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Unit 5 > BSF > Flashcards

BSF Flashcards

1
Q

Where is the feeding or hunger center located in the hypothalamus? What pathway is involved?

A

Lateral hypothalamic area. NPY edited pathway

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2
Q

Where is the satiety center located? What pathway is involved?

A

Ventromedial nuclei, melanocortin pathway (POMC)

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3
Q

What is the clinical effect of insulin?

A

Decrease appetite, increase metabolism

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4
Q

What is the source and effect of leptin?

A

Source: Fat cells, endocrine cells of the stomach
Effect: Decrease appetite, increase metabolism, decrease ghrelin release

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5
Q

What is the effect of CCK? Where is it released from?

A

Decrease appetite, decrease gastric emptying. CCK is released from I cells of the duodenum

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6
Q

What is the effect of PYY? What stimulates PYY?

A

Decrease appetite, increase metabolism, decrease gastric emptying and secretion

Stimulated by fat

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7
Q

What is the effect of ghrelin? Where is it released from?

A

Ghrelin increases appetite, decrease metabolism, decrease leptin release. It is released from endocrine cells (stomach), hypothalamus, and small & large intestines

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8
Q

What secretes gastrin? Where is it secreted? How is it stimulated? What are its actions?

A

G cells. Secreted in stomach, duodenum, all the way to the jejunum (diminished).
Stimulated by vagus nerves (direct), stomach distention and proteins.

Increases H+ and pepsinogen secretion, increases gastric distensibility. Stimulates growth of gastric mucosa

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9
Q

What secretes secretin? Where is it secreted How is it stimulated? What are its actions?

A

S cells of duodenum. Stimulated by presence of H+ and fatty acids in the duodenum.

Effect: stimulates bile and pancreatic duct secretion of H2O and bicabonate to neutralize pH. Increases pepsinogen secretion, inhibits gastric acid secretion and gastric motility.

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10
Q

What secretes CCK? Where is it secreted? How is it stimulated? What are its actions?

A

I cell, duodenum, jejunum, all the way to the ileum (diminishing). Fat/protein/vagal stimulation.

Increase enzyme secretion by pancreatic acinar cells, increase contraction of the gallbladder, inhibits gastric emptying

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11
Q

What secretes GIP? Where is it secreted? How is it stimulated? What are its actions? What does GIP stand for?

A

K cell, duodenum, jejunum. Released in response to high serum glucose in stomach.

Stimulates the release of insulin (or potentiates glucose-stimulated insulin secretion) and decreases gastric motility. Inhibits gastric secretion and emptying. GIP is why oral glucose is more effective than IV glucose at increasing insulin levels.

GIP = Glucose-dependent Insulinotropic Polypeptide

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12
Q

What secretes motilin? Where is it secreted How is it stimulated? What are its actions?

A

M cell, duodenum, jejunum, unknown stimulation

Increases motility and initiates MMC

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13
Q

What stimulates the release of pancreatic peptide? What is its action?

A

Stimulated by protein, fat, and glucose. It decreases bicarbonate and pancreatic enzyme secretion

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14
Q

What is the stimulus for enteroglucagon? What is its action?

A

Stimuli are fat and hexose. Primary action is to decrease gastric secretion and emptying, increases insulin release

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15
Q

Swallowing, pain, and defecation are what type of reflexes?

A

Long reflexes

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16
Q

What is the effect of parasympathetic stimulation on GI smooth muscle?

Mucosal secretory and/or endocrine cells?

Vascular smooth muscles?

A

Increase GI motility, decrease tone of GI smooth muscle sphincters

Increase secretion

Vasodilation, increase blood flow

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17
Q

What is the effect of sympathetic stimulation on GI smooth muscle?

Mucosal secretory and/or endocrine cells?

Vascular smooth muscle cell?

A

Decreased GI motility, increased tone of GI smooth muscle sphincters

Decreased secretion activity

Vasoconstriction, decreased blood flow

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18
Q

What does the submucosal plexus innervate? What action does it control

A

It innervates the glandular epithelium, intestinal endocrine cells, and submucosal blood vessels

It primarily controls GI secretion and local blood flow

It also regulates the contraction o fate muscular mucosa

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19
Q

What does the myenteric plexus control?

A

It primarily controls the GI movements

It regulates local and inter-regional motility activity through regulation of contraction/relaxation of circular and longitudinal smooth muscle layers

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20
Q

What is the purpose of interneurons (both inhibitory and excitatory)

A

Mainly responsible for integrating information, transmit signals from sensory to secretomotor neurons

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21
Q

What is VIP? What is its action?

A

It is a peptide neurotransmitter of the enteric nervous system . It relaxes the gut smooth muscle and stimulates intestinal and pancreatic secretion. Inhibits gastric secretion

VIP = vasoactive intestinal peptide

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22
Q

What do short reflexes (local) control?

