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GI block > Physiology > Flashcards

Physiology Flashcards

1
Q

Parasympathetic innervation of the GI system uses what two postsynaptic receptors?

A

Cholinergic–> ACh

Peptidergic–> substance P + VIP

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2
Q

What nerve relays the GI mechanoreceptors and chemoreceptors signals back to CNS?

A

VAGUS

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3
Q

Actions of ACh on GI system?

A 
Contraction of smooth muscle
Relax sphincters
Increase salivary secretions
Increase Gastric secretions
Increase pancreatic secretions
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4
Q

Actions of NE on GI?

A

Relax smooth muscle
Contract sphincters
Increase salivary secretions

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5
Q

Actions of VIP on GI?

A

Relax smooth muscle
Increase intestinal secretions
Increase pancreatic secretions

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6
Q

GRP (bombesin) actions on GI?

A

Gastrin releasing peptide

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7
Q

Enkephalins (opiates) actions on GI?

A

Contract smooth muscle

Decrease intestinal secretions

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8
Q

Neuropeptide Y actions on GI?

A

Relax smooth muscle

Decrease intestinal secretions

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9
Q

Substance P actions on GI?

A

Contraction of smooth muscle

increase salivary secretions

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10
Q

Stimulation / actions/ site of Gastrin secretion?

A 
Stimuli= small peptides + AA + GRP (distention)
Action= Increase H+ (parietal cells) &              gastric mucosa growth
Site= G cells of Stomach
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11
Q

Stimulation / actions / site of CCK secretion?

A 
Site= I cells of Duodenum + jejunum
Stimuli= small peptides + AA + FA 
Actions= increase pancreatic enzymes & HCO3 + contraction of Gallbladder + relax sphincter of iddi                             growth of exocrine pancreas + GB                     Inhibits Gastric emptying
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12
Q

Stimuli / actions/ site of secretin secretion?

A

Site= S cells of duodenum
stimuli= H+ & FA in duodenum
actions= increase pancreatic & biliary HCO3
Decrease gastic H+
inhibit trophic affects of gastrin on mucosa

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13
Q

Stimuli / site/ actions of GIP?

A 
Site= duodenum + jejunum 
stimuli= FA + AA + Oral Glucose 
Actions = increase Insulin secretion +            Decrease Gastric H secretion
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14
Q

What is the difference btwn “little” (17-amino acid) Gastrin and “big” (34 AA) gastrin?

A 
Little= secreted in response to meals
Big= secreted during inter-digestive periods
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15
Q

Two most potents AA for stimulation of GASTRIN secretion are?

A

Phenulalanine

Tryptophan

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16
Q

What are the affects of High levels of Gastrin (ZES= Gastrinoma)?

A

Increase H+ secretion from Parietal cells
Hypertrophy of Gastric mucosa
DUODENAL ULCERS–> High H+
FAT malabsorption (steatorrhea)

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17
Q

What is the Tx for Zollinger-Ellison syndrome?

A

H2 receptor blockers (Cimetidine)

H+ pump inhibitors (Omeprazole)

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18
Q

CCK- Gastrin are related how?

A

CCK –> has Gastrin activity

Gastrin–> Can activate CCKb receptor

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19
Q

Monoglycerides + FA + small peptides and AA Triglycerides

A

CCK

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20
Q

Stimuli/ site/ and action of Motilin?

A 
Site= upper duodenum 
Stimuli= Fasting
Actions= initiates interdigestive myoelectric complexes 90min intervals
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21
Q

Action / stimulation / site of Somatostatin?

A 
Site= D cells in GI mucosa
Stimuli= Decreased pH 
Action= inhibits Gastric H+ secretions
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22
Q

What action to Histamine and ACh have in common in GI?

A

Stimulate H+ secretion by parietal cells

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23
Q

What parts of the GI tract are Striated muscle instead of Smooth?

A

Pharynx
Upper 1/3 Esophagus
Anal sphincter

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24
Q

Which parts of the GI tract exhibit phasic contractions?

A

Esophagus
Gastric antrum
small intestines

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25
Q

Which parts of GI are involved in Tonic contractions?

A

Upper Stomach
Lower Esophageal sphincter
Ileocecal and internal anal sphincter

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26
Q

Contractions in GI smooth muscle has what unique feature?

A

SLOW waves= oscillating depolarization and repolarization that leads to AP when membrane potential reaches Threshold

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27
Q

What parts of the GI tract have the highest and lowest slow wave rates?

A 
Slowest = Stomach (3/min)
Fastest= Duodenum (12/min)
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28
Q

What sets the slow waves and how can it be modulated?

