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Physiology > Exam3Lec10GI:ExoPancreas,Liver/Gallbladder,LI > Flashcards

Exam3Lec10GI:ExoPancreas,Liver/Gallbladder,LI Flashcards

1
Q

Summary review of regulation of pancreatic secretion, fill in blanks

A
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2
Q

Which peptide enhances insulin secretion?

A

Oral Glucose-Stimulated Insulinotrophic Peptide

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3
Q

What stimulates GIP release at a larger magnitude? Intravenous glucose or oral glucose

GIP (gastrin inhibitor of peptide) aka K cells

A

Oral glucose

has less of a glycemic response (b/c releasing more insulin)

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4
Q

Does IV glucose stimulate GIP release?

A

No bc its not directly in the dudodenum but in BV, it bypasses the GI tract

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5
Q

How much enzymes are produced and secreted by the exocrine pancreas throughout lifee?

A

Excess, altough production decreases progressively as we age (~30-50 decrease @ ge 75 years)

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6
Q

When do nutrition problems arise?

A
  • If production of pancreatic enzyme falls by as little as 10%
  • Outflow of pancreatic juice is obstructed (ex. sphincter of oddi obstructed)

you get malabsoprtion, you arent digesting protein, faits, and carbohydrates

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7
Q

Review: List the sphincters that are present in the Gastrointenstinal Tract

A
  • Upper and lower esophageal sphincters
  • Pylorus
  • Sphincter of Oddi
  • Internal and external anal sphincter
  • Illeocecal valve

Know location and function

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8
Q

Which ducts drain to the Duodenum (in duodenal papilla)?

A

Common bile duct and Pancreatic Duct

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9
Q

What are the 8 major pancreatic enzymes?

A
  • Trypsin , Chymotrypsin, Elastase
  • Carboxypeptidase
  • Lipase
  • Amylase
  • Ribonuclease , Deoxyribonuclease
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10
Q

Enzymes: Trypsin, Chymotrypsin, & Elastase, what is the

  • Substrate
  • Action
A
  • Substrate: Proteins
  • Action: Breaks peptide bonds in proteins to form peptide fragments
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11
Q

Enzyme: Carboxypeptide, what is the

  • Substrate
  • Action
A
  • Substrate: Proteins
  • Action: Splits off terminal amino acid from carboxyl end of protein
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12
Q

Enzyme: Lipase, what is the

  • Substrate
  • Action
A
  • Substrate: Fats
  • Action: Splits off two fatty acids from triacylgcerols, forming free fatty acids and monoglycerides
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13
Q

Enzyme: Amylase, what is the
* Substrate
* Action

A
  • Substrate: Polysaccharides
  • Splits polysaccharieds into glucose and maltose
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14
Q

Enzyme: Ribonuclease, Deoxyribonuclease, what is the

  • Substrate
  • Action
A
  • Substrate: Nucleic Acids
  • Action: Splits muclei acids into free mononucleotides
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15
Q

The Exocrine Pancreas is a two-stage model utilizing _________ and ________.

A

Acinar cells; Ductal cells

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16
Q

List the cell types that play a part in pancreatic acinar cell regualtion and explain their functions

A
  1. Vasointestinal peptide (VIP) and Secretin
  • Both regulate the activation of cAMP
  1. GRP, ACh, CCK
  • All regulate the presence of intracelluar [Ca2+]

Both cAMP & Ca2+ play a role in the phosphorylation of structural and regulatory proteins→Fusion of granules w/ apical membrane and discharge of contents

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17
Q

Exocrine pancreas pancreatic acinar cell is under tight ____ regulation

A

hormonal

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18
Q

What cell dectects low pH in the duodenum?

HIGH yield

A

Acid sensing S-cells (aka ductal cells)

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19
Q

What hormone is stimulated pancreatic duct and what does it secrete when S-cells detect low pH?

S-cells: Ductal cells

HIGH yield

A

Secretin is stimulated and it secretes HCO3- to raise duodenum pH

Overall goal: ↑ pH of environment so that enzymes can fucntion properly

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20
Q

Secretin receptors are ____ expresed on ____

HIGH yield

A

Densely, Pancreatic Ductular Cells in Humans

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21
Q

What action(s) liberate free fatty acids?

A

Gastric mixing and triglyceride digestion by gastric lipase enzyme

Gastric lipase ↑ liberation of TAG

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22
Q

What are fatty acids a potent stimulate for?