A

Secretion, peristalsis, mixing contraction

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23
Q

How do pain reflexes affect the GI tract?

A

It is a general inhibitor of the entire GI tract

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24
Q

What regulates the longitudinal and circular muscles?

A

They are regulated by neural pathways integrated through the myenteric plexus

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25
Q

What is the function of mucosal muscle (usually longitudinal)?

A

It alters the mucosal surface area. It regulates lymph flow through the central lacteal into the lymphatic system

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26
Q

What is the difference between phasic and tonic contraction?

A

Phasic – contraction-relaxation cycles

Tonic – sustained. Found in GI sphincters and latch mechanisms

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27
Q

What is the major determinant of the phasic nature of contraction?

A

ICCs

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28
Q

What do slow waves determine?

A

SWs determine the maximum frequency and direction propagation

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29
Q

What are the different types of ICC and their actions?

A

Myenteric plexus level (ICC-MY) – generate slow waves, propagate, and coordinate propagation of slow waves

Smooth muscle layer (ICC-IM) – mediators of enteric motor neurotransmission, essential for cholinergic (ACh) excitatory and nitric (NO) inhibitory neurotransmission

Within the sepae (ICC-SEP) – convert and coordinate the spread of pacemaker activity

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30
Q

Which region has the highest frequency of slow waves?

A

Duodenum at 12 cycles/minute

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31
Q

What creates the depolarization of slow waves? Repolarization?

A

Depolarization – Na+ influx, T-type Ca2+ channels, Ca2+ activated Cl- efflux

Repolarization – K+ efflux

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32
Q

What causes depolarization that leads to action potential

A

L-type Ca2+ channels

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33
Q

Between tonic and phasic contractions, which is associated with BER?

A

Phasic is associated with BER

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34
Q

Does sphincter relaxation causes an increase or decrease in GI motility? What about contraction?

A

Sphincter relaxation causes an increase in GI motility while contraction decreases GI motility

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35
Q

Is the upper pharynx a part of voluntary control?

A

Yes

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36
Q

When you have a sympathetic stimulation, what happens to the motility? Sphincter?

A

Sympathetic stimulation contracts the sphincter, which decreases GI motility

Parasympathetic stimulation relaxes the sphincter and increases GI motility

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37
Q

What action of what muscle is responsible for segmentation (mixing)? Does this move the particle along the GI tract?

A

Focal contraction of the circular muscle layer. This does not result in significant net movement of material along the tract

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38
Q

What is the function of paneth cells?

A

They synthesize and secrete several antimicrobial agents such as secretory IgA

They are in the bases of small intestinal crypts and continually sense the microbiota to induce the production of antimicrobial peptides

39
Q

What is the function of Goblet cells?

A

They produce mucin, which is organized into a dense, highly cross-linked inner proteoglycan gel that forms an intestinal epithelial cell-adherent inner mucous layer and a less densely cross-linked outer mucous layer

40
Q

In the stomach, when is the acidity the lowest? Highest?

A

Acidity is lowest after digestion. It is highest after meals

41
Q

What characteristic must probiotics have?

A

They must be non-pathogenic and non-toxic, they must have a large number of viable cells

42
Q

What happens during the chewing reflex?

A

Bolus of food in the mouth inhibits contraction of the muscles of mastication, allowing the lower jaw to drop. The drop will induce a stretch reflex of the jaw muscles that leads to a rebound contraction

43
Q

What occurs during the voluntary stage and involuntary stage of swallowing?

A

Voluntary is only the oral phase

Involuntary begins at the beginning of the pharyngeal stage, which lasts for less than 1 second, esophageal lasts for about 8-10 seconds

44
Q

When swallowing, is respiration possible? Why or why not?

A

It’s not, the nasopharynx is closed as well as the epiglottis

45
Q

Propulsion through which sphincter occurs during the end of the pharyngeal phase?

A

Propulsion through the upper esophageal sphincter

46
Q

When does the esophageal phase begin?

A

It begins as the upper esophageal sphincter opens

47
Q

What initiates primary peristalsis? What controls it?

A

It is initiated through pharyngeal receptor contact (swallowing) and controlled by the vagus nerves in connection with the esophageal myenteric plexus

48
Q

What initiates secondary peristalsis? What controls it?

A

It is initiated by the distention (due to food bolus) of the esophagus. It is partly controlled by both intrinsic (myenteric) and extrinsic nervous systems

49
Q

In between swallows, how is regurgitation prevented? How is pressure involved?

A

Largely prevented through tonic constriction of the UES and LES, which produces greater pressure than their adjacent compartments

50
Q

What happens to the UES during and after swallowing?

