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Gastro > Stomach Physio > Flashcards

Stomach Physio Flashcards

1
Q

Types of muscles in GI (2)

A

smooth muscle
1. longitudinal muscle
2. circular muscle

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2
Q

what controls contraction of smooth muscle

A

pacemaker cell - interstitial cell of cajal (connects to both longitudinal & circular muscle)

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3
Q

what are the characteristics of action potentials interstitial cell of cajal creates? (2)

A
  • usually: slow waves without action potential (lower than threshold potential) and contraction
  • under certain conditions (food): action potential triggered, contraction occurs
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4
Q

Activity of smooth muscles in (1) sphincters; (2) blood vessels/ airways; (3) stomach/ intestines; (4) esophagus/ urinary bladder

A

(1) normally contracted, occasionally relax
(2) normally partially contracted and varies slightly (tone)
(3) phasically active (peristalsis etc)
(4) normally relaxed, occasionally contracted

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5
Q

What occurs in mastication? (4)

A
  • food broken down by chewing and mixed with saliva to enhance TASTE
  • mucous in saliva lubricate food, ease swallowing
  • salivary enzymes (a-amylase) mixed with food
  • increase SA of food by breaking into smaller pieces
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6
Q

process of swallowing (3)

A
  1. Oral (voluntary) phase - chewing, food bolus formation
  2. Pharyngeal phase (involuntary) (1-2 s)
  3. Oesophageal phase (involuntary) - pri peristalsis + sec peristalsis
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7
Q

steps in pharyngeal phase of swallowing (5)

A
  1. tongue block oral cavity (prevent backflow of food)
  2. vocal folds close to protect airway to lungs
  3. soft palate blocks entrance into nasal cavity
  4. larynx pulled up with epiglottis covering entrance to trachea (respiration inhibited)
  5. upper esophgeal sphincter opens to allow passage to esophagus
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8
Q

what is primary peristalsis

A
  • voluntary process
  • generated by swallowing signal
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9
Q

what is secondary peristalsis

A
  • involuntary process (smooth muscle)
  • generated by food bolus which stretches smooth muscle -> create peristaltic wave
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10
Q

arrangement of layers of stomach (8)

A

mucosa (outermost layer):
- epithelium - simple columnar
- lamina propria
- muscularis mucosae

submucosa

muscularis layer:
- oblique layer
- circular
- longitudinal (deepest)

**same as intestines & esophagus except no oblique muscles for both

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11
Q

what are the 3 motor functions of stomach and where do they occur

A
  • reservoir function [proximal, fundus] - relaxation, accommodation
  • churning function [distal, antrum]
  • emptying function [antrum-pylorus-duodenum unit]
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12
Q

2 types of stomach relaxation to serve as reservoir

A
  • receptive relaxation - swallowing signal + peristalsis triggers stomach relaxation
  • adaptive relaxation - accomodate increase volume of food, gastric stretch receptors send signal via vagal afferent to CNS -> CNS send signals back via vagal efferent to relax stomach (VAGO-VAGAL reflex) through NO and VIP (vasoactive intestinal peptide)
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13
Q

what happens to stomach after vagotomy (removal of vagus nerve)

A
  • loss of vago-vagal reflex -> stomach cannot expand despite food filling up -> intraluminal pressures increase
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14
Q

What is the purpose of gastric churning

A
  • break food down into smaller pieces
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15
Q

what happens during gastric churning & trituration (3)

A
  1. propulsion - peristaltic wave push food towards closed pylorus (food stuck at antrum)
  2. grinding - antrum churns trapped food via antral contraction
  3. food is pushed back into proximal stomach and is broken down in the process

*repeats to break food down into small size

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16
Q

what regulates gastric emptying

A
  • pyloric sphincter (part of the antro-pyloric-duodenal unit)
  • prevents duodenal-gastric reflux
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17
Q

what characteristics of food INHIBIT (slow down) gastric emptying

A
  • pH - acids inhibit
  • tonicity - hypertonic (less water) inhibits
  • fatty acids inhibits
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18
Q

factors affecting gastric motility

A

Neural control
- vagal nerve -> eg stress, nausea
- vago-vagal reflex

Hormonal control
- gastrin -> stimulate gastric motility
- CCK, secretin, GIP -> inhibit gastric motility

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19
Q

2 characteristics of intestinal motility

A
  • peristalsis
  • segmentation
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20
Q

describe intestinal peristalsis (2)

A

propulsive segment:
- longitudinal muscle relax, circular muscle contract
- contraction of lumen

receiving segment
- longitudinal muscle contract, circular muscle inhibits
- dilation of lumen

LONG RANGE - compared to segmentation (local)
**peristalsis is triggered by RADIAL STRETCH of intestinal wall

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21
Q

describe segmentation

A
  • back and forth movement (local reflex) -> allow mixing of bolus
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22
Q

what happens during interdigestive periods (no food in lumen)