A

Origin= Interstitial cells of CAJAL of Myenteric plx
Modulators= Hormone and neural inputs
PSNS + gastrin= increase AP freq + force contractn
SNS + GIP + secretin= decrease freq + force

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29
Q

What is considered to be the Pacemaker of GI motility?

A

Cells of CAJAL

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30
Q

Where is the swallowing center located?

A

Medulla

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31
Q

What mediates the relaxation of the lower esophageal sphincter?

A

Vagal peptidergic fibers== Release VIP

**Upper stomach (orad) also relaxes to receive food

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32
Q

What factors slow or inhibit gastric emptying?

A

Low pH

FAT (CCK)

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33
Q

What are the Neurotransmitters involved in contraction and relaxation during peristaltic contractions?

A 
Constrictors= ACh + Substance P
Relaxers= VIP + NO
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34
Q

Describe vomiting reflex?

A

Reverse peristalsis starting @ Small intestines
Relaxation of stomach and pylorus
Forced Expiration to increase abdominal pressure
Relaxation of Lower ESO sphincter

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35
Q

What is retching?

A

Act of vomiting without OPENing of Upper esophageal sphincter = contents fall back into stomach

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36
Q

What is the Gastrocolic reflex?

A

Distention of stomach increases Colon motility via afferent PSNS and efferent CKK and gastrin

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37
Q

What stimulates salivary glands?

A

Both SNS & PSNS

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38
Q

What is saliva made of?

A 
Water 
Electrolytes (high [HCO3] + [K+]) 
alpha Amylase
Lingual lipase
kallikrein
mucus
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39
Q

Describe the tonicity of Saliva?

A

HYPOTONIC
Higher K+ and HCO3
Lower Na+ & Cl-

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40
Q

Formation and secretion of Saliva?

A

Acinar cells produce initial saliva

Ductal cells modify the saliva

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41
Q

What do acinar cells produce in salivary glands?

A

Isotonic fluid–> normal (plasma) Na, K , HCO, Cl-

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42
Q

What factors decrease Saliva secretion?

A

Sleep
Dehydration
Atropine
Anticholinergics

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43
Q

What factors stimulate secretion of HCL in stomach?

A

Gastrin
ACh via GRP
Histamine

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44
Q

What factors decrease HCL secretion?

A 
LOW pH in stomach 
Chyme in duodenum
Somatostatin 
Atropine
Cimetidine 
Omeprazole
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45
Q

What are the characteristics of Pancreatic secretions?

A 
Pepsinogen 
Intrinsic Factor 
High [HCO3] 
Isotonic 
Lipase + amylase + protease
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46
Q

What factors stimulate Pancreatic secretions?

A

PSNS–> Pepsinogen + Lipase + protease + aml
Secretins–> HCO3
CCK-

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47
Q

What is overall function of ductal cells during salivary modification?

A

Absorb NaCl
Secrete K+ & HCO3
Cells are water impermeable creating HYPOtonic saliva

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48
Q

What is the function of Kallikrein?

A

cleaves High molecular wght Kininogen into bradykinin (potent vasodilator)

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49
Q

What are the four components of Gastric Secretions?

A

HCl
pepsinogen
Intrinsic factor
Mucus

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50
Q

What are the products of Oxyntic/Parietal cells and Chief/peptic cells located in the BODY of stomach?

A 
Parietal= HCl + IF (Absorption of HCO3)
Chief= Pepsinogen
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51
Q

Pyloric glands in the ANTRUM of stomach contains what 2 cells types/function?

A

G cells= Gastrin secretion

Mucus cells= mucus + HCO3 + pepsinogen

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52
Q

What is the MOA of omeprazole?

A

Block H+ K+ ATPase on the Apical side of Parietal cells

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53
Q

What is responsible for the pH of Gastric venous blood?

A

HIGH pH due to Absorption of HCO3–> Eventually released back into GI from Exocrine pancreas

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54
Q

MOA of HCl release from gastric cells via ACh + Histamine + Gastrin?

A

Vagus->ACh->M3->IP3/Ca->HCl release (xAtropine)
ECL cells->H2->cAMP->PKA->HCL (xCometidine)
Gcells-> Gastrin-> CCKb->IP3/Ca->HCL

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55
Q

How do Atropin and Cimetidine affect HCl release from Parietal cells?

A

Atropine blocks Vagal stimulation (anticholinergic)

Cimetidine Blocks H2 receptors/ blocks histamine action of Parietal cells

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56
Q

What is potentiation?

A

Ability of two stimuli to produce a combined response greater than the sum of individual responses –> ACh + Gastrin both increase Histamine release from ECL cells

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57
Q

How does Vagus nerve innervate parietal cells and G cells?

A

ACh->Parietal cells-> Direct stimulation of HCl

GRP-> G cells -> Gastrin-> HCl release

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58
Q

What can stimulate HCl release?

