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Physiology > GI Physiology > Flashcards

GI Physiology Flashcards

1
Q

What do contractions of the muscularis proporia do

A

Mix and circulate the content of the lumen and propel through the GI tract

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2
Q

What are the functional layers of the GI

A

Mucosal layer (interior)
Submucosa
Muscle layers
Serosa (exterior)

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3
Q

Mucosal layer from outside in

A

Villi
Epithelium
Lamina proporia muscularis mucosa (SM, that contracts to change shape and surface area of the epithelium)

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4
Q

Submucosa

A

Submucosa

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5
Q

Muscle layers (muscularis propria)

A

SM that give MOTILITY to the GI tract

Circular msucle
Longitudinal muscle

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6
Q

Serosa

A

Serosa

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7
Q

What is “the second brain or little brain in the gut”

A

Enteric nervous system

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8
Q

What makes up the enteric nervous system

A

Myenteric and submucosa plexuses

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9
Q

Describe ens

A

Sensory neurons get info from stimuli in the wall of gut and send into to interneurons which send into to motor neurons so u get response

The CNS gives and receives information (para and smympa too)

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10
Q

What are the sensory neurons of the enteric nervous system

A

Mechanoreceptors and chemoreceptors in mucosa

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11
Q

Can the integrating center of the ENS exert its functions without the CNS

A

Yup

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12
Q

What roles does the CS have in regulation of GI function

A

Vago-vagal reflex 9gastric receptive relaxation reflex)

Modulates ENS responses

Centers that control food intake are located int he brain

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13
Q

Vagal efferents from the ___ go to the gut and vagal afferent go from gut to ___

A

Nucleus of the tractus solitarius

Sensory ganglion of the vagal nerve (nodose ganglion)

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14
Q

How does the parasympathetic system innervated GI

A

Vagus and pelvic nerves

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15
Q

Where are preganglionic nerve cell bodies located for parasympathetic nervous system

A

Brainstem and sacral spinal cord

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16
Q

Where are postganglionic neurons of the parasympathetic nervous system

A

In the wall of the organ (enteric neuron in the gut wall)

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17
Q

The synapse between pre and post ganglionic parasympathetic cells is __

A

Nicotonic

NAChRs

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18
Q

How does the sympathetic nervous system innervated GI functions

A

Via nerves running between the spinal cord and the prevertebral ganglia and between these ganglia and GI organs

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19
Q

Preganglionic efferent fibers arise within the spinal cord and end in the ____ ____

A

Prevertebral ganglia

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20
Q

Postganglionic fibers from the prevertebral ganglia innervate myenteric and ___ ____

A

Submucosal plexuses

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21
Q

Mostly, preganglionic efferents fibers release __ which postganglionic efferent nerves release __

A

ACh

NE

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22
Q

Paracrine regulation

A

Action of peptides (somatostatin) or other messengermolecules (histamine)

Act locally

Reach their target cells by diffusion over short distances

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23
Q

Endocrine regulation

A

Action of hormones

Enteroendocrine cells contain secretary granules filled with hormones that are released upon stimulation

Hormones are secreted into circulation

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24
Q

Neural regulation

A

Action of neurotransmitters

Action potentials are needed for neurotransmitter release

Neurotransmitter molecules diffuse across the synapse and bind to their specific receptors int he post synaptic cell

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25
Q

Gastric secretion

A

G cells of stomach

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26
Q

Cholecsytokinin secretion

A

I cells of the duodenum and Jejunum

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27
Q

Secretion secretion

A

S cells of the duodenum

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28
Q

Glucose dependent insulinotropic peptide secretion

A

Duodenum and jejunum

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29
Q

What stimulates gastric secretion

A

Small peptides and aa

Distention of the stomach

Vagal stimulation (via GRP)

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30
Q

What stimulates CCK secretion

A

Small peptides and aa

Fatty acids

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31
Q

What stimulates secretin secretion

A

H in duodenum

Fatty acids in the duodenum

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32
Q

What stimulates GIP secretion

A

Fatty acids

Aa

Oral glucose

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33
Q

Actions of gastrin

A

Increase gastric H secretion

Stimulated growth of gastric mucosa

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34
Q

CCK actions

A

Increase Pancreatic enzyme secretion

Increase pancreatic HCO3 secretion

Stimulates contraction of the gallbladder and relaxation of oddi sphincter

Stimulates growth of the exocrine pancreas and gallbladder

Inhibits gastric emptying

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35
Q

Actions of secretin

A

Increase pancreatic HC)3 secretion

Increase biliary HCO3 secretion

Decrease gastric H secretion

Inhibits tropics effect of gastrin on gastric mucosa

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36
Q

Actions of GIP

A

Increase insulin secretion from pancreatic B cells (incretin effect)

Decrease gastric H secretion

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37
Q

What hormone families are gastrin, CCK, secretin, and GIP in

A

Gastrin and CCK are in gastrin -CCK hormone family

Secretin and GIP are in secretin-glucagon family

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38
Q

What is the incretin effect

A

Increased stimulation of insulin secretion elicited by oral as compared to IV glucose
Oral higher

DM lose incretin effect

Glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP) mediate the incretin effect

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39
Q

Ach source

A

Cholinergic neurons

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40
Q

Ach actions

A

Contraction of smooth muscle

Relaxation of sphincters

Increased salivary secretion

Increased gastric secretion

Increased pancreatic secretion

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41
Q

Source of NE

A

Adrenergic neurons

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42
Q

Actions of NE

A

Relaxation of smooth muscle in wall

Contraction of sphincters

Increased salivary secretion

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43
Q

Vasoactive intestinal peptide VIP source

A

Neurons of ENS

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44
Q

VIP actions

A

Relaxation of smooth muscle

Increased intestinal secretion

Increased pancreatic secretion

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45
Q

NO source

A

Neurons of ENS

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46
Q

NO action

A

Relaxation of smooth muscle

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47
Q

Gastrin-releasing peptide GRP source

A

Vagal neurons of gastric mucosa

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48
Q

GRP actions

A

Increase gastrin secretion

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49
Q

Enkephalins source

A

Neurons of the ENS

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50
Q

Actions of enkephalins

A

Contraction os smooth msucle

Decreased intestinal secretion

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51
Q

Neuropeptides Y source

A

Neurons of the ENS

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52
Q

Neuropeptides Y actions

A

Relaxation of smooth muscle

Decreased intestinal secretion

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53
Q

Substance P source

A

Co-release with Ach by neurons of the ENS

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54
Q

Substance P actions

A

Contraction of smooth muscle

Increased salivary secretion

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55
Q

Slow wave

A

Depolarization and depolarization of the membrane potential

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56
Q

Are slow waves action potentials

A

No

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57
Q

When do APs occur

A

When the depolarization moves the membrane potential to or above threshold (to more positive membrane potentials)

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58
Q

__ and __ activity modulate generation of APs and strength of contractions

A

Neural

Hormonal

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59
Q

What followselectrical response in GI

A

Mechanical response

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60
Q

Tension slow wave?

A

?

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61
Q

In GI smooth muscle, even ___ depolarization can produce weak contraction, like basal contractions

A

Subthreshold

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62
Q

The greater number of APs on top of the slow wave the larger the ___ contraction

A

Phasic

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63
Q

_ and _ contractions of smooth muscle are key for motility along the GI tract

A

Phasic

Tonic

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64
Q

Phasic contraction

A

Periodic contractions followed by relaxation

Esophagus, stomach (antrum), SI and all tissues involved in mixing and propulsion

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65
Q

Tonic contractions

A

Maintain a constant level of contraction without regular periods of relaxation

Stomach(orad), lower esophageal, ileocecal, and internal anal sphincter

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66
Q

Ach effect. On slow waves and AP

A

Increases amplitude of slow waves

Increased number or AP

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67
Q

NE effect on slow waves and AP

A

Decreases amplitude of slow waves

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68
Q

We normally have slow waves and get AP spikes on top of slow waves. What stimulated these spikes

A

Stretch, acetylcholine, parasympathetic

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69
Q

What stimulates hyperpolarization

A

NE and sympathetics

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70
Q

What are the pacemaker cells for the GI smo0th muscle

A

Interstitial cells of cajal

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71
Q

What do ICC generate and propagate

A

Slow waves

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72
Q

Slow waves occur spontaneously in the __ and spread rapidly to smooth muscle via _ junctions

