gastrin secretion due to G cell hyperplasia (enlarged)

34
Q

What are stress ulcers?

A

Ulcers due to cells damaged by hypoxic conditions (after trauma/stress: surgery, burn, etc.)

35
Q

What is Cushing’s ulcer

A

Due to head injuries → increased intercranial pressure → dorsal vasal nuclei → vagus nerve → gastrin secretion

36
Q

Can you have H. pylori without having an ulcer?

A

Yes

37
Q

areas of the world with high prevalence of H. pylori

A
  • South America

- Europe

38
Q

transmission of H. pylori

A
  • oral-oral

- oral-fecal

39
Q

Gastric lymphoma is most common in which type of people?

A

older people

40
Q

Gastric lymphoma = lymphoma of…

A

GALT (gut-associated lymphatic tissues)

41
Q

most people with gastric lymphoma have…

A

H. pylori in their stomach

42
Q

How does H. pylori survive in the stomach?

A

Synthesize enzyme “urease” which can create an ura of bicarb around them (prevent effects of HCl)

43
Q

What does H. pylori do in the stomach? (slide 20)

A
  1. use pH sensors to swim to mucus layer
  2. drill through mucus layer to epithelial cells
  3. touch, but not enter epithelial cells
  4. cause filaments to push up & form pedestal for H. pylori
  5. H. pylori on pedestal release proteins that draw in neutrophils
  6. formation of pedestal release interleukins, which attract even more neutrophils → inflammatory response
  7. neutrophils release ROIs (reacted oxygen intermediates) that break down bilayer of epithelial cell from ISF
  8. H. pylori also causes cell to secrete vesicles filled with HCl → break down mucus layer from apical side
  9. Lining is defective & broken down → bleeding into stomach
44
Q

most peptic ulcers reach ___ layers. Those that reach all 4 layers is called ____.

A

mucosal & submucosal;

perforated ulcers

45
Q

What is a clever way to test for presence of H. pylori?

A

Breath test:

  1. Drink urea containing radioactive C-14
  2. H. pylori change C-14 → ammonium + 14-HCO3- (radioactive bicarb)
  3. radioactive bicarb goes to bloodstream
  4. Breath out into a balloon (release 14-CO2 in breath)
  5. put into scintillation fluid that detect radiation
  6. if counts appear on result reading = there is H. pylori
46
Q

Ways to detect H. pylori

A

1) look for antibodies
2) grow from biopsy
3) breath test

47
Q

What will happen to breath test result if there is no H. pylori?

A

Excreted C-14 in urine, unchanged

48
Q

Ways to get rid of H. pylori

A

1) antibiotics

2) increase pH in stomach (allow best environment for antibiotic function)

49
Q

What can be used to increase pH in stomach?

A

1) H/K pump inhibitors
2) H2 antagonists: histamine can’t signal HCl secretion anymore
3) Bismuth: metal

50
Q

Intestinal phase is activated by…

A

chyme / distention in the small intestines

51
Q

Secretions during the intestinal phase

A
  • S cells → secretin
  • I cells → CCK
  • GIP & GLP-1
52
Q

Effect of CCK

A
  • secretion of pancreatic enzymes
  • increase contractilty of gall bladder → more bile
  • stop stomach motilty
53
Q

effect of secretin

A
  • fluid & bicarb secretion

- stop stomach motility

54
Q

enterogastric reflex is initiated when…

A

mechanoreceptors & chemoreceptors sense chyme entering the small intestines

55
Q

enterogastric reflex

A
  • stop peristalsis (stops myenteric plexus)
  • relaxation of stomach
  • contraction of pyloric sphincter
56
Q

myentric plexus controls…

A

motility patterns in the stomach

57
Q

effect of GIP & GLP-1

A
  • insulin secretion

- inhibit stomach motility

58
Q

There are osmoreceptors in the small intestines that…

A
  • identifies solutes in chyme
  • blood borne product
  • feedback to stop stomach motility
59
Q

CFTR channels are present on what cells?

A

Cells that secrete mucus

Salivary glands, Tear ducts, Intestinal cells, Lungs

60
Q

Why do people infected with cholera tend to have diarrhea?

A

Cholera toxin (CT)

  1. CT goes into cell → cleaved and activated
  2. activate G-proteins → produce way more cAMP and PKA than necessary
  3. (P)-CFTR → cause channel to be stuck open
  4. Cl- mass exit the cell to lumen, which pulls water into lumen (diarreha if in intestines)
  5. (P)-CFTR also blocks NHE, meaning Na can’t enter the bloodstream → less water in bloodstream → dehydration
61
Q

How to treat severe diarrhea?

A

Oral rehydration therapy (ORS) replaces electrolytes lost, give water, buffer against acidosis

  • Na+
  • Glucose (SGLT for water transport)
  • KCl
  • Citrate (more stable, same function as bicarb, buffer against acidosis)
62
Q

osmolarity of ORS

A

311 mmol/L

63
Q

fecal transplant is used to treat…

A

older individuals that have recurring C.difficile infection
- Take safe-feces and put into the individual that has recurrent C.difficile infection and replace the bad bacteria with good bacteria

PSL301 (29 decks)

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