A

migrating motor complex (MMC) - intestinal contractions every 90-120min
- housekeeping -> continual sweeping of food debris to colon
- inhibit migration of colonic bacteria into distal ileum

**triggered by motilin (hormone released during fasting)
MMC stops when food enters small intestine and starts again when it is empty

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23
Q

What is the function of ileocaecal sphincter

A

Valve-like structure between ileum & colon

  • Regulate flow pass ileocaecal junction
  • Prevent reflux of colonic bacteria

Distension of ileum -> cause relaxation of the sphincter
Distension of proximal colon -> cause contraction of the sphincter

24
Q

functions of large intestines (3)

A

storage -> most excreted within 72 hrs

non-propulsive segmentation
– mixing of colonic contents
– slow progression of contents distally
- retrograde movements

mass movements associated with defaecation (mass peristalsis)

25
Q

what can trigger defaecation

A
  • gastrocolic reflex (causes STRONG mass movements throughout the day)
  • initiated by distention of stomach (gastro colic) & duodenum (duodeno-colic)
  • occurs after meals
26
Q

what can decrease mass movements?

A

opiates (morphine, codeine) -> can cause constipation

27
Q

how does defaecation occur

A
  • passive distension of rectum until sufficiently large -> cause relaxation of internal anal sphincter (rectosphincteric reflex) -> feeling to defaecate
  • passive distension of rectum -> triggers contraction of rectal smooth muscle, contribute to increase pressure in rectum & relaxation of internal sphincter

defaecation NOT desirable:
- involuntary reflex (no need to hold your shit by will) by sacral nerves keep EXTERNAL sphincter contracted

defaecation desirable:
- relaxation of external
anal sphincter
- relaxation of pelvic wall muscles
- contraction of abdominal muscles

28
Q

problems with swallowing

A
  • dysphagia

presentations:
- pain (odynophagia), food stuck (solid/ liquid), choking,

29
Q

causes of dysphagia

A
  • abnormal oropharyngeal coordination cause choking (eg stroke pts)
  • obstruction -> press on esophagus/ inside esophagus
  • stricture -> scarring which restricts esophagus
  • dysmotility -> disruption of neurons thus peristalsis does not occur in esophagus
  • achlasia -> failure of LES (lower esophageal sphincter) to open -> food collects at lower esophagus causing vomiting etc
30
Q

Types of gastric secretions (2)

A
  • secretory: secreted into gastric lumen
  • hormonal: secreted into bloodstream
31
Q

What are the secretory products of stomach and what cells are they secreted by?

A
  • secrete pepsinogen + some lipase -> chief cells
  • secrete acid (HCl) -> parietal cells
  • intrinsic factor -> parietal cells
  • mucous & electrolytes to form a mucosal barrier
32
Q

what are the hormonal secretions from stomach

A
  • gastrin
  • ghrelin
33
Q

function of ghrelin

A
  • induce appetite, secreted on EMPTY stomach and reduced on FULL stomach
34
Q

function of gastrin and site of secretion

A
  • stimulate acid production, gastric secretions and intestinal motility, secreted on FULL stomach and reduced on EMPTY stomach
  • increase pancreatic secretion
  • growth hormone causing growth of GI mucosa
  • produced by G cell mainly found in antrum & duodenum
35
Q

what does a typical gastric gland (in corpus of stomach) contain

A

top to bottom:
- mucous cell
- parietal cells
- enterochromaffin cells -> secrete histamines
- chief cells
- D cells -> secrete somatostatin
- G cells

36
Q

morphological changes to a stimulated parietal cell (2)

A
  • canaliculi of cell becomes more prominent
  • tubulovesicles containing H+,K+,ATPase pumps gets embedded to membrane, begins pumping H+ into lumen
37
Q

process of acid production mechanism in parietal cells

A
  • CO2 + H2O converted to H2CO3 by carbonic anhydrase
  • H+ is pumped out of cell with exchange for K+ and use of ATP (H+,K+,ATPase), Cl- leaves cell via Cl- channel -> HCl secreted
  • other side of cell: HCO3- is pumped out of cell into blood with exchange for Cl- (maintains [Cl-] in cell)
38
Q

reason for alkaline tide after food

A
  • food ingested cause acid secretion and HCO3- production
  • HCO3- is pumped out of parietal cell into blood with exchange for Cl-
  • increase [HCO3-] in blood causes alkaline tide
39
Q

production and function of pepsinogen

A
  • pepsinogen secreted by chief cell is converted to pepsin (autocatalysis at low pH; highest activity at pH<3)
  • pepsin cleave and digests 10-20% of protein
  • inactivated irreversibly at duodenum pH (alkaline)
40
Q

production and function of intrinsic factor

A
  • secreted by parietal cells -> mainly in FUNDUS
  • absorb vit B12 -> forms digestion-resistant complex with B12 in intestines, IF-B12 complex is eventually absorbed at terminal ileum
  • same stimuli as those evoking HCl secretion
  • not affected by proton pump inhibitors
41
Q

how is gastric secretion stimulated (3)

