Gastric Disorders of Nutrient Processing Flashcards

1
Q

What is the goal of the stomach? (8)

A
  • Maximize efficient intake of energy/nutrients
  • Store rapidly ingested energy/nutrients with highly variable volume, consistency, particle size, energy density
  • Begin process of breaking down energy/nutrient sources for further digestion/absorption - Increase surface/volume
  • Delivery of energy/nutrients to small intestine and match its capacity
  • Expel indigestible components - Air up through esophagus (belch) or colon less; Solids: down to colon
  • Rapidly expel toxic material: vomiting
  • Help defend against invaders (which could eat our food/damage us)
  • Perform functions without damaging/digesting itself
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2
Q

What is proximal gastric motor function?
What is the purpose of this function?
What nerve mediates it?

A

Initially a receptive relaxation of fundus tone
Allows accommodation/storage of ingested meal
Reflex mediated via vagus nerve

Subsequent increase in tonic and phasic contractions
Push meal into antrum

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3
Q

What is the distal gastric motor function?
What mediates it?
What is the role of the pacemaker?
How do contractions propagate?

A

Baseline slow wave activity in muscle cell membrane potential
Mediated by interstitial cells of Cajal
Spread distally from pacemaker site: Frequency is 3/minute
Contractions (vagally mediated) sweep in a ring towards pylorus

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4
Q

What is the pyloric motor function?
How are its contractions timed?
What function does it serve?

A

Sphincter to block egress of large food particles (sieve)
Closure timed with oncoming antral ring contractions
1-2 mm in size and liquids pass through

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5
Q

What is the role of duodenal motor activity?

A

Pattern of coordination of duodenal contractions can facilitate or inhibit emptying of gastric contents into small bowel lumen
Preparation for vomiting

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6
Q

What neural receptors are responsible motor feedback control?
What afferents do they use?
What is the rate of energy delivery?

A

Receptors in small intestine identify nutrient delivery
Act via vagal afferents to alter gastric motility, retard emptying
Results in relatively constant (1-4 kcal/min) delivery of energy to small intestine

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7
Q

What is the feedback control roles (in response to and effect of) of secretin, somatostatin, cholecystokinin?

A

Secretin

Released in response to entry of lipids, amino acids or HCl into duodenum
Relaxes gastric tone, inhibits contractions, increases non-propulsive duodenal contractions

Somatostatin

Release in response to acid/peptides
Inhibits gastric emptying

Cholecystokinin

In response to delivery of fat
Inhibits gastric motility

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8
Q

What is the role of PYY, GLP-1/Glucose-dependent insulinotropic peptide, Ghrelin in terms of motor feedback control?

A

PYY – Illeal brake

Shuts down stomach movement
Nutrients to distal small intestine

GLP-1 and Glucose-dependent insulinotropic peptide

Secreted in small intestine in response to glucose delivery
GLP-1 also in response to colonic fermentation
Inhibition on gastric motility before insulin

Ghrelin

Increases emptying speed

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9
Q

What is the rate of glucose emptying?
What did the insulin-glucose clamp studies reveal?

A

Constant linear (1-4 kcal/min) emptying of glucose from stomach regardless of concentration

Increased blood sugar levels result in delayed solid and liquid meal emptying

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10
Q

What is role of chornic caloric intake on gastric motility?
What is anorexia nervosa?
How is motility in the obsese?

A

GI tract adapts to ongoing nutritional intake
Reduced calorie intake/weight loss causes delayed gastric emptying
Anorexia nervosa: Reverses on refeeding
Brief overfeeding accelerates gastric emptying in normal eeight subjects
Gastric emptying faster in the obese

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11
Q

What is a scintigraphy?

What is its limitation and what needs to be controlled for?

A

Nuclear medicine test to assess emptying non-invasively
Radiolabeling of solid or liquid
Detects amount at specific timepoints

Does not measure total emptying

Normal values depend on the type of food

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12
Q

When does fasting occur?

What is the characteristic of the contractions in fasting activity?

What solids can pass?

A

Occurs at end of meal
Onset delayed 1 hour for each 200 kcal ingested
Every 90 min (1 to 6 hours) with fast

Maximum strength, frequency (3/min) and coordination of contractions

Allows clearance of large (> 7 mm) indigestible solids from gut and enteric coated meds

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13
Q

What is the consequence of contraction failure?