A

ICC

Gap

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73
Q

__ activity in the ICC drives the frequency of contractions

A

Electrical

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74
Q

How do smooth muscle cells respond to slow wave depolarizations

A

Increased Ca channel open probability

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75
Q

_ and _ condition the smooth muscle syncytium to generate the desired response

A

NT

Hormones

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76
Q

Swallowing is initiated __ int he mouth and after that it is under __ __ control

A

Voluntarily

Involuntary reflex

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77
Q

Oral phase

A

VOLUNTARY

Initiates swallowing process

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78
Q

Pharyngeal phase

A

INVOLUNTARY
Soft palate is pulled up->epiglottis moves->UES relaxes->peristaltic wave of contractions is initiated in pharynx->food is propelled through open UES

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79
Q

Esophageal phase

A

INVOLUNTARY

Control by the swallowing reflex and the ENS

Primary peristaltic wave

Secondary peristaltic wave

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80
Q

The involuntary swallowing phase is controlled by the __

A

Medulla

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81
Q

How does the medulla control the involuntary swallowing phase

A

Food in pharynx->afferent sensory input via vagus/glossopharyngeal N-> swallowing center (MEDULLA)->brain stem nuclei-> efferent input to pharynx

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82
Q

What are the two types of peristaltic waves in the esophageal phase

A

Primary and secondary

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83
Q

Primary peristaltic waves

A

Continuation of pharyngeal peristalsis

Controlled by medulla

Cannot occur after vagotomy

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84
Q

Secondary peristaltic waves

A

Occurs if primary wave fails to empty the esophagus or if gastric contents reflex into the esophagus

Medulla and ENS are involved

Can occur in the absence of oral and pharyngeal phases
Occurs even after vagotomy

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85
Q

Effect of vagotomy on swallowing

A

Can’t do primary peristaltic wave

Can do secondary peristaltic wave

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86
Q

During swallowing there are changes in ___along the esophagus as food bolus passes through it

A

Pressure

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87
Q

Between swallows both the UES and LES are ___

A

Closed

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88
Q

Between swallows the body of the esophagus is ___

A

Flaccid

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89
Q

Between swallows pressure int he UES _ parhynx and body of esophagus )60mmHg)

A

>

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90
Q

Between swallows the LE has an _ pressure

A

Elevated

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91
Q

Pressures in the body of the esophagus are similar to those within the body cavity in which the esophagus lies in between swallows

A

In the thorax the pressures are subatmospheric and vary with respiration

Fluctuations in pressure with respiration reverse below the diaphragm

Intraluminal esophageal pressure reflects intra abdominal pressure

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92
Q

During swallowing the _ relaxes and opens-decreasing pressure

A

UES

*once the bolus passes, the sphincter closes and assumes its resting tone

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93
Q

During swallowing there is a peristaltic wave. Describe this

A

Body of the esophagus undergoes peristaltic contraction;wave of high pressures moving along the esophagus in direction to the stomach

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94
Q

During swallowing the LES and upper part (orad) of the stomach relax-receptive relaxation (pressure decreases)

A

Ok

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95
Q

Opening of the LES is mediated by what

A

Peptedergic fibers in the vagal nerve

  • release of VIP
  • role of NO
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96
Q

___ ___ decreases the pressure in the upper region of the stomach (orad region)

A

Receptive relaxation

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97
Q

After bolus enters stomach, ___ contracts (pressure increases

A

LES

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98
Q

Where does receptive relaxation occur

A

Orad

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99
Q

What is receptive relaxation

A

A vagovagal reflex

Get decreased pressure and increased volume of the orad

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100
Q

What are the parts of the stomach (anatomical divisions)

A

Fundus, body, antrum

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101
Q

What are the two regions of the stomach

A

Orad and caudal

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102
Q

In the caudad region, why are most of the gastric contents propelled back into the stomach

RETROPULSION

A

For further mixing and reduction of particle size

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103
Q

213213how are large particles of undigested residue remaining in the stomach emptied

A

Migrating myoelectric complex MMC

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104
Q

What are migrating myoelectric complexes

A

Periodic, bursting peristaltic contractions that occur at 90 minute intervals during fasting

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105
Q

___ plays a significant role in mediating MMC

A

Motilitn

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106
Q

When are MMC inhibited

A

During feeding

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107
Q

How long does gastric emptying take

A

3 hours

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108
Q

What increases the rate of gastric emptying

A

Decreased distensibility of the orad (distensibility is ability to become stretched)

Increased force of peristaltic contractions of the caudad stomach

Decreased tone of the pylorus

Increased diameter and inhibition of segmenting contractions of the proximal duodenum

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109
Q

What factors inhibit gastric emptying

A

Relaxation of orad

Decreased force of peristaltic contractions

Increased tone of pyloric sphincter
Segmentation contractions in intestine

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110
Q

What is the entero-gastric reflex

A

Negative feedback from duodenum will slow down the rate of gastric emptying

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111
Q

-acid in the duodenum (entero-gastric reflex)

A

Stimulates secretin release which inhibited stomach motility via gastrin inhibition

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112
Q

Fats in the duodenum (entero-gastric reflex)

A

Stimulate CCK and GIP which inhibits stomach motility

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113
Q

Hypertonicity in the duodenum (entero-gastric reflex)

A

Unknown hormone causes inhibition of gastric emptying

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114
Q

What are segmentation contractions

A

Produces no forward, propulsive movement along the small intestine

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115
Q

What are peristaltic contractions

A

Circular and longitudinal muscles work in opposition to complement each there’s actions
-are reciprocally innervated

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116
Q

Circular and longitudinal muscles are ___ innervated

A

Reciprocally

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117
Q

____ —- are always present whether contractions are occurring or not

A

Slow waves

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118
Q

Unlike in the stomach, slow waves themselves __ __ initiate contractions in the SI

A

DO NOT

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119
Q

In the SI _ potentials (AP) are necessary for muscle contraction to occur

A

Spike

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120
Q

What do slow waves in SI do

A

Set the maximum frequency of contractions

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121
Q

What signals peristalsis in SI

A

Distension of muscle

Chemical/mechanical stimulation of the mucosa

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122
Q

What regulates peristaltic contractions in the SI

A

The myenteric plexus mainly regulates the relaxation and contraction of the intestinal wall. The submucosal (Meissner) plexus senses the lumen environment)

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123
Q

How is peristaltic reflex initiated

A

Serotonin 5HT is released by ECC and binds to receptors in IPANs, initiation the peristaltic reflex

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124
Q

What does distension of stomach signal

A

Interneurons-.excitatory motor neurons (Ach, Subastance P) and inhibitory motor neurons (VIP and NO) and intrinsic primary afferent neurons(serotonin)

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125
Q

What controls contractions of the intestine

A

ICC, SM, neural and hormonal responses

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126
Q

Neural input to intestine

A

Peristaltic reflex mediated by ENS

In general, parasympathetic stimulates and sympathetic inhibits contractions

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127
Q

Hormonal control of contractions in intestine

A

Serotonin stimulates contractions
Certain prostagladins can stimulate contractions

Epinephrine , released from adrenal, inhibitis contractions

Gastrin, CCK, motilin and insulin stimulate contractions

Selegine and glucagon inhibit contractions

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128
Q

Does parasympathetic stimulation increase or inhibit contractions of intestine

A

Increase

Sympathetic inhibitors

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129
Q

T/F serotonin does not cause contractions of intestin

A

False, it does

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130
Q

Does epinephrine inhibit or increase contractions

A

Inhibit

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131
Q

Gastrin, CCK, motilin , insulin effect on intestine contractions

A

Stimulate

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132
Q

Secretin and glucagon effect on contractions

A

Inhibit

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133
Q

Mass movements

A

Occur in colon over large distances
1-3 times a day

Stimulate defecation reflex

A final mass movement propels the fecal content into the rectum

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134
Q

The _ motility in the proximal large intestine causes greater absorption while _ motility in distal large intestine results in less absorption

A

Poor

Excess

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135
Q

How does the rectum fill

A

Mass movements and segmentation contractions

Happens intermittently

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136
Q

What happens are rectum sills with feces

A

SM wall of the rectum contracts and internal anal sphincter relaxes (rectosphincteric reflex)

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137
Q

The external anal sphincter is ___ closed

A

Tonically-under voluntary control

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138
Q

The rectosphincteric reflex and defectaion are under neural control

A

Controlled partially by ENS

Reinforced by activity of neurons within the spinal cord

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139
Q

Sensation of rectal distention and voluntary control of the external anal sphincter are mediated by pathways within the spinal cord that lead to the __ __-

A

Cerebral cortex

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140
Q

Destruction of pathways from external anal sphincter to spinal cord that lead to cerebral cortex

A

Loss of voluntary control over defectaion

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141
Q

Vomiting reflex is coordinated by the ___

A

Medulla

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142
Q

How does the vomiting reflex work

A

Nerve impulses are transmitted by vagus and sympathetic afferents from stomach to multiple brain stem nuclei

Then get response

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143
Q

What occurs when vagal and sympathetic afferents send impulses to medulla(vomit center)

A

Reverse peristalsis in SI

Stomach and pylorus relaxation

Forced inspiration to increase abdominal pressure

Movement of the larynx

LES relaxation

Glottis closes

Forceful expulsion of gastric contents

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144
Q

What is in the medulla that vagal and sympathetic afferents are sent to

A

Chemical trigger zone and vomiting center

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145
Q

What medications stimulate the chemical trigger zone

A

Apomorphine and morphine

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146
Q

Vago-vagal reflex (long reflex)

A

Generally stimulators (increase motility, secretomotor, vasodilatory activities)

Vagus carries both afferents (75% ) and efferents 25%

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147
Q

Intestinointestinal reflex (short reflex0

A

Generally inhibitory, involving only the ENS, and completely independent of the extrinsic ANS (atropine has no effect!!)