A

Vagus
Gastin
Caffeine
ETOH

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59
Q

What are the 3 phases of HCl release?

A

Cephalic-> Taste/smell/ Vagal ACh or Gastrin
Gastric-> Distention Vagus ACh/Gastrin + AA and small peptides
Intestinal Phase-> AA and peptides Gastrin

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60
Q

What are the direct and indirect ways Somatostatins block HCl secretions?

A

Direct-> inhibit Adenylyl cyclase on Parietal cells

Indrect-> inhibits Histamine and Gastrin release

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61
Q

What is the affect of Prostaglandins in HCl secretions?

A

Inhibits Histamine’s stimulatory action of parietal cells (inhibits Adenylyl cyclase)

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62
Q

What are the two major barriers of Peptic ulcers?

A
  1. Mucus (contains alkaline buffers HCO3)
  2. HCO3 contained in mucus and beneath mucus
  3. Mucosal blood flow
  4. Growth factors
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63
Q

What leads to peptic ulcers?

A

Loss of mucous barriers
Excessive H+ or pepsin release
Combine the TWO

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64
Q

What are the damaging factors affecting GI mucosa?

A 
H+ and pepsin 
H. pylori
NSAIDS
Stress
Smoking
ETOH
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65
Q

What is the pathogenesis of H pylori causing Gastric ulcers?

A 
G- bacterium colonizes Mucus and epithelial cells.
Releases Cytotoxins (cagA toxin)
cag A breaks down mucus
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66
Q

What permits H pylori to colonize the LOW pH stomach environment?

A

Urease-> generates NH3 to alkalinize the environment

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67
Q

What is a Diagnostic test for H pylori infections?

A

C-urea -> CO2 + NH3

CO2 is then measured

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68
Q

How does a H pylori cause a duodenal ulcer?

A

bacteria inhibits Somatostatin release

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69
Q

What are the affects of a Zollinger Ellison syndrome (gastrinoma)?

A

High Gastrin = High H+ & increased Parietal cells mass
high H+ overwhelms duodenal HCO3= Ulcers
High H+ inactivates Pancreatic Lipase= Steatorrhea

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70
Q

When/where is Pepsinogen secreted?

A

Chief cells

Vagal stimulation->High H+ -> Pepsinogen= Pepsin

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71
Q

What happens in the absence of Intrinsic factor secretion by Parietal cells?

A

Pernicious anemia

**Beware of Gastrectomies= Vit B12 supplements required

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72
Q

Sites of release & actions of Gastrin?

A 
Release= Antrum + duodenum 
Action= Antrum + Duodenum + Jejunum
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73
Q

Sites of release and action of CCK?

A

BOTH= Duodenum + Jejunum + ileum

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74
Q

Sites of Secretin secretion and action?

A 
Secretion= Duodenum
Action= Duodenum + Jejunum + Ileum
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75
Q

Site of GIP & Motilin secretion and action?

A

BOTH= Duodenum + Jejunum

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76
Q

Stimulatory and inhibitory factors for Gastrin release?

A 
Stimuli= Proteins + Distention + Vagus
Inhibitory= LOW pH
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77
Q

Stimuli for actions of Secretins?

A 
Stimuli= LOW pH 
Actions= Inhibit Acid secretion + stimulate pancreatic HCO3 and enzymes + growth
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78
Q

ALL secretins have what action in common?

A

Secretin + GIP + VIP + Glucagon= Inhibit Acid release

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79
Q

What are the GI hormones + Neurocrines + paracrines?

A 
Hormones= Gastrin + CCK + Secretin + GIP + motilin 
Neurocrines= VIP + Bombesin (GRP) + Enkephalin 
Paracrine= Somatostatins + Histamine
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80
Q

Site of release and actions of VIP?

A 
Site of release= mucosa and Smooth muscle
Actions= Relax sphincters
relax circular muscle
Stimulate Intestinal secretions
Stimulate pancreatic secretions
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81
Q

SIte of release and actions of Bombesin (GRP)?

A 
Site= Gastric mucosa
Action= Stimulate Gastrin release (via VAGUS)
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82
Q

Site of release and actions of Enkephalins?

A 
Site= mucosa + smooth muscle
Action= Simulate smooth muscle contractions + inhibits intestinal secretion

**used in Diarrhea

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83
Q

What are the stimuli & inhibitors of Somatostatin release?

A 
Stimuli= ACID
Inhibitory= Vagus nerve
84
Q

Four high yield facts about Zollinger-Ellison syndrome (gastrinoma)?

A

Over production of Gastrin
Duodenal ulcer, Diarrhea, Steatorrhea
High rates of Acid secretion
Inactivation of pancreatic LIPASE

85
Q

Three high yield points about Werner-Morison syndrome or Pancreatic Cholera?