A

During swallowing, it relaxes, immediately after, it constricts, which prevents air reflux

51
Q

Relative to peristaltic wave, describe the contraction or relaxation of the orad stomach and LES

What causes the receptive relaxation?

A

LES and orad stomach relaxes shortly before the peristaltic wave arrives. They constrict after the bolus passes into the FUNDUS in order to prevent acid reflux

Receptive relaxation is mediated by a vagovagal inhibitory reflex due to a release of inhibitory NTs (NO and VIP) from intrinsic nerves

52
Q

What causes pyrosis (heartburn)

A

Weak secondary peristalsis, increase in gastric pressure, low LES tone, causing gastric acid reflux

53
Q

What causes achalasia?

A

Degeneration of the postganglionic inhibitory neurons (NO/VIP) in the myenteric plexus

Loss of peristalsis, elevated resting LES pressure

Loss of LES relaxation in response to swallowing

54
Q

What level of pressure is maintained during eating? Why?

A

Low intragastric pressure is maintained during eating (stomach filling). This minimizes gastric reflux into the esophagus and prevents excessive stomach distention (which leads to vomiting)

55
Q

What can increase gastric distensibility during the gastric phase of digestion?

A

Ants such as VIP and NO, as well as GI hormones CCK and gastrin. This increases gastric distensibility during the gastric phase of digestion

56
Q

Describe gastric content mixing

A

Contraction begins in the mid-region of the stomach.

As contraction increases in force and velocity, some of the contents are passed over and forced back into the body of the stomach.

Contraction force and velocity are great enough to cause rapid and almost complete closure of the distal antrum.

Before and after this contraction, some of the contents is propelled into the duodenum but most stays in the stomach

During these contractions, there is no gross movement of gastric content

57
Q

Where do contractions begin in gastric content mixing? Emptying?

A

Mid-region in mixing

Stomach antrum in emptying

58
Q

What conditions of the stomach favors gastric emptying?

A

Increased tone of the orad region of the stomach

Forceful peristaltic contraction of the caudad region of the stomach

Relaxation of the pylorus, absence of segmenting contractions of the duodenum

59
Q

What are the effects of motilin, somatostatin, and GIP in motility?

A

Motilin increases contraction of the caudad stomach (increases motility)

Somatostatin and GIP suppress motility

60
Q

What is the role of pH in relation to gastric emptying?

A

The lower the gastric pH, the slower the gastric emptying

61
Q

Greater pyloric sphincter resistance increases or decreases the rate of gastric emptying?

What happened when duodenal pressure is increased?

A

It decreases the rate of gastric emptying

It slows gastric emptying

62
Q

If material is present in the small intestine, how is the stomach affected when it comes to parasympathetic and sympathetic responses?

A

Parasympathetic – decreased

Sympathetic – increases

63
Q

What can be a result of slow digestion? Rapid?

A

Slow digestion interrupts flow of nutrients to the body, it may also stimulate excess gastric acid secretion. This results in poor digestion and absorption

Rapid digestion overwhelms the digestive and absorptive capacity of the small intestine. It fails to fully buffer acidic chyme

64
Q

What can inhibit or stimulate BER waves?

A

Neural and hormonal controls

Inhibition – epi, VIP, NO, secretin, and glucagon

Stimulation – gastrin, CCK, motilin, and serotonin

65
Q

What are the complications due to vomiting?

A

Loss of gastric contents – loss of fluid, H+, and ions (K+), metabolic alkalosis, and hypokalemia

Loss of small intestine – additional loss of ions, fluid, bicarbonates, bile, and metabolic acidosis

Nutritional deficiency, ulceration, weakening of UES, and LES, tooth decay

66
Q

What is the function of haustrations? How are their contractions in comparison to those in the small intestine?

A

Mixing, used for segmenting contractions

Contraction is more forceful and longer (12-60 seconds)

It performs mass movements toward the rectum, less frequent but longer duration (20-30 seconds) and distance than SI

67
Q

What activates the ileocecal reflex? What does it do?

A

It is activated by the distention of the ileum. It increases the motility of the ileum and relaxes the ileocecal sphincter, allowing chyme to pass from the ileum to the cecum

68
Q

What activates the colonoileal reflex? What does it do?

A

It is activated by the distention of the colon. It causes the ileocecal sphincter to contract, preventing the emptying of ileal content into the colon, and providing protection against reflux of colonic contents

69
Q

What activates the gastroileal reflex? What mediates it? What does it do?

A

It is activated by a distended stomach. It is mediated by gastrin and CCK. It increases ileal motility and movement through the ileocecal sphincter

70
Q

Which reflex is responsible for the defecation sensation?

Which reflex stimulates a colonic mass movement?

A

Duodenalcolic reflex

Gastrocolic reflex and duodenalcolic both augment colonic mass movement

71
Q

What is relaxed and what is contracted during defecation?