A

Impaired triturtion of solids
Delayed delivery of nutrients
Retention of gastric contents
Pain, early saiety, nausea, vomiting, poor delivery

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14
Q

What are the consequences of accomodation failure?

A

Limits amount that can be ingested without discomfort
Pain/bloating
Early satiety
Nausea/vomiting
Weight loss
Food moves too rapidly into small bowel

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15
Q

What are the consequences of small bowel?

A

Extensive distension
Bloating, pain, symptomatic hypotension
Particles too large
Poorly timed for biliary secretions
Inadequate time for nutrient absorption (weight loss, nutrient deficiencies)
Colonic bacterial fermentation (flatus, bloating, osmotic diarrhea, cramps)
Humoral lag in response resulting in initial rising blood glucose followed by compensatory hypoglycemia (Reduced glucose delivery)
Unbuffered HCl to duodenum

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16
Q
A
17
Q

What are the consequences of unbuffered HCl to duodenum?

A

Ulcer to mucosa
Destruction of pancreatic enzymes
Pain, maldigestion

18
Q

What are consequences of MMC failure?

A

Failure to clear indigestible material from stomach (including meds)
Bezoar formation, poor drug delivery, small intestinal bacterial overgrowth

19
Q

What is gastroparesis?
What are the characteristic signs?
What is the most important diagnostic characteristic of gastroparesis?

A

Objectively delayed gastric emptying in absence of mechanical obstruction
Early satiety, postprandial fullness, nausea, vomiting, bloating, upper abdominal pain
Diagnosis requires exclusion of other causes

20
Q

What are the three types of causes for gastroparesis?

A

Intact structures with gastroparesis
Muscular injury
Neurologic injury

21
Q

What are the causes for gastroparesis if intact structures?

A

Electrolyte disturbances
Hyperglycemia
Renal failure with uremia
Hypothyroidism
Mesenteric ischemia
Cortical effects (motion sickness, stress)
Medications

22
Q

What medications can cause gastroparesis?

A

Anti-cholinergics
Opiates
NSAIDs (PG inhibition)
Pramlintide (amylin analog)
Exenatide (GLP-1 receptor agonist)
Cyclosporine - Unknown mechanism

23
Q

What kinds of muscular injury can cause gastroparesis?

A

Infantile pyloric stenosis
Hollow visceral myopathies
Connective tissue disease (scleroderma)
Gastric resection (ulcer surgery)
Fundoplication wrap for reflux disease

24
Q

What neurologic injuries cause gastroparesis?

A

Parkinson’s
Multiple sclerosis
Amyloidosis
Viral infection/auto-immune
Hereditary neuropathies
Paraneoplastic syndrome
Trauma/surgical injury

25
Q

What causes vagal injury?
What are the effects on solids/liquids

A

Usually iatrogenic – Thoracic, esophageal, gastric surgery
May be intentional (ulcer surgery)

Opposite effects on solids/liquids
Poor accommodation : Liquids empty rapidly
Poor antral grinding: Solids empty slowly

26
Q

What is visceral hypersensitivity seem with?
What is the pain threshold?
What is it associated with?
What is the mechanism?
What does it put the patient at risk for?

A

Seen with post-prandial pain but no ulcer (non-ulcer dyspepsia)

Lower threshold for pain with:
Gastric distension with balloon and gastric/duodenal acid infusion
Thresholds are lowered with stress

Associated with anxiety/depression, aging, diabetes, drugs, analgesics

Possible mast cell mechanism
Reduced ability to detect and respond to pathologic processes

Greater complications: Ulcer disease

27
Q

What is diabetic dysfunction requires what kind of diabetes?
What mechanism is affiliated with it?
What is the effect of hyperglycemia?
What is the effect on gastric emptying?
How do symptoms relate with the severity of gastric emptying?

A

Long-term of either type

Extrinsic vagal dysfunction
Loss of enteric neurons, interstitial cells of Cajal

Hypergylcemia affects motor function

Rapid or slow gastric emptying

Symptoms correlate poorly with severity of gastric emptying abnormality