A

Overproduction of VIP
Diarrhea, Metabolic acidosis, Dehydration, HypoK
High rates of Intestinal secretions
**Watery diarrhea= ALL night does not stop

86
Q

Name 5 features of GERD (causes and symptoms)?

A 
Acid reflux
Heartburn
HIatal hernia
Pregnancy 
Failure of 2nd peristalsis
87
Q

What mediates the pressure change in the Fundus of the stomach right before food enters via relaxation of LES?

A

Accommodating/ Relaxing reflex= Vago-vagal

88
Q

What is the contraction method for gastric emptying?

A

Segmental constriction= Used to propel some food into Duodenum while some back into stomach
**MIXING food

89
Q

How long does the average gastric emptying process last?

A

2-3 hrs

90
Q

How do High fat, High CCK, and High acid affect Gastric emptying?

A 
Fat= Slow gastric emptying (CCK)
CCK= relax smooth muscle= decrease 
Acid= increases Peristalsis= Increase 
Tonicity= Isotonic rapidly empties
91
Q

What causes fullness, loss of appetite, nausea, obstruction ulcer, Cancer, and vagotomy?

A

Decreased/ failure of Gastric Emptying

92
Q

What causes inadequate regulation, diarrhea, and duodenal ulcers?

A

Increased Gastric Emptying

93
Q

What affects to Vagal and SNS stimulation have on Slow waves?

A

They either Increase (vagal) or decrease (SNS) the AMPLITUDE of the slow wave= affects the strength and # of AP contraction respectively

94
Q

What determines Gastric AP contractions?

A

AMPLITUDE of Slow wave

95
Q

Small intestine Fed motor pattern is described as?

A

Segmentation contractions used to Increase SA coming in contact with Food to increase Absorption

96
Q

During the FED state what is the pattern of Small bowl motility?

A

Migrating Motor complex-> caused by MOTILIN secretion= contraction/90min

97
Q

How is contraction and slow wave different in small intestines from that of stomach?

A

Small intestines= Slow waves have Constant Amplitude

**Contractions are triggered by AP @ peak of slow wave NOT By the change in amplitude as seen in stomach

98
Q

How are slow waves, APs, and contractions affected by vagal and SNS stimulation in the small intestines?

A

NO Change in Slow wave FREQUENCY

Vagus= increase # of AP + Contractions

99
Q

How do contraction # increase from FED state to Fasting state in small intestines?

A

Increase in the # of SPIKES (APs)–> approaching the MAX (same as Slow wave frequency)

100
Q

What is the Rectosphinteric reflex?

A

Passive filling of the Rectum causes Active peristalsis which causes the Relaxation of the Internal Anal sphincter= Want to poop feeling

101
Q

What is the cause of Achalasia and megacolon?

A

Absence of Ganglia (NO VIP) causing Failure to RELAX smooth muscle

102
Q

What are the most important function of the Acid in the stomach?

A

Inhibit bacterial growth

2nd: activate pepsin

103
Q

What kind of cells are located in the Antrum of the stomach?

A

G cells –> secrete Gastrin

** NO parietal cells because LOW pH inhibits Gastrin release

104
Q

What is the function of Parietal cells during fasting?

A

Release SMALL amounts of HCL–> inhibit Gastrin release

105
Q

What is the Alkaline tide?

A

Stomach venous blood has HIGHER pH than arterial blood due to Reabsorption of HCO3 and secretion of H+

106
Q

WHat is the function of Carbonic anhydrase in the parietal cells?

A

CA turns the OH- left over from break down of H2O and combines it with CO2 to Form HCO3, THIS allows for Continuous H+ production while also increasing the [Cl-] inside the cells (HCO3/Cl- exchanger on Basolateral membrane)

107
Q

Where are the K+ H+ ATPase located inside the Parietal cells?

A

Lumenal side of Tubulovesicles–> NEVER face cytoplasmic side

108
Q

What change occurs form resting -> secreting parietal cells that allows for K+ H+ ATPase secretion into lumen of stomach?

A

Tubulovesicles are triggered to fuse with Intracellular Canaliculus–> Proton pump is then fused with membrane facing outward

109
Q

What are the four features of Parietal cells that allow it to Secrete High [H+]?

A
  1. Carbonic anhydrase
  2. Proton pump (K+H+ ATPase)
  3. Tubulovesicles containing proton pump
  4. Electrical gradients (mucosal side VERY negative due to HIGH Cl-)
  5. Gastric mucosal barrier
110
Q

How are Cl- and H+ ions transported across lumenal membrane relative to concentration and electrical charge?

A 
Cl-= against both 
H+= With Electrical Against Concentration
111
Q

What products breakdown the the Gastric mucosal barrier?