A

CCK release

after gastric mixing and trig digestion, you get an emulsion of monoglycerodes and FFA activing CCK release in duod

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23
Q

Which cells in the duodenum releases CCK and how is it activated?

A
  • I-cells
  • Free fatty acids(high protein or high carb meal)
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24
Q

What are the roles of CCK?

A
  • Relaxes Stomach
  • Can influence eating behavior (satiating effect)

Satiation: Process that causes on to stop eating

25
Q

How much of TAGs are digested in the stomach?

TAG: Triglycerides

A

Approx. 10%

26
Q

Which enzymes are required for the activation of some pancreatic digestive enzymes?

HIGH yield

A
  • Brush Border Entrokinase (aka. Entropeptidase)
  • Luminal Tyrsin

trypsin willl turn proenzymes into their enzymatic form

27
Q

What does CCK stimulate and by which methods?

A
  • Stimulates Gallbladder contraction & Sphincter of Oddi Relaxation
  • Neural and Humoral Pathways
28
Q

The sphincter of Oddi is ____ by the hormone ____ via ____

HIGH yield

A

The sphincter of Oddi is relaxed by the hormone cholecystokinin (CCK) via vasoactive intestinal peptide (VIP)

29
Q

CCK stimulates pancreatic enzyme secretion by what pathway(s)?

A

Neural and hormonal

30
Q

What materials are entering the large intestine (colon) via what structure?

HIGH yield

A
  • Entry of undigestible/unabsorbed material through the ileocecal sphincter

Unabsorbed material= soluble (ex. pectin)/unsoluble (ex.cellulose) fibers

31
Q

What the the Colon (LI) a final site for?

HIGH yield

A
  • FInal site for absorption of water and ions (many under hormonal control)
32
Q

What happens to undigested nutrients (fibers) in the colon?

HIGH yield

A

Are metabolized by intestinal flora(bacteria) and converted to short chain fatty acids (SCFAs), neurotransmitters (ex. 5HT-3, dopamine) and vitamins (VIT K)

Fiber→colonic bacteria→SCFAs→feed colonocytes

33
Q

What triggers Peptide YY production and release in the Colon?

YY=tyrosine-tyrosine

A

Protein and Fat

Also in Ileum before food reaches circulation

34
Q

Fat in ileum and colon release peptide YY does what?

A

It inhibits meal-stimulated GI functions

slows dig and transit rate so we can absorb food better

35
Q

How does the release of PYY inhibit meal stimulated GI fxns?

A
  • ↓ Gastric acid secretion
  • ↓ Gastric emptying
  • ↓ Pancreatic secretion
  • ↓ decreased transit rate
  • ↓ Colonic motility

PYY has very strong anti appetite effet

36
Q

List the parts of the Colon

A
  • Terminal Ileum
  • Ileocecal valve
  • Cecum
  • Ascending colon (site of most colon cancers)
  • Transverse colon
  • Descending colon (↑ [microbome])
  • Sigmoid colon
  • Rectum

70% of gut microbiome is in DC

37
Q

What is the main difference in the right and left colon and why?

A

Function and Slow Wave Propagation differ to help ↑ H2O and electrolyes reabsorption

38
Q

What is the function of the right and left colon?

A
  • Right colon: Absorption of water and electrolytes
  • Left colon: Formation and storage of feces

note diff direction of right, its compacts food in a way that optimizes H20 and electrolyte absorption

39
Q

What are the three contraction pattern displayed by the colon?

A
  1. Mixing Movements
  2. Haustral Migration
  3. Mass Movement
40
Q

Explain the three contraction patterns

  • Mixing Movements
  • Haustral Migration
  • Mass Movements
A
  • Mixing Movements: Strong contraction of circular muscles to ↑ SA→to help main absorption
  • Haustral Migration: Back and forth contraction to ↑ H2O extraction
  • Mass Movements: Stimulated by eating, laxatives, exercise by enteric NS to ↑ contraction
41
Q

What occurs with sympathetic nerve stimulation in the colon?

A

Sympathetic nerve stimulation decreases spike frequency and inhibits colonic contractions

decr AP that is responsible for muscle contraction

42
Q

What are Interstital Cells of Cajal (ICC)?

A
  • “Pacemakers” and generate slow waves
  • aka: BER; basal electrical rhythm
43
Q

How is the colonic response to a meal initated?

A

By signals from the stomach, intestines and brain

Gastrocolonic Reflex: neural and hormonal controlled and contributes to defacation

44
Q

What role does Aldosterone play in the colon?