-eg ileocecal sphincter SM acts by intestinointestino reflexes

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148
Q

Enterogastric reflex

A

Negative feedback from duodenum will slow down the rate of gastric emptying

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149
Q

Gastroileal reflex (gastroenteritic)

A

Gastric distention relaxes ileocecal sphincter

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150
Q

Gastro and duodeno-colic reflexes

A

Distention of stomach/duodenum initiates mass movements

Transmitted by way of the ANS

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151
Q

Defectaion reflex (rectosphincteric)

A

Rectal distention initiates defecation

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152
Q

What causes GERD

A

Changes in the barrier between the esophagus and stomach (eg LES relaxes abnormally or weakens)

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153
Q

Why get GERD

A

Motor abnormalities that result in abnormally low pressures in the LES; if intragastric pressure increases, as may occur following a large meal, during heavy lifting, or during pregnancy

Persistent reflux and resulting inflammation lead to GERD

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154
Q

What can GERD cause

A

Backwash of acid, pepsin and bile into the esophagus

Lead to heartburn and acid regurgitation

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155
Q

Complications of GERD

A

Irritation of the lining of the esophagus (esophagitis), scar tissue in the esophagus (stricture of esophagus) and Barrett’s esophagus

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156
Q

What happens in achalasia

A

Impaired peristalsis
Incomplete LES relaxation during swallowing (LES stays closed during swallowing, resulting in the back up of food)

Elevation of LES resting pressure

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157
Q

Why get achlasia

A

Lack of VIP or enteric nervous system has been knocked out

Damage to nerves in the esophagus, preventing it from squeezing food into the stomach

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158
Q

What can achlasia result in

A

Backflow of food int he throat (regurgitation), difficulty in swallowing to both liquid and sold (dysphagia), chest pain

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159
Q

What is gastroparesis

A

Slow emptying of the stomach/paralysis of stomach int he absence of mechanical obstruction

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160
Q

What is a common cause of gastroparesis

A

Diabetes mellitus

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161
Q

What is a less common cause of gastroparesis

A

Injury to the vagus nerve

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162
Q

Symptoms of gastroparesis

A

Nausea, vomiting, an early feeling of fullness when eating, weight loss, abdominal bloating, abdominal discomfort

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163
Q

What causes hirschsprung disease

A

Ganglion cells are absent from segment of colon

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164
Q

What happens in hirschsprung

A

VIP levels low->SM constriction/loss of coordinated movement->colon contents accumulate

Colon equilivent of achalasia

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165
Q

Clinical presentation hirschsprung

A

Newborn cant pass meconium

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166
Q

Composition of saliva in the primary secretion

A

H2O, electrolytes, a amylase, lingual lipase, lakkikrein and mucus

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167
Q

Alive compared to plasma

A

Hypotonic

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168
Q

Saliva has high _ __ and low _ _ concentrations due to active/passive absorption and secretion

A

K, HCO3

Na Cl

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169
Q

What are the two main steps in the formation of saliva

A
  1. Formation of isotonic, plasma like solution by acinar cells
  2. Modification of the isotonic solution by the ductal cells
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170
Q

What happens at the ductal cells

A

Absorption Na (active), Cl(passive) and secretion K(active), HCO3

Absorption is out
Secretion is in

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171
Q

Luminal side of ductal cell

A

Na/H exchange
Cl/HCO3 exchange
H/K exchange
(K, HCO3, H in)

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172
Q

Blood (basolateral side) ductal cell

A

NaK ATPase and Cl channels

Cl Na out
K and HCO3 and Na in

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173
Q

What gives saliva its concentration

A

Combined action of SBS option of Na and Cl and secretion of K and HCO3

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174
Q

In salivary formation there is net absorption of __

A

Solute

More NaCl is absorbed than KHCO3 secretion

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175
Q

Does the parasympathetic or sympathetic nervous system dominate in salivary secretion

A

Parasympathetic

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176
Q

What stimuli increase parasympathetic signaling for salivation and what stimuli decrease parasymapthic stimulation for salivation

A

Conditioning, food, nausea, smell

Dehydration , fear, sleep

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177
Q

How does the parasympathetic nervous system cntrol salivation

A

CNVII and CNIX send AcH to mAChR on acinar or ductal cells

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178
Q

___ stops the binding of AcH to mACHR on acinar and ductal cells, decreasing salivation

A

Atropine

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179
Q

What happens when AcH binds mAChR on acinar or ductal cells

A

Increase IP3 and Ca

Stimulation of salivary cells

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180
Q

How does the sympathectomy nervous system stimulate salivary cells (acinar or ductal)

A

T1-T3 send NE to Beta AR

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181
Q

What happens when NE binds beta AR on acinar or ductal cells

A

CAMP

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182
Q

What happens when the parasympathetic or sympathectomy nervoussysem stimulated acinar or ductal cells

A

Increased saliva production
Increased HCO3 and enzyme secretions

Contraction of myoepithelial cells

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183
Q

Salivary is exclusively under the control of the ___

A

ANS

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184
Q

Salivary secretion is increased by both ___ and ___ stimulation

A

Parasympathetic and sympathetic

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185
Q

In general parasympathetic and sympathectic stimulation have opposite effects. Salivary

A

Same

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186
Q

The gastric mucosa is divided into the _ gland area and the _ gland area

A

Oxynitic gland

Pyloric gland

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187
Q

Where is the oxynitic gland and what does it secrete

A

Located in the e proximal 80% of the stomach (body and fundus)

Secretes acid

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188
Q

Where is the pyloric gland and what does it do

A

Located int he distal 20% of the stomach (antrum)

Synthesizes and releases gastrin

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189
Q

What cells are in the body of the stomach

A

Parietal

Chief

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190
Q

What cells are in the antrum

A

Mucus and G cells

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191
Q

What do parietal cells secrete

A

IF and HCl

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192
Q

What do chief cells secrete

A

Pepsinogen

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193
Q

What do G cells secrete

A

Gastrin

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194
Q

What do mucus cells secrete

A

Mucus, HCO3 and pepsinogen

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195
Q

What do chief cells secrete

A

Pepsinogen

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196
Q

HCl and pepsin

A

Initiate protein digestion

Necessary for the conversion of pepsinogen to pepsin

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197
Q

Pepsinogen

A

Inactivate precursor; converted to pepsin

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198
Q

Mucus

A

Lines the wall of the stomach and protects it from damage

Lubricant

Together with HCO3, it neutralizes acid and maintains the surface of the mucosa at neutral pH

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199
Q

IF

A

Required for the absorption of vitamin B12 in the ileum

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200
Q

H2O

A

Medium for the action of HCl and enzymes

Solubililzes much of the ingested materials

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201
Q

Pepsinogen is secreted by what

A

Chief cells and mucus cells in oxyntic glands

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202
Q

What does pepsinogen require

A

H+ secretion from parietal cells to lower pH of gastric contents (pH<5)

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203
Q

What is the most important stimulus for pepsinogen secretion

A

Vagus nerve

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204
Q

_ triggers local cholinergic reflexes that stimulate chief cells to secrete pepsinogen

A

H+

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205
Q

__ converts more pepsinogen to pepsin

A

Pepsin

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206
Q

Cellular mechanism of HCl secretion by gastric parietal cells

A

Lumen-HCl is secreted(Cl follows H)

