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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
If you are vegan, will the gastric phase still stimulate secretions for protein digestion in the stomach? Why?
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
26
in the ____, there will be correct enzyme secretion based on what was in the diet because...
duodenum; | absorption of nutrients allow body to know what is needed
27
___ enzyme secretion is affected by diet
pancreatic
28
symptoms of gastric ulcer
- nausea after meals - burning sensation in stomach that gets worse a few hours after meal & at night - poor appetite - weak
29
Contributions of Dr. Marshall & Dr. Warren to ulcer discovery
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
Caues of peptic ulcers
Primary: H. pylori Secondary: drugs, excess acid, stress ulcers, others
31
example of a drug that causes ulcers
NSAIDs: decrease secretion of prostaglandins (responsible for secretion of mucus & bicarb in the stomach)
32
which disease may cause peptic ulcers?
- ZE syndrome | - pseudo ZE syndrom
33
ZE syndrome vs. pseudo ZE syndrome
ZE: increased gastrin secretion due to pancreatic tumour pseudo ZE: increased gastrin secretion due to G cell hyperplasia (enlarged)
34
What are stress ulcers?
Ulcers due to cells damaged by hypoxic conditions (after trauma/stress: surgery, burn, etc.)
35
What is Cushing's ulcer
Due to head injuries → increased intercranial pressure → dorsal vasal nuclei → vagus nerve → gastrin secretion
36
Can you have H. pylori without having an ulcer?
Yes
37
areas of the world with high prevalence of H. pylori
- South America | - Europe
38
transmission of H. pylori
- oral-oral | - oral-fecal
39
Gastric lymphoma is most common in which type of people?
older people
40
Gastric lymphoma = lymphoma of...
GALT (gut-associated lymphatic tissues)
41
most people with gastric lymphoma have...
H. pylori in their stomach
42
How does H. pylori survive in the stomach?
Synthesize enzyme "urease" which can create an ura of bicarb around them (prevent effects of HCl)
43
What does H. pylori do in the stomach? (slide 20)
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
most peptic ulcers reach ___ layers. Those that reach all 4 layers is called ____.
mucosal & submucosal; | perforated ulcers
45
What is a clever way to test for presence of H. pylori?
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
Ways to detect H. pylori
1) look for antibodies 2) grow from biopsy 3) breath test
47
What will happen to breath test result if there is no H. pylori?
Excreted C-14 in urine, unchanged
48
Ways to get rid of H. pylori
1) antibiotics | 2) increase pH in stomach (allow best environment for antibiotic function)
49
What can be used to increase pH in stomach?
1) H/K pump inhibitors 2) H2 antagonists: histamine can't signal HCl secretion anymore 3) Bismuth: metal
50
Intestinal phase is activated by...
chyme / distention in the small intestines
51
Secretions during the intestinal phase
- S cells → secretin - I cells → CCK - GIP & GLP-1
52
Effect of CCK
- secretion of pancreatic enzymes - increase contractilty of gall bladder → more bile - stop stomach motilty
53
effect of secretin
- fluid & bicarb secretion | - stop stomach motility
54
enterogastric reflex is initiated when...
mechanoreceptors & chemoreceptors sense chyme entering the small intestines
55
enterogastric reflex
- stop peristalsis (stops myenteric plexus) - relaxation of stomach - contraction of pyloric sphincter
56
myentric plexus controls...
motility patterns in the stomach
57
effect of GIP & GLP-1
- insulin secretion | - inhibit stomach motility
58
There are osmoreceptors in the small intestines that...
- identifies solutes in chyme - blood borne product - feedback to stop stomach motility
59
CFTR channels are present on what cells?
Cells that secrete mucus | Salivary glands, Tear ducts, Intestinal cells, Lungs
60
Why do people infected with cholera tend to have diarrhea?
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
How to treat severe diarrhea?
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
osmolarity of ORS
311 mmol/L
63
fecal transplant is used to treat...
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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