A

BOTH IAS and EAS are relaxed. This is accompanied by a peristaltic contraction f the rectum and distal colon

Contraction of the chest muscles against a closed glottis and full lungs (valsalva) and contraction of abdominal muscle raise intrathoracic and intra-abdominal pressure and enhances the propulsion of feces

Relaxation of the pelvic floor allows the increased abdominal pressure to force the floor downward. It straightens the rectum and facilitates the passage of feces

72
Q

When does fasting motor activities occur during fasting?

Where do MMCs originate from?

A

After about 90 minutes and are associated with MMCs

They originate from the mid-stomach region

73
Q

What is the difference between phase I, II and II of MMC?

A

Phase I – no spikes, no contractions

Phase II – irregular spikes and contractions (~50% of slow waves are associated with contractions)

Phase III – bursts of regular spikes and contractions (~100% of SWs are associated with contractions), gastric material is moved to longer distances

74
Q

What is the character of MMC in the stomach? Where is it initiated?

A

It is vigorous and prolonged peristaltic wave

It is initiated at the mid-body of stomach and moves distally over the caudad region and through the pylorus

75
Q

What is the function of MMC?

A

Clear the stomach of debris between meals. It keeps the SI clean of indigestible meal residua, bacteria, and desquamated cells only during fasting

76
Q

What happens to the ileocecal sphincter as the MMC approaches?

A

It relaxes

77
Q

Is saliva isotonic, hypotonic, or hypertonic?

A

It is INITIALLY isotonic with neutral pH, then because of electrolyte modification, it becomes HYPOTONIC with pH between 6-7

78
Q

What is the effect of PSNS and SNS in salivary secretion rate?

What is the difference in the two secretions?

A

Both increase salivary secretion rate, however, PSNS is dominant

PSNS is watery and causes vasodilation

SNS is viscous and thick, causes vasoconstriction

79
Q

What is the difference between oxyntic glands and pyloric glands?

A

Oxyntic – parietal cells (HCl, IF), chief cells (pepsinogen), mucus (mucus)

Pyloric glands – mucus cells (mucus), G cells (gastrin)

80
Q

What converts pepsinogen to pepsin?

A

HCl, pH has to be less than 5

81
Q

How is H+ and HCO3- produced in parietal cells? What enzyme is used?

A

They are produced from CO2 and water using the enzyme carbonic anhydrase

82
Q

In the H,K+ ATPases in parietal cells, in which direction does H+ go and in which direction does K+ go?

A

H+ goes out to the lumen to form HCl

K+ goes inside the parietal cell

83
Q

In the parietal cell, between gastrin and ACh, which one binds to M3 and which one binds to CCK receptors?

What do they activate?

A

Gastrin binds to CCK, ACh binds to M3 receptors

Their binding activates the PLC pathway through Gq, which opens calcium channels from the ER

Eventually activates H+/K+ pumps

84
Q

What receptor does histamine bind to in the parietal cell? What does it activate?

What are its antagonists? Through which pathway

A

Histamine binds to H2 receptors, which activate the Gs protein, which activates adenylyl cyclase, activating PKA. It eventually activates H+/K+ ATPase

Its antagonists are somatostatin and prostaglandins. Both activate Gi, which inactivates adenylyl cyclase

85
Q

What secretes somatostatin?

What happens during this cell’s vagal stimulation?

A

D cells

Vagal stimulation inhibits its release

86
Q

How does the vagus nerve stimulate parietal cells? G cells?

A

Directly by releasing ACh and also through ECL cells

Stimulates G cells through GRP, promoting gastrin release

87
Q

What is the effect of luminal H+ on D cells?

A

It directly stimulates the D cells to release somatostatin, which inhibits gastrin release from G cells, thereby reducing gastric acid secretion

88
Q

What is the effect of somatostatin on gastric secretion?

A

It inhibits gastrin secretion

89
Q

During which time of day is gastric acid secretion the highest? Lowest?

A

Lowest in the morning and highest in the evening

90
Q

In the cephalic phase, what stimulates gastric secretion? Gastric phase? Intestinal phase?

A

Cephalic – chewing and swallowing, smell, and sight of food

Gastric – mechanically through wall distention, chemically through partially digested protein products in chyme

Intestinal – distention of the intestinal wall, circulating amino acids (major stimulus)

91
Q

What happens to gastric secretion during the first hour of a meal?

A

Gastric secretion increases and reaches maximum, pH reaches maximum

92
Q

How is gastrin secretion affected by low pH?

A

Low pH inhibits gastrin release, stipulates release of somatostatin, which directly inhibits acid secretion

93
Q

What stimulates the release of secretin? What is its primary effect?

A

It is triggered by acidic pH such as HCl in the duodenum. It increases the release of bicarbonate from pancreatic ductal cells and liver

Unit 5 (11 decks)

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