A 
Aspirin= turns to acid and overwhelms the buffers
ETOH= toxic to the cells
112
Q

What are the measured affects of Loss of Gastric mucosal barrier?

A
  1. Loss of H+–> leaks back into damaged cells
  2. HyperK+ due to damaged cells releasing it into lumen
  3. Increased Na+
113
Q

What are the ion vs flow rate affects in the Stomach?

A

1 Increased Flow= Increased H+ & Increased K+

Decreased Na+ & level Cl-

114
Q

What are the blood findings in a person with Chronic vomiting?

A

Metabolic Alkalosis

HYPOKalemia

115
Q

What are the lab findings in a person with Chronic Diarrhea?

A

Metabolic Acidosis

116
Q

What is the makeup of secretion in a NON-oxyntic fluid secretion? non stimulated stomach

A

Isotonic Fluid= NaCl + HCO3 + K+

117
Q

What is the makeup of Oxyntic fluid secretion in a stimulated stomach?

A

HCl + K+

118
Q

What are the receptors located on Parietal cells that trigger HCl release?

A

ACh + Gastrin–> PL-C/ IP3

Histamine–> cAMP

119
Q

What are the ways that Gastrin increases HCl release from Parietal cells?

A

Direct-> Bind IP3/ Ca receptor

Indirect= Binds ECL cells and stimulates Histamine production and release

120
Q

What is the relationship btwn Gastrin and histamine in response to HCl release?

A

Potentiation-> Both together increase HCl release higher than the sum of individual stimulation

** Histamine Potentiates ACh as well

121
Q

Normal diurnal basal gastric secretion shows that highest when?

A

Midnight= GERD worst around that time

122
Q

30% of Gastrin secretion is during the Cephalic phase (Vagus). The Amount of acid secreted is affected by what?

A

Self-selected preference for the foods LIKED= More Acid secretion

123
Q

What are the triggers for the Cephalic phase of Gastrin secretion?

A 
Smell|
Taste
Chewing
Swallowing
Hypoglycemia 
**ALL potentiated by VAGUS
124
Q

How does Vagus potentiates Cephalic gastrin release?

A

Direct ACh to Parietal cells

GRP directed to G cell to release Gastrin= Increases HCl release from parietal cells

125
Q

What are the effects of Dilatation/ distention of stomach?

A

HCl release via 3 mechanisms:

1: short intramural reflex= ACh= stimulate parietal
2: Vago-vagal= direct ACh
3: Vago-vagal= GRP/ Gastrin

126
Q

What are the mechanisms for Gastrin release?

A 
Vagus= ACh -> GRP-> Gastrin release 
Vagus= ACh> inhibits Somatostatin 
Distention= ACh-> Gastrin release
127
Q

How does Protein meal affect Somatostatin release?

A

Proteins neutralize pH= Inhibiting the stimulatory actions of LOW pH on SS release

128
Q

What is the majority of the pancreas made up of?

A 
90%= Exocrine (HCO3 + enzymes)
2%= Endocrine (Islets of Langerhaan)
129
Q

DIscuss the enzyme and aqueous secretions of the Exocrine pancreas?

A

Acinar cells= secrete Enzymes
Centroacinar = secrete aqueous (HCO3)
Ductal cells= Modify Aqueous secretion

130
Q

Exocrine pancreas enzymes are synthesized where and secreted due to what?

A

synthesized-> RER

Stimuli= PSNS + CCK

131
Q

What are the Carbohydrate digesting enzymes and where are they synthesized?

A

Salivary gland= Amylase

Pancreas= Amylase

Intestinal mucosa= Sucrase + Maltase + Lactase + Trehalase + alpha Dextrinase

132
Q

What are the protein digestive enzymes and where are they synthesized?

A

Stomach= Pepsin

Pancreas= Trypsin + Chymotrypsin + Carboxypeptidase + Elastase

Intestinal mucose= Amino-oligopeptidase, Dipeptidase + Enterokinase

133
Q

What are the Lipid digestive enzymes and where are they synthesized?

A

Saliva= Lingual lipase

Pancreas= Lipase, Phospholipase A2, Cholesterol ester hydrolase

134
Q

What is the net result of pancreatic secretion?

A

HCO3 into Pancreatic ductal juice

Net absorption of H+ in venous blood

135
Q

What happens to the content of pancreatic juice when the rate of secretion in Increased?

A

K + Na = Constant
HCO3 = Increases -> levels off
Cl-= Decreases -> levels off

136
Q

How does Increased Salivary flow alter the content of Saliva?

A 
K+ = Constant
Na+ = Increases Dramatically
Cl- = Increases steadily
HCO3 = Increases and then Levels off
137
Q

What is the explanation for the affect of Rate of flow on Pancreatic juice content?

