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Year 2 Med > Ingestion > Flashcards

Ingestion Flashcards

1
Q

What are the layers of the GI tract?

A
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2
Q

Describe smooth muscle

A
  • Non-striated
  • Ratio of thick to thin filaments is 12:1 to 18:1
  • Intermediate filaments eg. desmin can serve as anchor points for the contractile filaments
  • Specialised for long term and maintained contraction using limited ATP
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3
Q

What is the mechanism of calcium dependent smooth muscle contraction vs relaxation?

A
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4
Q

What is pharmomechanical vs electromechanical coupling?

A

Pharmacomechanical coupling:

  • Ca2+ levels required for contraction rise from SR and entry via non voltage gated channels
  • Chemicals bind to membrane receptors and activate G protein
  • PLC activation leads to an increase in the concentration of
    1P3 and DAG - initiates the rise in concentration of Ca2+
  • STIM1 is a Ca2+ sensor that activates the store operated Ca2+ channels
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5
Q

What is the mechanism of non-calcium dependent contraction?

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6
Q

What is the latch state?

A

Latch state- dephosphorylating myosin already on actin reduces its off rate, decrease in detachment rate would allow a greater number of cross-bridges resulting in lower rate of cross-bridge cycling and ATP hydrolysis meaning low energy consumption

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7
Q

What are slow waves and what causes them?

A

Slow waves- cyclical changes in membrane potential seen in GI smooth muscle cells which underlie physical contraction and relaxation, this is a result of interstitial cells of cajal (ICCs)- they are the electrical pacemakers for smooth muscle cells, they dont cause calcium to enter the muscle fibres but the spike potentials from peaks of slow waves cause calcium entry

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8
Q

The rate of passage through the gastrointestinal tract can be controlled by:

A
  • Contraction of sphincters
  • Changing the rate of peristalsis
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9
Q

What is the gastroileal, gastrocolic, enterogastric, intestinointestinal and colonileal reflexes?

A
  • Gastroileal reflex - Stomach activity promotes the opening of the ileocaecal sphincter
  • Gastrocolic/Duodenocolic reflexes - food entering the stomach or duodenum promotes the motility of the colon.
  • Enterogastric reflex - Distension of the small and large intestines inhibits stomach motility and secretion
  • Intestinointestinal reflex - over distension of one part of the intestine leads to relaxation of the rest of the intestine.
  • Colonoileal reflex - Inhibits ileal emptying when the colon is stretched
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10
Q

What is receptive relaxation of the stomach?

A
  • Receptive relaxation is a vasovagal reflex meaning both afferent and efferent limbs of the reflex are carried in the vagus nerve
  • The neurotransmitter released from the postganglionic vagal nerve fibres is VIP
  • If the vagus nerve is transected then receptive relaxation is impaired and the stomach becomes less distensible
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11
Q

What are the 2 main plexi in the ENS?

A
  • Myenteric (Auerbach’s) plexus (between circular and longitudinal muscle layers of the gut) that controls GI motility
  • Submucosal (Meissner’s) plexus (between the muscularis mucosa and the circular muscle layer of the gut) that controls GI motility and secretion
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12
Q

What is the function of the CNS in motility and secretion?

A
  • Parasympathetic - Promotes motility/secretion. Fibres reach the gut through the vagus nerve and sacral outflow tracts. Vagal innervation of GI smooth muscle is indirect via the ENS
  • Sympathetic - Inhibits motility/secretion and contracts sphincters. Originates in preganglionic cholinergic neurons. Decrease release of acetylcholine (ACh) from enteric neurons = inhibits Gl motor and secretory function
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13
Q

What are the GI peptides?

A
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14
Q

What are the neurocrines of the ENS and their functions?

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15
Q

What is segmentation?

A

Segmentation- fed pattern: non propagated focal contractions of intestine that occur simultaneous at multiple locations in the intestine. Typically lasts 4-6 hrs following a meal. Different regions of the circular muscle of the gut contract to pinch off lengths of gut contents. This helps mix the contents of the Gl tract with digestive secretions and bring them into close contact with the mucosa. Food contact is further improved by contractions of the villi and muscularis mucosae

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16
Q

What is peristalsis?

A

Peristalsis- intrinsic local reflex that helps moves the food through the Gl tract towards the anus. Peristaltic movements are orchestrated by ICC but occurrence and force of contraction is dependent on the ENS. The CNS can also elicit effects through its stimulation of the ENS (promotion inhibition of motility and secretion).

  • excitatory neurons cause the longitudinal muscle in the segment ahead of the bolus to contract
  • inhibitory neurons cause the circular muscle layer relaxes in the same segment = expansion of the lumen
  • excitatory neurons cause contraction of the circular muscle layer in the segment behind the bolus
  • inhibitory neurons cause the longitudinal muscle layer in this segment to relax simultaneously = propulsion of the luminal contents ahead
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17
Q

What does luminal distension trigger?