Blood(basolateral side)-net absorption of HCO3 (alkaline tide)

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207
Q

Omperazole and HCL secretion by parietal cells

A

Inhibits the H/K ATPase, stopping the release of HCL by patietal

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208
Q

Alkaline tides hat is omeprazole used for

A

HCO3 is secreted into blood on basolateral sidetreatment of ulcers

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209
Q

Omperaolecimetidine

A

Antagonist of H2R

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210
Q

What is cimetidine used for

A

Treat peptic ulcers, GERD

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211
Q

A passive mechanism regulates HCl secretion

A

As pH falls, gastrin release is inhibited; decreases HCl secretion

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212
Q

What receptors influences parietal cells to secrete H

A

M3

CCKB

H2

Somatostatin receptor

Prostagladin receptor

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213
Q

M3 receptor

A

On gastric parietal cells

Vagus secretes AcH on it

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214
Q

CCKB receptor in gastric parietal cell

A

Bind gastrin from G cells

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215
Q

Effect of M3 and CCKB in gastric parietal cells

A

Activate Gq which increase IP3/Ca

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216
Q

H2 receptor

A

Binds histamine from ECL cells

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217
Q

What stimulates ECL cells to secrete histamine

A

Ach, gastrin,

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218
Q

What stops ECL cells from secreting histamine

A

Somatostatin and prostagladin

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219
Q

Atropine

A

Stop Ach from binding M3

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220
Q

Cimetidine

A

Stop histamine from binding H2

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221
Q

What cells secrete somatostatin

A

D cells

222
Q

What is the effect of H2 activation and activation of somatostatin and prostagladin binding to their receptors on the gastric parietal cells

A

H2-Gs increased cAMP

Somatostatin and prostagladin-Gi decreased cAMP

223
Q

What does increased cAMP (H2) and IP3/Ca (M3 and CCKB) have on parietal cell

A

Increase H K ATPase

224
Q

What is the effect o decreased cAMP in the parietal cell (somatostatin and prostagladin)

A

Decreased K H ATPase

225
Q

Omeprazole

A

Stops H K ATPase

226
Q

Potentiation

A

Combined response to two stimulants exceeds the sum of their individual responses
-requires the presence of separate receptors on the target cell for each stimulant

227
Q

Examples of potentiation

A

Histamine potentials the actions of AcH and gastrin

Ach potentiation the actions of histamine and gastrin

228
Q

What is cimetidine

A

H2 antagonist

229
Q

What does cimetidine do

A

Block the direct action of histamine and also block potentiaed effects of ACh and gastrin

230
Q

What is atropine

A

Antagonist of mACHRs

231
Q

What does atropine do

A

Block the direct effects of ACh and the ACh potentiation effects of histamine and gastrin

232
Q

__ acts on G cels to inhibit gastrin release

A

Somatostatin

233
Q

__ activation stimulates gastrin release by releasing GRP and inhibiting the release of somatostatin

A

Vagal

234
Q

How does gastrin itself increase somatostatin

A

Negative feedback

235
Q

__ in the gastric lumen stimulates release of somatostatin

A

H

236
Q

What are the three phases of gastric HCL secretion

A

Cephalic

Gastric

Intestinal

237
Q

Cephalic phase of gastric HCL secretion

A

Via vagus (vagal center in medulla)

238
Q

__ excite pepsin and acid production

A

Parasympathetics

239
Q

Gastric phase

A
  1. Local nervous secretory reflexes
  2. Vagal reflexes
  3. Gastrin -histamine stimulation
240
Q

Intestinal phase

A
  1. Nervous mechanisms

2. hormonal mechanisms

241
Q

How is the role of the vagus nerve on HCl secretion from parietal cells twofold

A

Direct and indirect pathway

242
Q

Direct vagus pathway

A

To parietal cells to secrete HCL

243
Q

Indirect vagus pathways for HCL secretion

A

Vagus release GRP in G cells which send gastrin to circulation to parietal cells to increase HCL

244
Q

Does atropine block the direct or indirect pathway of HCL secretion

A

Direct

245
Q

Why wont atropine block the vagal effects on gastrin secretion

A

The NT at the synapse on G cells is GRP

246
Q

Small intestinal phase of the integrated response to a meal

A

Decrease pH in duodenum. Which stimulates S cells to secrete secretin which causes ductular bicarbonate secretion which increases pH in duodenum

Full circle

247
Q

What is IF

A

Mucoprotein secreted by parietal cells

Binds to vitamin B12

248
Q

What is the only essential secretion by the stomach (required)

A

IF

249
Q

Failure to screte IF

A

Pernicious anemia

250
Q

What are causes of pernicious anemia

A
  • destruction of gastric parietal cells(as in strophic gastritis)
  • autoimmune metaplastic strophic gastritis-immune system attacks IF or gastric parietal cells
251
Q

What protects the gastric mucosal epithelium against the HCL and pepsin

A

Mucosal barrier

252
Q

How do we get the mucosal layer

A

Gastric epithelium secretes HCO3 and mucus to form gel like mucosal abrrier

253
Q

What secretes mucus

A

Mucus neck

254
Q

What secretes HCO# for the mucosal barrier

A

Gastric epithelial cells

255
Q

How does the mucosal abrrier protect the gastric mucosa

A

HCO3, mucus, prostagladins, mucosal blood flow and growth factors

256
Q

What causes damage to the gastric mucosa

A

Acid, pepsin, NSAID (asprin), H pylori, alcohol, bile, and stress

257
Q

What could cause peptic ulcer disease

A

Loss of protective mucosal barrier

Excessive H and pepsin secretions

Combo

258
Q

What are the two types of peptic ulcers

A

Gastric

Duodenal

259
Q

H pylori

A

Releases cytotoxic that breakdown the mucosal barrier and underlying cells

The enzyme urease allows the bacteria to colonize the gastric mucosa
-urease converts urea to NH3 which alkalinizes the local environment

260
Q

How diagnose H pylori

A

Urease activity

261
Q

Gastric ulcers

A

Usually form on the lining of the stomach
Form mainly because gastric mucosal barrier is defective
A major causative agonist is H pylori

262
Q

Duodenal ulcers

A

Usually form on the lining of the duodenum
More common than gastric ulcers
Do not become malignant

H+ secretion rates are higher than normal

H pylori is a major etiology factor in duodenal ulcers

263
Q

Zollinger ellison ydnrome

A

H+ secretory rates are the highest compared to peptic ulcer diseases

Tumor, usually in the pancreas, secretes large quantities of gastrin

264
Q

Zollinger-Ellison syndrome

A

H+ secretory rates are the highest compared to peptic ulcer diseases

265
Q

What causeszollinger Ellison syndrome

A

Tumor, usually in the pancreas, secretes large quantities of gastrin

  • increased H+ secretion by parietal cells
  • increased parietal mass (tropic effect)
266
Q

In zollinger-Ellison what happens when get excessive H+ in the duodenum

A

Overwhelms the buffer capacity of HCO3 in pancreatic juice, creating an ulcer

267
Q

What happens when there is low duodenal pH

A

Inactivated pancreatic lipases—>steatorrhea

268
Q

Secretin stimulation test is for diagnosing what

A

Gastrin secreting tumours

269
Q

Under normal conditions, what does secretin administration do

A

Inhibit gastrin release

270
Q

In gastrinomas, what does injection of secretin cause

A

Paradoxical increase in gastrin release

271
Q

Gastric ulcer H+ secretion and gastrin levels

A

Decreased H+ and increased gastrin levels because of decreased H secretion

272
Q

What does gastric ulcer cause

A

Damage to protective barrier of gastric mucosa

273
Q

Duodenal ulcer H secretion and gastrin levels

A

Increased H secretion and increased gastrin levels because gastrin reponse to ingestion of food

274
Q

Damage from duodenal ulcer

A

Increased parietal cell mass due to increased gastrin levels

275
Q

Zollinger Ellison syndrome H secretion and gastrin levels

A

INCREASED H secretion and INCREASED gastrin levels

276
Q

Damage from zollinger Ellison syndrome

A

Gastrin is secreted by pancreatic tumor

Increased parietal cell mass due to trophies effect of increased gastrin levels

277
Q

Pancreatic juice contains _ for the neutralization of H from the stomach, and enzyme secretions to digest _, _ and _

A

HCO3

Carb, proteins, lipids

278
Q

What are the two components of pancreatic secretions

A

Aqueous secretion by centroacinar and ductal cells

Enzymatic secretion by acinar cells

279
Q

Centroacinar and ductal cells produce the initial aqueous solutionwhich is __ and contains what