A

Basal flow (slow) = Isotonic NaCl + H2O solution

Stimulated Flow= activates centroacinar and ductal cells to Increase HCO3 and decrease Cl
HCO3 Na + H2O

138
Q

What activates the release of Aqueous and enzymatic pancreatic secretions?

A

Aqueous= H+ in the Duodenum
Enzymatic= Digestive products in duodenum
(proteins,AA, FA)

139
Q

Describe the 3 phases of Pancreatic juice secretion?

A
  1. Cephalic= smell, taste, conditioning-> Vagus
    * Enzymes ONLY
  2. Gastric= Distention–> Vagus
    * *Enzymes ONLY
  3. Intestinal= CCK + ACh + Secretins
    * *80% Both enzymatic + aqueous
140
Q

What is the stimulus for the secretion of Enzymes from the Acinar cells in the Pancreas?

A

CCK-A + ACh receptors

I cells in Duodenum= secrete CCK in presence of AA, peptides, FA-

ACh from Vago-vagal reflex directly acts on Acinar cells

141
Q

Most important Amino acids in relation to CCK secretion are?

A

Tryptophan
Methionine
Phenylalanine

142
Q

What are the stimuli for the secretion of Aqueous solution from the Ductal cells?

A

CCK + ACh + Secretins

143
Q

What part of the GI is involved in Enterohepatic circulation of bile salts?

A

Ileum

144
Q

What is the composition of bile?

A 
50% Bile salts
40% phospholipids
4% cholesterol
2% bilirubin 
H2O + NaCl
145
Q

What are the primary & secondary bile acids?

A

Primary= hepatocyte synthesized–> cholic acid + chenodeoxycholic acid

Secondary= dehydroxylated primaries by intestinal bacteria–> deoxycholic + lithocholic acids

146
Q

What two amino acids are conjugated by the liver to form bile acids?

A

Taurine

Glycine

147
Q

What is the role of bile salts and what property allows them to do that?

A

Emulsify lipids= Amphipathic properties

  • *Form Micelles
  • Phospholipids are also amphipathic
148
Q

Yellow colored byproduct of Hemoglobin metabolism?

A

Bilirubin

149
Q

Describe the process from hemoglobin breakdown to urobilinogen in Urine and feces (Sterobilin)?

A

Hemoglobin degraded by RE cells (spleen)
Deconjugated Bilirubin circulates bound to Albumin
Liver extracts + conjugates with Glucuronide
“Direct” conjugated bilirubin enters BILE
Intestinal bacteria convert it into Urobilinogen
Gives Feces and Urine its color

150
Q

What is the mechanism for Carbohydrate absorption?

A

Mechanism: Na/Glucose cotransport
Na/galactose cotransport
Facilitated diffusion

151
Q

What is the mechanism of protein absorption?

A

Mechanism: Na/amino acid cotransport
H+ dipeptide cotransport
H+ tripeptide contransport

152
Q

What is the mechanism of Lipid absorption?

A

Bile salts form micelles in the small intestines
Diffusion of FA + monoglycerides and cholesterol into intestinal cells
Reesterification in the cell to Triglycerides and phospholipids
Chylomicrons form in the cell (apoprotein 100) and transferred to LYMPH

153
Q

What is the mechanism of Fat & water soluble vitamin absorption?

A
  1. Micelles form with bile salts and products of lipids
    DIffusion into intestinal cells
  2. Na+ dependent cotransport
154
Q

Where and what is the mechanism for absorption of?

  1. B12
  2. Bile salts
  3. Ca++
  4. Fe++
A
  1. Ileum–> Intrinsic Factor
  2. Ileum–> Na/ bile cotransport
  3. small intestine–> vitamin D dependent binding
  4. small intestine-> binds apoferritin in cell then BINDS transferrin in Blood
155
Q

What are the only carbs absorbed in the GI system?

A

Monosaccharides–> Glucose, galactose, fructose

156
Q

Describe the digestion of starch from mouth to absorption?

A

Mouth-> salivary amylase-> dectivated in stomach

Pancreatic amylase cleaves 1,4 glycosidic bonds
yielding dextrins, maltose, or maltotriose

These disaccharides are broken into Glucose which is absorbed

157
Q

What is the mechanism of Glucose, fructose, and galactose absorption?

A

Glucose + galactose= Na+ cotransport (SGLT 1)

Fructose= GLUT 5 facilitated diffusion

158
Q

What is lactose intolerance?

A

Lactase deficiency= Brush boarder enzyme

**Causes Osmotic diarrhea because Lactose is not broken down and absorbed

159
Q

What are the two classes of proteases?