A
  • direct activation of mechanoreceptive endings of intrinsic primary afferent neurons (IPANs)
  • indirect activation of IPANs upon serotonin release by enterochromaffin cells in the epithelium.
18
Q

What do IPANs activate?

A
  • ascending interneurons - stimulate excitatory motor neurons
  • descending interneurons - stimulate inhibitory motor neurons
  • Motor neuron activity leads to oral contraction and anal relaxation of intestinal smooth muscle = propulsion of luminal contents in the proximal-distal direction.
19
Q

What is the migrating motor complex?

A
20
Q

What is Achalasia?

A
21
Q

What is gastroparesis?

A
22
Q

What is Hirschsprung’s disease?

A
23
Q

What can vomiting be induced by?

A
24
Q

What happens in emesis- nerve signals?

A
25
Q

What happens in emesis- propulsion of stomach contents?

A
26
Q

Internal vs external rectal sphincter

A
  • Internal - Smooth Muscle - Subconsciously controlled
  • External - Skeletal Muscle - Voluntarily controlled
27
Q

What is colonic motility?

A
  • Entry into the colon is controlled by the ileocecal sphincter - enteric contents are continually delivered to the colon in the fed and fasting states.
  • The colon stores faces until such time as it can be evacuated conveniently - allows maximal absorption of water, electrolytes, short-chain fatty acids, and bacterial metabolites.
  • Colon contents generally pushed caudally by mass movement - under autonomic control (can be initiated by stimulation of parasympathetic sacral outflow tracts)
  • The gastrocolic reflex increases colonic motility within 30 min of a meal.
  • It is stimulated by food in the duodenum and appears to be a neurally mediated response that involves cholecystokinin (CCK) release.
  • The giant peristaltic contraction is a peristaltic reflex characterised by high amplitude and long-duration contractions.
  • Water absorption occurs in the distal colon, making the fecal contents of the large intestine semisolid and increasingly difficult to move - a final mass movement propels the fecal contents into the rectum
28
Q

How is drinking regulated?

A
29
Q

How is thirst regulated?

A
30
Q

What is plasma osmolality?

A

the level of different solutes (mainly sodium, chloride, bicarbonate, glucose & urea) in plasma. Osmoreceptors - neurons that identify CF osmolality change.

31
Q

What are the stimuli for thirst?

A

increased plasma osmolarity, reduced blood volume, reduced blood pressure, increased Ang II levels, and dry month. It is the opposite for decreased thirst for all factors and also gastric distension decreases thirst.

32
Q

The lateral vs ventromedial hypothalamus

A
33
Q

What do stretch receptors do?

A

in the stomach activate sensory afferent pathways in the vagus nerve = inhibit food intake

34
Q

What hormones are released by the ingestion of food?

A

Peptide YY (PYY), cholecystokinin(CCK), and insulin are GI hormones that are released by the ingestion of food = suppress further feeding. PPY is released by the small intestine after meals in amounts proportional to the calories ingested. CKK is related to the amount of nutrients (particularly fats) that the duodenum receives from the stomach, receptors for it are located in the junction between the stomach and the duodenum

35
Q

What is the role of lectin?

A

is a hormone produced in increasing amounts by fat cells as they increase in size. It inhibits food intake

36
Q

What is the role of ghrelin?

A

is released by the stomach, especially during fasting = stimulates appetite, it binds to the hypothalamus

37
Q

Which hormones decrease vs increase feeding?

A
  • Decrease feeding hormones: leptin, serotonin, noradrenaline, insulin, CCK, PYY
  • Increase feeding hormones: endorphins, glutamate, cortisol, ghrelin
38
Q

What are the 5 modalities of taste?

A
  1. Sour - acids (H+ ion)
  2. Salty - ionised salts e.g. Na+
  3. Sweet - e.g. sugars, glycols, alcohols, aldehydes, ketones, amides, esters, some amino acids, some acids
  4. Bitter - long chain organic substances that contain nitrogen and alkaloids (e.g. quinine, caffeine, nicotine)
  5. Umami (“delicious”) - food containing L-glutamate e.g. meat extracts and aging cheese
39
Q

What modulates taste?

A
  • Angiotensin II decreases sensitivity to salty tastes & increases sensitivity to sweet tastes
  • Glucagon increases sensitivity to sweet tastes
  • TNF-alpha decreases sensitivity to some bitter tasting foods
40
Q

What is sodium appetite?

A

Sodium appetite- Sodium appetite is an increased palatability and drive to ingest salty substances. Elicited by sodium depletion. Research has identified aldosterone-activated HSD2 neurons in the nucleus tracts solitarii (contain c-Fos-immunoreactive nuclei) as being responsible for eliciting this effect

Year 2 Med (60 decks)

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