A

Isotonic

Na, K, Cl, HCO3

280
Q

What happens to the aqueous solution secreted by centroacinar and ductal cells

A

Modified by transport processes in the ductal epithelial cells

281
Q

Enzymatic secretion by acinar cells contains what

A

Pancreatic amylase and lipases are secreted as active enzymes

Pancreatic proteases SECRETED IN THEIR inactive forms and converted to their active forms in the lumen of the duodenum

282
Q

What is the net result of modification of initial pancreatic secretion by ductal cells

A

Secretion of HCO3 into pancreatic ductal juice and net absorption of H

283
Q

What are the phases of pancreatic secretion

A

Cephalic
Gastric
Intestinal

284
Q

Cephalic phase of pancreatic secretion

A

Initiated by smell, taste and conditioning
Mediated by vagus nerve
PRODUCES MAINLY AN ENZYMATIC SECRETION

285
Q

Gastric phase pancreatic secretion

A

Initiated by distention of the stomach
Mediated by the vagus nerve
PRODUCES MAINLY AN ENZYMATIC SECRETION

286
Q

Intestinal phase pancreatic secretion

A

80% of pancreatic secretion *

ENZYMATIC AND AQUEOUS SECRETIOS ARE STIMULATED

287
Q

What do I cells secrete

A

CCK

288
Q

What stimulates I cells to secrete CCK

A

Phenylalanine, methionine, tryptophan

Small peptides

Fatty acids

289
Q

What does CCK do

A

Binds to acinar cells (ACh potentiates) to increase IP3 and CA

290
Q

What happens when IP3 and Ca increase in acinar cells due to CCK

A

Enzymes

291
Q

What do S cells secrete

A

Secretin

292
Q

What stimulates S cells to secrete secretin

A

H+

293
Q

What does secretin bind to

A

Receptor on ductal cells (also Ach and CCK potentiates)

294
Q

What happens when secretin (potentiates by ACh and CCK) binds to ductal cells

A

CAMP

295
Q

What happens when cAMP increases in ductal cells

A

Aqueous secretion (Na, HCO3)

296
Q

Cystic fibrosis mutation

A

CFTR:regulated Cl channel in the apical surface of the duct cell

297
Q

In CF, the __ is one of the fist organs to fail

A

Pancreas

298
Q

Some CFTR mutations seem to be associated with a loss of _ secretion

A

HCO#

299
Q

What happens if lose HCO3 secretion

A

Ability to flush active enzymes out of the duct may be lost

May lead to recurrent acute and chronic pancreatitis

300
Q

Metabolic functions of the liver

A

Carbohydrate metabolism

Protein metabolism

Lipid metabolism

301
Q

Liver carbohydrate metabolism

A

Gluconeogenesis
Storage of glucose as glycogen

Release of glucose

302
Q

Liver protein metabolism

A

Synthesis of nonessential aa

Modification of aa for use in biosynthetic pathways for carbohydrate

Synthesis of almost all plasma proteins

Conversion of ammonia (byproduct of protein catabolism) to urea

303
Q

Liver failure can result in ___, which may lead to ___

A

Hypoalbuminemia

Edema

304
Q

Liver lipid metabolism

A

Fatty acid oxidation

Synthesis of lipoproteins , cholesterol and phospholipids

305
Q

Cirrhosis

A

Chronic livers disease in which normal liver cells are damaged and replaced by scar tissue

306
Q

What causes liver cirrhosis

A

Excessive alcohol intake is most common cause

307
Q

How does excessive alcohol cause cirrhosis

A

Leads to accumulation of fat within hepatocytes

Fatty liver leads to steatohepatitis

308
Q

What is steatohepatitis

A

Fatty liver accompanied by inflammation, which leads to scarring of liver and cirrhosis

309
Q

One of the most common causes of ___ ___ is cirrhosis

A

Portal hypertension

310
Q

Why does portal hypertension develop

A

When there is resistance to portal blood flow, which most often occurs in the liver

311
Q

How can liver dysfunction lead to hepatic encephalopathy

A

Decreased hepatic urea cycle metabolism in the context of liver cirrhosis or portosystemic shunting leads to accumulation of ammonia in the systemic circulation
-ammonia readily crosses the BBB and alters brain function

Get increased brain water, direct neuronal toxicity, increased intracranial pressure, altered neurotransmission

312
Q

__ is produced and secreted by the liver

A

Bile

313
Q

Bile composition

A 
Bile salts (50%)
Bile pigments (2%)-bilirubin
Cholesterol(4%)
Phospholipids (40%)-lecithin
Ions
H2O
314
Q

Function of bile

A

Vehicle for the elimination of substances from the body

Solves the insolubility problem of lipids

315
Q

What are the biliary system organs

A 
Liver
Gallbladder and bile duct
Duodenum
Ileum
Portal circulation
316
Q

Steps in bile secretion

A
  1. Synthesis and secretion of bile salts
  2. Bile salts are stored and concentrated in gallbladder (absorption of ions and H2O
  3. CCK induced gallbladder contraction and sphincter of Oddi relaxation
  4. Absorption of bile salts into the portal circulation
  5. Delivery of bile salts to the liver
317
Q

Bile salts are recirculated to the liver via the ___ ___

A

Enterohepatic circulation

318
Q

Steps of bile salts recirculating to the liver via the enterohepatic circulation

A
  1. Bile salts are transported from the ileum to the portal blood
  2. Bile salts back to the liver
  3. Synthesis of bile salts to replace the amount that was lost
319
Q

What are the two system that mediate uptake across the basolateral membrane of the hepatocytes

A

1.Na dependent transport protein, sodium taurocholate cotransport int polypeptide(NTCP)
Na independent transport protein, organic anion transport proteins OATPS

320
Q

Describe recirculation of bile salts to liver

A

Biles leave the hepatocyte at bile canaliculus through BSEP and MRP2(both using ATP) thought biliary excretion and enter the enterocyte though ASBT

Then leave enterocyte into portal circulation by OSTa-OSTb

Then renter the hepatocyte through NTCP

321
Q

BSEP

A

Bile salt excretory pump

Uses ATP

322
Q

MRP2

A

Mltidrug resistance protein 2

Uses ATP

323
Q

ASBT

A

Apical sodium dependent bile acid transporter

Cotransport bile acid with Na

324
Q

OSTa OSTb

A

Organic solute transporter alpha beta

325
Q

NTCP

A

Sodium taurocholate cotransport int polypeptide

Cotransport Na

326
Q

The enterohepatic circulation of bile acids is carried out by both active and passive processes

A

The ideal transport process is highly efficient, delivering more than 90% of the bile acids to the portal blood

Only a small portion of bile acids (3-5%) are excreted into the feces

327
Q

How is bilirubin made

A

Red cell destruction, heme protein catabolism, and bone marrow erythropoiesis cause breakdown of hemoglobin->biliverdin->bilirubin

Bilirubin binds to albumin/unconjugated in the bloodstream

328
Q

Bilirubin/unconjugated enters the liver

A

Conjugated by UDP glucuronyl transferase

329
Q

What happens to conjugated bilirubin

A

Goes to enterohepatic circulation of small intestine

330
Q

What happens to conjugated bilirubin in the small intestine

A

Turned to urobilinogen then urobilin stercobilin

331
Q

Some new borns synthesize _ slowly and develop jaundice

A

UDP glucuronyl transferase

332
Q

What makes stool a dark color

A

Urobilin and stercobilin

333
Q

How do we quantify jaundice

A

Measure total serum bilirubin

334
Q

How do we express bilirubin tests

A

Direct conjugated

Indirect unconjugated

Total bilirubin

335
Q

Hemolytic anemia

A

Form of anemia due to hemolysis

336
Q

Hemolytic anemia is associated with increased production of ___, what does this cause

A

Bilirubin

Overwhelm livers capacity to produce conjugated bilirubin, resulting in increased unconjugated bilirubin

337
Q

What is neonatal jaundice

A

Increased unconjugated bilirubin in blood during 1st week of postnatal age

338
Q

Neonatal jaundice prognosis

A

Transient and resolves within 2 weeks after birth

339
Q

Two main causes of neonatal jaundice

A
  • bilirubin production is elevated because of increased breakdown of fetal erythrocytes-shortened lifespan of fetal erythrocytes
  • low activity of UDP glucuronyl treansferase
340
Q

Gilbert syndrome

A

Increased levels of unconjugated bilirubin in the blood

341
Q

Prognosis gilbert

A

Mild

342
Q

When is Gilbert recognized

A

Adolescence

343
Q

When do people with Gilbert get episodes of hyperbilirubinemia

A

Physiological Stressed!