A 
Endopeptidases= hydrolyze INterior peptide bond
Exopeptidases= hydrolyze one AA @ a time from C terminal side
160
Q

What are examples of endopeptidases and exopeptidases?

A 
Endo= Pepsin + Trypsin + chymotrypsin + elastase
Exopep= Carboxypeptidases A & B
161
Q

Describe the role of pepsin in protein digestion?

A

Begins the process @ Low stomach pH
Inactivated in high pH of duodenum
NOT essential to digestion

162
Q

After proteins enter duodenum, what are the next steps in digestion?

A

Trypsin activated by Enterokinase
Trypsin activates all other brush boarder enzymes
Break down proteins and absorb
Pancreatic proteases digest themselves and each other

163
Q

In what form are proteins absorbed?

A

AA + Dipeptides + tripeptides

164
Q

What is the mechanism of absorption for L- amino acids and dipeptides/ tripeptides?

A 
L-AA= Na+ cotransport 
Di/tripeptides= H+ cotransport
165
Q

The absence of what enzymes affects all other pancreatic enzymes and Drastically affects protein absorption?

A

TRYPSIN

166
Q

Genetic disorder in which cotransporters for Dibasic amino acids cystine, lysine, arginine, ornithine is absent in both small intestines and kidneys?

A

Cystinuria

167
Q

What is the function of the stomach in lipid absorption?

A

Initiates enzymatic digestion by mixing, increasing SA, and hydrolyzing using Lingual and gastric Lipases

  • *slowly empties Lipids into Duodenum so it can ALL properly come in contact with BILE
  • *CCK slows gastric emptying for this reason
168
Q

What is the role of the small intestines in lipid digestion?

A

Pancreatic lipase= hydrolyzes TGs into MAG+2FAs

**Inactivated by Bile salts thus NEEDS Colipase to maintain activity

169
Q

Explain the absorption of lipids digestion products cholesterol, monoglycerides, lysolecthin, and FFA?

A

All are bound to Micelles–> diffuse TO brush-boarder-> Lipids are released and diffuse into cell-> Most lipids absorbed by midJejunum.

**Micelles DO NOT enter cell

170
Q

What happens to the lipid digestive products once they enter intestinal cells?

A

They are RE-esterified with FFA and packed into CHYLOMICRONS

171
Q

What is a chylomicron composed of?

A

TGs
Cholesterol
Core of Phospholipids
Apoprotein B 48

172
Q

What is the fate of chylomicrons?

A

They are Exocytosed into Lymphatics as Lacteals

173
Q

What are the affects of ileal resection?

A

Pernicious anemia

Steatorrhea–> No enterohepatic circulation of Bile salts so Bile storage is depleted

174
Q

Decreased intestinal absorption due to decreased in intestinal cells and reduced microvillar surface area?

A

Tropical sprue

175
Q

What are the water-soluble vitamins and mechanism of absorption?

A

Vitamins B1, B2, B6, biotin, folic acid, nicotinic acid, and pantothenic acid–> Na dependent cotransport in small intestines
**Except for Cobalamin (B12)

176
Q

Describe the absorption of Vitamin B12 (cobalamin)?

A
  1. released from food by Pepsin
  2. Free B12 binds R protein from Saliva
  3. Pancreatic proteases degrade R protein
  4. B12 then binds Intrinsic factor
  5. B12+ IF resistant to pancreatic proteases
  6. Ileum absorption via special transporter
177
Q

Describe the absorption of Fe++ (iron)?

A
  1. Absorbed as either Free iron or heme iron
  2. Digested by lysosomal enzymes inside intestinal cells
  3. Binds Apoferritin and transports across basolateral membrane into blood.
  4. Binds Transferrin during circulation
178
Q

Paracellular movement of H2O and electrolytes is possible at what part of the GI?

A

Small intestines= Leaky tight junctions= paracellular movement possible
COLON= “Tight” tight junctions= no PC movement

179
Q

Neonate with failure to pass meconium in the immediate postnatal period followed by obstructive constipation. Dx?

A

Hirschsprung Disease= Congenital Aganglionic Megacolon

180
Q

What is the pathogenesis of Hirschsprung disease?

A

Failure of Neural crest cells to migrate and produce the Meissner submucosal plexus and Auerbach myenteric plexus
**Tyrosine kinase RET mutation in familial form

181
Q

What is the difference btwn mucosal infaction and mural infarction?

A 
Mucosal= NO deeper than muscularis mucosa 
Mural= Mucosa and submucosa 
Transmural= all three layers
182
Q

What are the causes of mucosa, mural, and transmural infarctions?

A

Mucosal + mural= acute/chronic hypo perfusion

Transmural= Acute vascular obstruction

183
Q

What are some common causes of acute arterial obstruction?