A
  1. cephalic phase (30%) via vagus nerve -> smell & sight of food cause vagal center of medulla to transmit signals to increase secretion via vagal trunk
  2. local gastric phase (60%) -> 1)local secretory reflexes 2)vagal reflexes 3)gastrin-histamine stimulation acting on parietal cell to increase secretion/ intestinal cell to increase motility
  3. intestinal phase (10%) -> when food passes into intestines and there is abnormal amounts of acidity -> feedback to stomach to increase/reduce secretion
42
Q

describe the stimuli and mechanism of cephalic phase

A

stimuli:
- smell, taste, conditioning

mechanism:
- vagus nerve -> directly act on parietal cell
- vagus nerve -> act on gastrin producing cell (G cell) -> gastrin acts on parietal cell

43
Q

describe the stimuli and mechanism of gastric phase

A

stimuli:
- distension
mechanism:
- vagus directly act on parietal cell
- vagus act on gastrin cell -> gastrin act on parietal cell

stimuli:
- distension of antrum
mechanism:
- local reflex -> act on gastrin cell -> gastrin act on parietal cell

stimuli:
- amino acid, small peptides from breakdown of food
mechanims:
- gastrin -> act on parietal cell

44
Q

neurotransmitters used at synapse between vagus nerve and G cell/ parietal cell

A
  • G cell -> GRP (gastrin releasing peptide)
  • parietal cell -> ACh
45
Q

how is gastrin production in G cell regulated

A
  • production is stimulated by GRP released from vagus nerve
  • presence of negative feedback by G cell pH sensors -> reduce secretion of gastrin under high acidity
  • inhibited by D cells in presence of high [H+] -> D cells produce somatostatins -> downregulate gastrin production
46
Q

how is H+ production in parietal cell regulated

A
  • gastrin binds to parietal cell directly causing H+ release
  • stimulation by ACh from vagus nerve directly causing H+ release
  • gastrin/ ACh (from vagus nerve) binds to enterochromaffin like cells (ECL) -> histamine production -> bind to parietal cell and release H+

**histamine produced by ECL can also bind to chief cell to stimulate pepsinogen release. OR gastrin can bind directly to chief cell to stimulate pepsinogen release (PRIMARY PEPSINOGEN PRODUCTION STIMULUS)
OR ACh from vagus nerve stimulate chief cell directly

47
Q

effect of chemical mediators (histamine, ACh, gastrin) on parietal cell

A

histamine
- binds to H2 histamine receptors -> release cAMP

ACh
- binds to M3 receptors -> release Ca2+

gastrin
- binds to CCK-B receptors -> release Ca2+

Ca2+, cAMP -> cause confirmation change of canaliculus + insertion of proton pump

48
Q

purpose of gastric mucosal barrier

A

protect against abrasion, HCl and pepsin

49
Q

components of thick mucous layer (1mm)

A
  • MUCINS, HCO3- -> UNSTIRRED LAYER slows inward diffusion of H+ & outward diffusion of HCO3-
  • certain PROSTAGLANDINS enhance mucus & HCO3- secretion
  • TREFOIL FACTORS (peptides) -> allow epithelial repair & formation of mucosal barrier
50
Q

why does gastric mucosal barrier have stem cell & renewal capacity

A
  • high turnover rate as gastric cells die frequently, requires constant replacement
51
Q

components of mucin

A

main constituent of gastric mucous
- large molecules (MW = 2x10^6) with carbohydrate side chain -> resistant to digestion

52
Q

function of mucin

A
  • coat & lubricate mucosal surface
53
Q

regulation of mucin production

A
  • same mechanisms that enhance HCl secretion (eg ACh)
  • mechanical stimulation (in presence of food)
54
Q

functions of prostaglandins

A
  • gastric epithelial defence/repair
  • regulate mucosal HCO3 & mucous
  • inhibit parietal cell secretion
  • mucosal blood flow
  • epithelial restitution
55
Q

Problems of stomach

A
  • GERD (gastrooesophageal reflux disease)
  • Gastritis
  • Intestinal metaplasia
  • Peptic ulcers
  • Gastric cancers
56
Q

Types of peptic ulcers (peptic ulcer disease)

A
  • gastric ulcers
  • duodenal ulcers

pathology:
– Helicobacter pylori
– Drugs eg.NSAIDs
– Zollinger Ellison syndrome (gastrinoma)

57
Q

what is atrophic gastritis

A
  • chronic inflammation of gastric lining -> atrophy & thinning of mucosal layer

Gastro (20 decks)

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