Usually mild

344
Q

_ of People with Gilbert have no signs or symptoms of the condition

A

30%

345
Q

Mutation Gilbert

A

Mutation in gene that code UDP glucuronyltransferase

346
Q

Crigler najjar syndrome

A

Increased levels of unconjugated bilirubin in the blood

347
Q

What does crigler najjar syndrome cause

A

Nonhemolytic jaundice

348
Q

Mutation crigler najjar syndrome mutation

A

Mutations in the gene that code for UDP glucuronyltransferase

349
Q

Two types of crigler najjar

A

Type I very severe

Type 2 less severe

350
Q

Crigler najjar syndrome type I

A

Starts earlier in life

Jaundice is apparent at birth or in infancy

351
Q

Genetic mutation crigler najjar type I

A

NO function of UDP glucuronyltransferase

352
Q

Kernicterus and crigler najjar type I

A

Form of brain damage caused by the accumulation of unconjugated bilirubin in the brain and nerve tissues

353
Q

What sort of damage does unconjugated bilirubin toxicity inthe CNS cause

A

Oligodendrocytes, microglia, astrocytes,neurons

354
Q

How does the CNS protect from unconjugated bilirubin

A

Increase bilirubin oxidase

Increase cytochrome P450

Increase ABCB1 and ABCC1 export

355
Q

Crigler najjar syndrome type 2

A

Starts later in life

356
Q

Genetic mutation crigler najjar syndrome 2

A

Less than 20% function of UDP glucuronyltransferase

357
Q

Crigler najjar type 2 and kernicterus

A

Less likely

358
Q

Life span crigler najjar 2

A

Most affected individuals survive into adulthood

359
Q

Dublin Johnson

A

Increased CONJUGATED bilirubin in the serum without elevation of liver enzymes

360
Q

Genetic defect dubin Johnson

A

Defectint he ability of hepatocytes to secrete conjugated bilirubin into the bile
-mutations in multidrug resistance protein 2 (MRP2)

361
Q

What does MRP2 do

A

Transports bilirubin out of liver cells and into bile

362
Q

Slinical dubin johnson

A

Mild jaundice throughout life
Which may not appear until puberty or adulthood

LIVER HAS BLACK PIGMENTATION

363
Q

Why does the liver have black pigmentation in dubin johnson

A

Result of an intracellular melanin like substance but is otherwise histologically normal

364
Q

Rotor syndrome

A

Buildup of both unconjugated and conjugated bilirubin in the blood, but the majority is conjugatedsimilar to dubin johnson

365
Q

Genetics rotor syndrome

A

Set abnormally short, nonfunctional OATP1B1 and OATP1B3 proteins or an absence of these proteins

366
Q

What do OAT1B1 and OAT1B3 normally do

A

Transport bilirubin and other compounds from the blood into the liver so that they can be cleared from the body

367
Q

Are liver cells pigmented in rotor

A

No

368
Q

How is unconjugated bilirubin formed

A

RBC breakdown (get increase in hemolytic anemia)

369
Q

Why would u have decreased delivery of bilirubin for conjugation

A

Heart failure

370
Q

What disease decreases uptake to the liver

A

Gilbert

371
Q

What disease decreases conjugation of bilirubin

A

Gilbert syndrome

Crigler najjar

372
Q

What disease prevents conjugated bilirubin secretion to bile

A

Dubin johnson and rotor syndrome

373
Q

What disease decreases passage of conjugated bile

A

Biliary tree obstruction

374
Q

What are the five known hereditary defects in bilirubin metabolism

A

Crigler najjar
Gilbert
Dubin johnson
Rotor

375
Q

Gallstones

A

Excess in either pigment of bilirubin breakdown or cholesterol

376
Q

Causes of gallstones

A
  1. too much absorption of water from bile
  2. Too much absorption of bile acids from bile
  3. Inflammation of epithelium
377
Q

What is the fate of gallstones

A

75% large gallstones stay in gallbladder and are asymptomatic

10% smalls tones intermittently blocking cystic duct, causing intermittent biliary pain

10% smalls tones impacted in cystic duct; causing acute cholecystitis

5% small stones impacted in distal bile duct; causing jaundice, biliary type pain and risk of cholangitis and pancreatitis

378
Q

The surface of the small intestine is arranged in longitudinal folds-what are these called

A

Folds of kerckring

379
Q

Villi are longest in the __ and shorter in the ___

A

Duodenum

Terminal ileum

380
Q

Microvillar surface/brush border

A

Site of activity for a number of digestive enzymes

Barrier that use be traversed by nutrients , water, and electrolytes onthe way to the blood or lymph

381
Q

Transmural movement of absorption: solute moving across the enterocyte, from the lumen to the blood must cross several barriers

A 
I stirred layer of fluid
Glycocalyx
Apical membrane
Cytoplasm of the cell
Basolateral membrane
Basement membrane
Wall of the blood capillary or wall f the capillary of the lymphatic vessel
382
Q

What are enterocyte:epithelial cells for

A

Digestion, absorption and secretion

383
Q

Turnover rate of enterocyte:epithelial cells

A

3-6 days

384
Q

What are enterocyte susceptible to

A

Irradiation and chemotherapy

385
Q

Paneth cells do what

A

Part of the mucosal defenses against infection

Secrete agents that destruct bacteria or produce inflammatory responses

386
Q

Goblet cell function

A

Mucus secreting

Physical, chemical and immunologic protection

387
Q

Only — are absorbed by enterocyte

A

Monosaccharides

388
Q

What are the monosaccchraides

A

Glucose, galactose, and fructose

389
Q

Lactose broken down by lactase

A

Glucose and galactose

390
Q

Sucrose broken down by sucrase

A

Glucose and fructose

391
Q

Trehalose broken down by trehalase

A

Glucose and glucose

392
Q

Starch broken down by a-amylase

A

A dextrins, maltose, and maltotriose

393
Q

A destrins broken down by a dextrinase

A

Glucose glucose

394
Q

Maltose broken down by malaise

A

Glucose glucose

395
Q

Maltotriose broken down by sucrase

A

Glucose glucose

396
Q

How are carbohydrates absorbed lumen

A

SGLT1-secondary active transport

GLUT5

397
Q

How are carbohydrates absorbed blood basolateral side

A

GLUT2 for glucose, galactose and fructose driven by NaK ATPasw

398
Q

SGLT1

A

Cotransport Na and glucose or Na and galactose

399
Q

GLUT5

A

For fructose

400
Q

Lactose intolerance

A

Brush border lactase is decreased or absent and undigested lactose remains in the lumen and holds H2O and causes osmotic diarrhea

401
Q

In lactose intolerance what happens to the undigested and unabsorbed lactose

A

Fermented into methane and H gas, causing excess gas

402
Q

Ingested proteins are digested to absorbable forms by __ in the stomach and small intestine

A

Protesases

403
Q

In the __ pepsinogen becomes pepsin from low pH

A

Stomach

404
Q

Pancreatic enzymes are secreted in the inactive form into the small intestine . What are the endopeptidases and exopeptidases

A

Endopeptidases-trypsin, chymotrypsin, elastase

Exopeptidases-carboxypeptidase A, carboxypeptidase B

Also have pancreas proteases

405
Q

In the __ __ enterokinase turns trypsinogen to trypsin

A

Brush border

406
Q

What then turns trypsinogen to trypsin

A

Trypsin

407
Q

What turns chymotrypsinogen to chymotrypsin

A

Trypsin

408
Q

What turns proelastase to elastase

A

Trypsin

409
Q

What turns pro-carboxypeptidase A to carboxypeptidase A

A

Trypsin

410
Q

What turns procarboxypeptidase B to carboxypeptidase B

A

Trypsin

411
Q

How are proteins digested in the stomach

A

Protein->aa and oligopeptides

By pepsin

412
Q

How get inactivation of pancreatic protesases

A

Trypsin catalyze the hydrolysis of trypsinogen (autocatalysis)

Pancreatic proteases digest themselves and each other

413
Q

How is protein digested int he SI

A

By trypsin, chymotrypsin, elastase, carboxypeptidase A, and carboxypeptidase B

Into aa, dipeptide, tripeptide

And oligopeptides->aa, dipeptide, and tripeptide by peptides (brush border)

