Week 1 Flashcards

1
Q

What is the first line of defense in GI tract against pathogens?

A

Mucosa which contains antibodies against pathogens

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2
Q

Ratio of GI immune cells vs Body

A

GI & Body immune cells have equal numbers showing how significant immunity for GI is

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3
Q

Histamine effect on GI

A

Stimulates Motility & Secretion

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4
Q

Further GI defense lines

A

1) GALT (waldeyer’s ring)
2) Inflammatory mediators (cytokines/histamine)
3) Host microbe interactions (flora)

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5
Q

2 Types of GI afferent neurons

A
  • Intrinsic afferent (to inter n.)
  • Visceral afferent (from organs)
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6
Q

GI sympathetic DIRECT innervation

A
  • Vasoconstriction (a1-R)
  • SM of GI (B2-R)
  • Sphincter constriction (a1-R)
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7
Q

GI sympathetic INDIRECT innervation

A

Decreased motility and secretion
(a2-R)

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8
Q

G-cell

A

Gastrin
(Acid secretion)

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9
Q

I-cell

A

Cholecyctokinin (CCK)
(pancreas secretion & gallbladder emptying)

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10
Q

S-cell

A

Secretin
(pancreas & bile secretion)
Low pH in duo. stims this

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11
Q

L-cell

A
  • Proglucagon
  • GLP-1/2
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12
Q

GIP-cell

A

Gastric inhibitory peptide (GIP)
Oral glucose stims this
(inh. gastric emptying)
(K-cells)

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13
Q

P/D1-cell

A

ghrelin
(hunger / food intake)

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14
Q

D-cell

A

Somatostatin
(generally inhibitory)

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15
Q

F-cell

A

Pancreatic Polypeptide (PP)

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16
Q

M-cell

A

Motilin

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17
Q

EC-cell

A

Serotonin (enterochromaffin/EC cells)

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18
Q

ECL-cell

A

Histamine (enterochromaffin-like cell)
(motility & secretion stim.)

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19
Q

Hormones made in the GI but act somewhere else

A
  • CCK
  • Ghrelin
  • Gastrin
  • Secretin
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20
Q

Hormones made somewhere else & act on GI

A
  • Aldosterone
  • PTH
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21
Q

What % of the body’s immune cells are in the GI-tract

A

80%

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22
Q

Sympathetic regulation of GI

A
  • a1 causes contraction of SM sphincters
  • a2/B2 cause SM wall relaxation
  • a1 Vasoconstriction of splanchnic circulation
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22
Q

3 GI control mechanisms

A
  • Neural
  • Paracrine
  • Endocrine
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23
Q

What cells in GI secrete hormones

A

Enteroendocrine cells

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24
Q

What are the wave-like movements in GI

A
  • Not APs
  • Originate from interstitial cells of Cajal
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25
Q

Where are Cajal cells found & their function

A

Myenteric / Submucosal Plexus
Origin of the slow-wave movement of GI
(GI-tract pacemaker)

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26
Q

Phases of Swallowing

A

1) Oral phase (voluntary)
2) Pharyngeal phase (in-v)
3) Esophageal phase (in-v)

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27
Q

Upper Esophageal Sphincter (UES)

A
  • Striated muscle
  • Voluntary
  • Relaxed by Bolus detection
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28
Q

Lower Esophageal Sphincter (LES)

A
  • Smooth Muscle
  • Involuntary
  • Vagovagal reflex
  • Relaxed by NO
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29
Q

Retropulsion

A

Pushback of Chyme from pylorus due to small opening and slow-waves of stomach

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30
Q

Movements in Small Intestine

A
  • Segmentation (mixing)
  • Peristalsis (propulsion)
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31
Q

How long does it take for food to go from Pylorus to Ileocecal valve?

A

3 to 5 hours

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32
Q

What promotes / inhibits Peristalsis of small intestine?

A

+ : Gastrin, CCK, Insulin, Serotonin
- : Secretin, Glucagon

33
Q

How does Peristalsis in Small intestine start?