HIGH yield

A
  • Promotes expression of transporters required for sodium absorption
  • Water follows sodium concentration

absoprtion of H20 and water

sodium intake (diet) alter amt of aldoosterone

45
Q

List the main functions of SCFAs from gut microbiome (5)

SCFAs= Short Chain Fatty Acids

HIGH yield

A
  • Main fuel for coloncytes
  • Tumor supressor effect
  • Crosesses Blood Brain Barrier (BBB)
  • HDAC activity
  • Downregulates VEGF and has other epigentic effects
46
Q

What enhances the production of SCFAs?

A

Prebiotics and Probiotics fibers that influence colonic bacteria

47
Q

What mediates the transport of SCFA in the gut?

HIGH yield

A

Sodium coupled monocarboxylate transporters (SMCT1)

SCFA is absrorbed into circ by SMCT1 (which is coupled with Na+)

48
Q

What are the different causes of constipation?

A
  • Usually d/t diet
  • Drugs
  • Diseases
49
Q

List the dietary aspects that cause constipation (3)

HIGH yield

A
  • Not enough dietary fiber
  • High Calcium + Diary
  • Dehydration
50
Q

List the drugs the cause constipation (2)

A
  • Opiates
  • Calcium antacids

can decr gastric motillity

51
Q

List the diseases that cause constipation (5)

A
  • Irritable Bowel Disease
  • Hirchsprung’s Disease: lack of ENS in distal colon
  • Physiological Stress
  • Hypothyroid
  • GI cancers
52
Q

List the causes of Diarrhea (5)

A
  • Viral, bacterial, or parasitic infection in the colon (most common). Drugs too (Antibiotics, PPIs, Chemo, etc)
  • Inflammatory bowel syndrome/Crohn’s disease
  • Food intolerances: Wheat and diary products, sugar
  • Ischemic bowel disease (older individuals)
  • Colon

NOTE: Diarrhea kills more children than malaria, measles, and AIDs combined

53
Q

List the four types of Diarrhea (4)

HIGH yield

A
  • Secretory diarrhea: e.g. Cholera toxin
  • Osmotic diarrhea: maldigestion, hyperosomtic
  • Motilty-related diarrhea: vagotomy, neuropathy
  • Inflammatory: Brush border damage from infection
54
Q

What are treatments for Diarrhea?

A
  • Antimotility agents (Immodium=Loperamide)
  • Nonspecific agents (Pepto-Bismol=bismuth subsalicylate) buffer and anti-inflammatory effects

Loperamide=opioid receptor agonist that stays in stomach (works locally in the gut)

55
Q

How do you treat Traveler’s Diarrhea?

A

CDC recommends antibiotics (3 day regimen) or Pepto Bismol (8 doses over 4 hours)

56
Q

What is Gastritis (inflammatory) ?
What does it cause?
How do you treat it?

HIGH yield

A
  • Serious diarrhea combined with vomiting and retching over several hours
  • The fluid loss from the colon will cause metabolic acidosis
  • Treatment: Go to ER for anti-emetic, IV fluids, and anti-diarrheal

Anti-emetic: anti-vomiting

57
Q

What is Irritable Bowel Disease (IBD)

NOT IBS and Celiac

HIGH yield

A
  • Chronic inflammation of bowel; unknown reasons
  • Include Crohn’s Disease and Ulcerative Colitis
58
Q

List the 4 abnormalities found in IBD

HIGH yield

A
  • Inapproriate immune response to normally innocuous gut flora
  • Damage to intestinal: maldigestion/malabsorption; defects in barrier function
  • Malabsorption of bile acids in terminal ileum impacts colonic electrolyte transport, leading to diarrhea
59
Q

List the 6 abnormalities reported in Irritable Bowel Syndrome (IBS)

A
  • ↑ incidence of 3/min slow waves (↑ motility=diarrhea)
  • ↓ myoelectric response to feeding (↓ motility=constipation)
  • ↑ response to CCK and cholinergic agents (↑ pancreatic secretions)
  • ↓ stressed-related small bowel dysmotility (slowed digestion)
  • ↓ threshold for pain caused by distension (hypersensitve b/c cytokine & chemokine receptors increase)
  • ↑ psychophsiologic scores

you can have incr ir decr in slow waves whichc an cause diahrrea or constipation
nerve pathways in enteric ns are hyperactivates b/c incr cytokine elease making nerve ending more senstitive to distensing pain

Physiology (22 decks)

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