414
Q

_ and _ _ are key transport mechanisms in the absorption f proteins

A

Cotransport and facilitated diffusion

415
Q

What are the 4 separated cotransporters in lumen

A

One for neutral, acidic, basic and imino aa

416
Q

Basolateral side has 4 separate facilitated diffusion mechanisms

A

One for each neutral, acidic, basic and imino aa

417
Q

_ and _ lipases initiate lipid digestion in the stomach

A

Lingual

Gastric

418
Q

What happens to lipids in stomach

A

10% ingested TG are hydrolyzed to glycerol and fatty acids

Lipids are broken down into small droplets

Lipids droplets are emulsified I tot he stomach (no bile acids in the stomach, dietary proteins perform the emulsifying action

419
Q

In order to allow sufficient time for lipids to get digested properly, __ is released in stomach

A

CCK

420
Q

When is CCK secreted

A

When dietary lipids first appear in the small intestine

421
Q

What does CCK do

A

Slows the rate of gastric emptying

422
Q

Most lipid digestion occurs in the ___

A

SI

423
Q

__ __ emulsify lipids

A

Bile salts

424
Q

Pancreatic enzymes are secreted into he SI to complete digestion

A

Ok

425
Q

Pancreatic lipase

A

Secreted as the active enzyme

Inactivated by bile salts; colipase solves this problem

426
Q

Colipase

A

Secreted as an inactive form (procolipase) it is activated by trypsin

Once activated, it binds to pancreatic lipase displacing bile salts

427
Q

Cholesterol ester hydrolase

A

In addition to catalyze the production of cholesterol, it also hydrolyzes triglycerides to produce glycerol

428
Q

Phospholipase A2

A

It’s proenzyme is activated by trypsin

429
Q

Ingested lipids are digested to absorbable forms by lipases int he stomach and small intestine

A

Ok

430
Q

Triglycerides are broken down by

A

Lingual, gastric and pancreatic lipases

431
Q

What are triglycerides broken down into

A

Monoglyceride, FA, FA

432
Q

Cholesterol ester are broken down by

A

Cholesterol ester hydrolase

433
Q

What are cholesterol ester broken down into

A

Cholesterol, FA

434
Q

Phospholipid are broken down by

A

Phospholipase A2

435
Q

What are phospholipid broken down by

A

Lysolecithin

FA

436
Q

Insolubilits of lipids complicates their assimilation

A

Lipids need to be solubilized in micelles and transported to the apical membrane of intestinal epithelial cells for absorption

437
Q

Steps in lipids processing

A
  1. Solubilization by micelles
  2. Diffusion of micelles content across apical membrane
  3. Reesterification
  4. Chylomicron formation
  5. Exocytosis of chylomicron
438
Q

No ApoB

A

Abetalipoproteinemia and no absorption of dietary lipids

439
Q

Regulation of __ of duodenal content is critical for the integrity of pancreatic enzyme function

A

Acidity

440
Q

The duodenum needs to be adequately neutralized by _ contains pancreatic secretions

A

HCO3

441
Q

Pancreatic insufficiency

A

Failure to secrete adequate amounts of pancreatic enzymes

442
Q

Zollinger Ellison syndrome

A

Gastrin secreting tumor of the pancreas

Increased H secretion by gastric parietal cells

Overload of acid in the duodenum

443
Q

Pancreatitis

A

Impaired HCO3 and enzyme secretions

444
Q

Defiency of bile acid problem

A

Interferes with the formation of micelles

445
Q

Factors that cause deficits in bile acid

A

Ideal resection

  • interrupts enterohepatic circulation of bile salts
  • Total bile salt pool is reduced

Small intestinal bacterial overgrowth SIBO

  • bacteria deconjugate bile salts, impairing micelle formation and fat malabsorption
  • severe bacterial overgrowth damages the intestinal mucosa
  • two main causes: decreased gastric acis secretions nd small testing dysmotility
446
Q

Tropical sprue

A

Decreased intestinal epithelial cells affects lipid absorption

447
Q

Cause of tropical sprue

A

Cause not identified, putatively due to an intestinal infection

448
Q

Problem with tropical sprue

A

Decreased number of intestinal epithelial cells; reduces the microvillar surface ares
THIS CAUSES IMPAIRED LIPID ABSORPTION BC THE SURFACE AREA TOR ABSORPTION IS DECREASED—>STEATORRHEA

Nutritional deficncies (B12, folate)

449
Q

Main symptom of tropical sprue

A

Diarrhea

450
Q

Other symptoms of tropical sprue

A

Cramps, nausea, weight loss, gas and indigestion

451
Q

Celiac sprue

A

Autoimmune disorder; there is a hereditary component

452
Q

In celiac sprue there are antibodies against what

A

A gluten component-gliadin

453
Q

What does celiac sprue lead to

A

Destruction of small intestine villi (atrophy), as well as hyperplasia of the intestinal crypts

454
Q

What malabsorption related deficiencies do people with celiac sprue have

A

Folate, iron, calcium, vitamins a B12 and D

455
Q

Water soluble vitamins

A

B1, 2, 3, 12, C, biotin, folic acid, nicotonic acid, pantothenic acid

456
Q

How are water soluble vitamins absorbed

A

Na dependent cotransport mechanism in the small bowel

457
Q

How is B12 absorbed (cobalmin)

A

Forms complexes with other proteins to be absorbed

R proteins (secreted in salivary juices)
IF
Transcobalmin II

458
Q

B12 absorption

A

B12 attached to food is released with pepsin and H+ and forms B12 R protein complex in stomach which travels to SI
In SI pancreatic protesases release B12 from R protein and then in the SI it attaches to IF
B12-IF is absorbed in the ileum by binding to IF receptors

In the mucosa B12 binds TCII and goes into circulation with it (transcobalmin II)

459
Q

Gastectome

A

Loss of parietal cells(source of IF)

460
Q

Gastric bypass

A

Exclusion of the stomach, duodenum, and proximal jejunum alters absorption of B12

461
Q

Duodenum transport between interstitial fluid and intestinal lumen

A

Intestinal lumen is isotonic and receives H20 which it sends Na, H2O, Ca and Fe into interstitial fluid

462
Q

Jejunum

A

Send Na, Cl, K, H2O and HCO3 from lumen into interstitial fluid

463
Q

Ileum

A

Send Na, Cl, K, H2O, bile salts, IF,-b12 into interstitial fluid and
Receive HCO3 into lumen

464
Q

Colon

A

Smallest absorption

Send Na, Cl, and H2O into interstitial fluid and receive K HCO3

Look at pic

465
Q

What is absorbed in the proximal small intestine

A

Fat, sugar, peptides and aa, iron, folate, calcium, water, electrolytes

466
Q

What is absorbed int he middle small intestine

A

Sugars, peptides and aa, calcium, water, electrolytes

467
Q

Distal small intestine

A

Bile acids, vitamin B12, water, electrolytes

468
Q

What is absorbed in the colon

A

Water, electrolytes, medium chain triglycerides, calcium, aa

469
Q

Where are carbs, proteins and lipids absorbed

A

Most duodenum, middle jejunum least ileum

470
Q

Where are calcium, iron and folate absorbed

A

Duodenum

471
Q

Where is calcium absorbed

A

Duodenum most

Also jejunum and ileum

472
Q

Where are bile acids absorbed

A

Least duodenum

Middle jejunum
Most ileum
Middle large intestin

473
Q

Where is cobalmin absorbed

A

Ileum

474
Q

Cholera

A

Cholera toxin produced by virbio cholera she causes uncontrolled secretion of Cl I tot he intestinal lumen resulting in copious secretory diarrhea

475
Q

What does cholera B subunit bind to (also has A subunit)

A

GM1 ganglioside

476
Q

What happens with cholera toxin binds to GM1

A

Get retrograde transport through golgi and into ER by PD1

477
Q

What happens to cholera toxin in ER

A

Unfolded segment A

478
Q

What does unfolded subunit A do

A

Transport and remolding into cytosolic and binds ARF

479
Q

What dose ARF bound to a subunit do

A

Activate NAD to bind Gsa G protein which blah blah blah increase cAMP and open CFTR which releases chloride

480
Q

Ileum antiporter

A

Cl HCO3

481
Q

Colon antiported

A

HCO3, Cl

482
Q

NAD bound to active Gsa..what happens to NAD

A

Turns to ADP ribose which activated adenylate cyclists which turns ATP to cAMP which opens CFTR to release Cl

483
Q

What reflexes signal defecation

A

Duodenocolic and gastrocolic

484
Q

What stimulates gastrocolic and duodenocolic reflex

A

Distention of stomach and duodenum

485
Q

What pathology would create no reflex to poop

A

Removal of autonomic nerves to colon

486
Q

What transmits the gastrocolic and duodenocolic reflexes

A

Autonomic nervous system

487
Q

Enterogastric reflex

A

Signal from intestine inhibits gastric motility and gastric secretion

488
Q

Intestino intestinal reflec

A

Over distention or injury to a bowel segment signals he bowel to relax

489
Q

Rectosphincteric reflex

A

Also called the defecation reflec

Initiated when feces enter the rectum and stimulate the urge to defecate

490
Q

What happens when lactose intolerant person eats lactose

A

Not absorbed cant break down so gut bacteria ferment

H and methane

491
Q

94% of biles salts are reabsorbed into the blood from the small intestine, with about Hal of this by diffusion through the mucosa in the early portions and remainder by _- ___ through intestinal mucosa in distal ileum

A

Active transport

492
Q

Where is B12 absorbed

A

Ileum

493
Q

What is required for B12 absorption

A

IF (glycoprotein_ from parietal cells in stomach bind B12 in ___ for receptors in brush border of the ileum

494
Q

Atrophic gastriris

A

Autoimmune gastritis mainly confined to the acid secreting corpus mucosa.