A 
Atherosclerosis 
Aortic aneurysm
Hypercoagulable states
Oral contraceptives
Embolization of cardiac vegetation
184
Q

Intestinal hypoperfusion can be associated with what causes?

A

cardiac failure
Shock
dehydration
vasoconstrictive drugs

185
Q

What are the variables that determine the severity of ischemic bowel disease?

A

Severity of vascular compromise
Time frame
Vessel affected

186
Q

What areas of the GI system are particularly susceptible to ischemia?

A

Watershed zones= Splenic flexure

Sigmoid colon

187
Q

What causes GI surface epithelial atrophy and necrosis with consequent sloughing BUT normal or hyperproliferative crypts?

A

Ischemic intestinal disease= Crypts have majority of blood supply because they house the regenerative cells

188
Q

Older patient with history of cardiac and vascular disease with sudden onset severe abdominal pain and tenderness, N/V, bloody diarrhea?

A

Ischemic Bowel disease

189
Q

What viral infection can cause ischemic GI disease as a consequence of tropism and infection of endothelial cells?

A

CMV

190
Q

Most common acquired GI emergency of neonates, particularly prematures and low birth weights often beginning with Oral feeding?

A

Necrotizing enterocolitis

191
Q

Malformation of submucosa and mucosal blood vessels in cecum of Right colon presenting @ 6th decade with Lower intestinal bleeding, hemorrhage?

A

Angiodysplasia

192
Q

Thin walled dilated submucosal vessels that protrude beneath anal or rectal mucosa above the anorectal (pectinate) line?

A

Internal hemorrhoids

193
Q

Passing of Isotonic stool that persists during Fasting?

A

Secretory diarrhea

**Osmotic ceases with fasting

194
Q

Excess stool caused by inadequate nutrient absorption with Steatorrhea and relieved by Fasting?

A

Malabsorptive diarrhea

195
Q

What are the four phases of nutrient absorption?

A
  1. intraluminal digestion=breaking down to absorbable size
  2. Terminal digestion= hydrolysis by enzymes @ the brush boarder of intestinal mucosa
  3. Transepithelial transport
  4. Lymphatic transport of Lipids
196
Q

What are the signs and symptoms of malabsorption?

A

Diarrhea
flatus
abdominal pain
weight loss

197
Q

What is the cause of Cystic fibrosis malabsorption?

A

Mutated CFTR (Cl- channel) interferes with HCO3, Na, H2O secretion= causes thickened secretion

  • *Meconium Ileus newborn
  • *Pancreatic insufficiency in adults
198
Q

Autoimmune mediated enteropathy triggered by the ingestion of gluten-containing foods?

A

Celiac disease

199
Q

Biopsy of Duodenum mucosa shows Increased numbers of intraepithelial CD8+ T cells with intraepithelial lymphocytosis, crypt hyperplasia and VIllous atrophy?

A 
Celiac disease (Gluten sensitive enteropathy)
**Often affects Duodenum heavily due to high gluten exposure
200
Q

Pt 30-60 yo with Iron deficiency anemia, diarrhea, bloating, and fatigue. GI biopsy shows lymphocytosis and villous atrophy?

A

Celiac disease

201
Q

Children btwn 6-24 mo presenting with irritability, abdominal pain, distention, anorexia, diarrhea, failure to thrive, weight loss, and muscle wasting with Characteristic Pruritic skin blisters?

A

Pediatric Celiac disease = Dermatitis Herpetiformis

202
Q

What is the differential for a celiac disease pt On Strict Gluten FREE diet with sudden onset of abdominal pain, diarrhea, and weight loss?

A

High RISK for:
Enteropathy associated Tcell Lymphoma
Intestinal Adenocarcinoma
Refractory sprue (no longer responding to Diet)

203
Q

syndrome of stunted growth and impaired intestinal function that is common in developing countries?

A

Environmental Sprue (tropical)

204
Q

Pt with recent enteric viral or bacterial inception presents with explosive diarrhea with watery, frothy stools and abdominal distention?

A

Acquired Lactose deficiency

205
Q

Mutation in the microsomal triglyceride transfer protein rendering the enterocytes unable to to export lipoproteins and FFA?

A

Abetalipoproteinemia = Spur cells in peripheral blood

206
Q

Chronic and relapsing abdominal pain, bloating, changes in bowel habits including diarrhea and constipation?

A

IBS (irritable bowel syndrome)

207
Q

Middle-aged women with chronic watery diarrhea, grossly normal intestines BUT presence of dense subepithelial collagen layer, increased numbers of intraepithelial lymphocytes, and mixed inflammatory infiltrates within lamina proria?

A

Collagenous colitis

**lymphocytic colitis= same without Thickened collagen layer

GI block (6 decks)

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