495
Q

Saliva composition basal

A

K bicarbonate high

Low Na Cl

496
Q

What is the only gastrointestinal hormone released by all three major foodstuffs-fat, proteins, and carbohydrates

A

GLIP

497
Q

What is secreted by fat and protein

A

CCK

498
Q

Protein in antrum of stomach

A

Gastrin release

499
Q

GLIP

A

Strong stimulator of insulin release and is responsible for the observation that an oral glucose load releases more insulin

500
Q

Where is there subatmospheric pressure in the esophagus

A

Where it passes through the chest cavity

501
Q

What secretes pepsinogen

A

Chief cells

502
Q

What is an oxyntic gland

A

Gastric gland

503
Q

What does pepsin digest

A

Collagen and CT in meats

504
Q

__ is the only gastrointestinal hormone that inhibits gastri emptying under physiological conditions.

A

CCK

505
Q

Why does a breakfast of fat a protein stick with you better than one of carbs

A

CCK

506
Q

Please describe saliva secretion

A

Primary secretion by acini has ionic composition similar to plasma
As flow through ducts, sodium ions are actively reabsorbed and potassium are actively secreted in exchange for sodium

Bc sodium is absorbed in excess Cl follow causing Cl in saliva to decrease

Bicarbonate secreted by an active transport process causing an elevation of bicarbonate concentration in alive

507
Q

Secretin and GLIP inhibit acid secretion through a ___ action on parietal cells and __ through suppression of gastrin secretion

A

Direct

Indirect

508
Q

What does gastrin stimulate

A

Gastric acid secretion

509
Q

What do GLIP and secretin do

A

Inhibit gastrin secretion

510
Q

Cephalic phase gastric secretion

A

Before food enters stomach. See, smell, chew, mechanoreceptors in mouth, hypoglycemia

Brain anticipates food

511
Q

What mediates cephalic phase

A

Vagus nerve

512
Q

Vagotomy and cephalic phase

A

Gone

513
Q

Antacids

A

Neutralize gastric acid

514
Q

H2 blocker

A

Attenuate the cephalic phase of gastric secretion but not abolish

515
Q

MMC

A

Peristaltic waves of contractions hat begin in the stomach and slowly migrate in an abnormal direction along entire small intestine to the colon. This sweeps undigested food residue from stomach trough small intestine into colon

516
Q

Purpose of MMC

A

Maintain low bacterial count

517
Q

Why get bacterial overgrowth syndrome

A

No MMC

518
Q

What conditions favor gastric emptying

A

Increased tone of orad
Forceful peristaltic contractions
Relaxation pylorus
Absence of segmentation contractions

519
Q

V cholera

A

Irreversible increase in cAMP levels in enterocytes located in the crypts of lieberkuhn of the small intestine

Irreversible opening of chloride channels on the luminal membrane. Movement into gut causes secondary movement of na which water follows

Severe diarrhea

520
Q

How are enterocytes made

A

From stem cells in crypts of lieberkuhn of SI. They mature as they migrate upward toward the villus tip, where they are extruded into the gut lumen,

521
Q

How often are epithelial cells replaced

A

3-6 days

522
Q

When is pH stomach lowest

A

Immediately before meal

523
Q

How long does it take stomach to empty after eat

A

3-4 hours

524
Q

Gastrin and CCK do not share any effects on GI function at normal physiological conditions ; however, they have identical actions on GI function when pharmacological doses are administered

A

Gastrin stimulates gastric acid secretion and mucosal growth throughout the stomach and intestines under physiological conditions

CCK stimulates growth of the exocrine pancreas and inhibits gastric emptying under normal conditions , al

525
Q

Describe swallow

A

Palatopharyngeal folds on either side of pharynx pulled medially, forming a sagittal slitthrough which the bolus of food must pass

Soft palate pulled up to close posterior Nareen
Vocal cords of larynxstrongly approximated during swallowing and the larynx is pulled up and anterior by neck muscles

Epiglottis swings back over opening of larynx allowing food to go from posterior pharynx to upper esophagus

526
Q

Frequency slow waves stomach, duodenum, jejunum, ileum

A

3 a min, 12, 10, 8

527
Q

What happens when feces enter rectum

A

Distention of fetal wall signals spread through the myenteric plexus to initiate peristaltic waves in descending colon, sigmoid colon and rectum
Internal anal sphincter relaxes

528
Q

Defectaion and transacted spinal cord

A

Defectaion reflexes can cause autonomic emptying of the bowel because the external anal sphincter is normally controlled by the conscious brain through signals transmitted in the spinal cord

529
Q

NSAID gastritis and peptic disease

A

Yup

530
Q

Vomiting

A

Deep breath
Relaxation of upper esophageal sphincter
Closure of the glottis
Strong contractions of the abdominal muscles and diaphragm

531
Q

Diagnose gastrinoma of zollinger ellison

A

Gastrin over 110

532
Q

Small wave frequency effected by anything

A

Nope

533
Q

Rectosphinteric reflex

A

Mass movement enters rectum

When rectum stretched internal anal sphincter relaxes and the rectum contracts pushing the feces toward the anus the external anal sphincter is controlled voluntarily

534
Q

When get relaxation ileocecal sphincter

A

Shortly after eat

Gastroileal reflec

535
Q

Gastric mucosal barrier damage allow h ions to back leak into the mucosa in exchange for Na ions

A

Low pH mast cells to leak histamine which damages the vasculature causing ischemia

536
Q

Fat digestion

A

In SI emulsified in bile
Colipase and lipase digest int monoglycerides and FFA
Surrounded by bile acids to form micelles
Michelle contacts enterocyte monoglycerides and ffa diffuse in
In enterocyte form triglycerides
Then packaged by golgi into chylomicrons
Exoctose and enter lymphatic capillary in villus

537
Q

CFTR protein

A

CAMP regulated Cl channel

538
Q

Absence of CFTR

A

CF

539
Q

What happens when mucosa damages

A

H leak into
Intracellular buffered saturate
PH decreases cell death

Also damage mast cells

540
Q

Receptive relaxation

A

Fundus and lower esophageal sphincter both relax during a swallow while the bolus of food is still higher in the esophagus

541
Q

Haustrations

A

Bulges in large intestine caused by contraction of adjacent circular and longitudinal smooth muscle

542
Q

Gastroparesis

A

Delayed emptying

Can be cause by diabetes

543
Q

__, __, and __ can directly stimulate parietal cells to secrete acid

A

Gastrin
Acetylcholine
Histamine

544
Q

Ptyalin

A

Salivary amylase for carb digestion in mount

545
Q

Celiac

A

Cell mediated immune espouse to gliadin

546
Q

Why pH increase in stomach after food

A

Food buffers the acid inthe stomach this ph increase suppressses release of omatostatin which allows acid to secrete

547
Q

Intestinal absorption of immunoglobulins from colostrum

A

Endocytosis-only first few months

Normally just facilitated diffusion, passive diffusion, and primary and secondary active transport

548
Q

hypernatremia and low bp

A

Dehydrated

549
Q

CentralDiabetes insipidus

A

Low ADH

Low specific urine gravity despite hypernatremia
Pee a lot

550
Q

Nephrogenic diabetes insipidus

A

Not responding to ADH

Low urine specific gravity despite hypernatremia

Pee a lot

Physiology (7 decks)

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