A

Enterochromaffin (EC) cells detect bolus in mucosa and release Serotonin
= Activation of Peristalsis

34
Q

What happens in Proximal colon

A

Anti-peristalsis

35
Q

What induces opening of Ileocecal valve?

A
  • Gastrin
  • Gastroileal reflex
36
Q

Daily Salivary secretion

A

800 - 1500 mL / day (pH 7)
(90% during meals)

37
Q

Saliva composition

A
  • H2O
  • Electrolytes
  • Salivary Amylase
  • Lingual Lipase
  • IgA
  • Lysozyme
  • Mucin
38
Q

Salivary secretion Pathway

A

1) Intralobular Intercalated
2) Intralobular Striated
3) Interlobular ducts
4) Interlobular excretory d.
5) Main excretory d.

39
Q

Parotid Gland is mostly…

40
Q

Sublingual Gland is mostly…

41
Q

Submandibular Gland is mostly…

42
Q

Intrinsic Salivary Glands

A
  • Buccal
  • Labial
  • Palatine
    (constant mucous secretion)
43
Q

Parasympathetic Effect on Saliva Secretion

A
  • VIP (vessels): Gs, Vasodilation
  • ACh (acini): M3-ACh-R (Gq), Ca2+ signal, Constriction & Exocytosis
44
Q

Sympathetic Effect on Saliva Secretion

A

NE mediated
- B2-AR, Mucin secretion, Viscous
- a1-AR, Vasoconstriction, less secretion

45
Q

Daily Gastric Secretion

A

1 - 1.5 L /day

46
Q

What is essential for Vitamin B12 absorption

A

Intrinsic factor secreted in gastric juice (parietal cells)

47
Q

Gastric Parietal Cells secrete

A
  • HCl
  • Intrinsic factor
48
Q

Gastric Chief Cells

A

Pepsinogen

49
Q

Omeprazol

A

Inhibits the H+/K+ ATPase in Parietal cell acid secretion

50
Q

What does prolonged vomiting cause?

A

Metabolic Alkalosis
Stomach acidity needs to be replenished, so HCO3/Cl exchanger works more, pumping more HCO3 bicarbonate into the blood

51
Q

Regulators of Parietal cells

A
  • Gastrin from G-cells (main)
  • Histamine (paracrine)
  • ACh (neural)
52
Q

What can activate G-cells?

A
  • ACh
  • GRP (gastrin releasing peptide)
  • Wall tension
  • Alcohol
  • H.Pylori = ulcers
  • NE on B2-AR
53
Q

What Inhibits G-cells?

A
  • Somatostatin
  • Prostaglandins
54
Q

ECL-cells effect on gastric acid

A
  • Activated by PARA or Gastrin
  • Release Histamine which stimulates parietal cell secretion
55
Q

Gastric acid secretion Cephalic phase

A
  • Smell & Taste of food
  • Vagal N stim. GA secretion
56
Q

Gastric acid secretion phases

A
  • Cephalic phase
  • Gastric phase
57
Q

Vagovagal Reflex

A
  • Activated by presence of food in stomach
  • By wall-distension taken by vagal N efferents
58
Q

Feedback reg. of GA secretion

A

When low pH is sensed in antrum & pylorus, somatostatin is released from D-cells

59
Q

Basal G.acid output (BAO)

A

1.5 - 2.5 mmol H+/hour

60
Q

Peak G.acid output (PAO)

A
  • F: 25 mmol H+/hour
  • M: 35 mmol H+/hour
61
Q

What stimulates Pepsinogen secretion?

A
  • Gastrin (Gq)
  • ACh (M3) via ENS
  • Histamine (Gs)
  • Secretin
62
Q

Daily secretion of Small intestine

A

1.5 - 2 L / day

63
Q

What does Diarrhea cause?

A

Metabolic Acidosis
Continuous fluid produced in small intestines which is high in HCO3, so it is lost from blood causing lower pH

64
Q

PARA effects on Large intestine

A

VIP (Gs) stimulates cAMP signal, causes translocation of CFTR channels.
= Effects of Cholera toxin making more watery diarrhea

65
Q

Paracrine mediators of Large intestine

A

Local immune system activated by Serotonin production so Diarrhea happens to wash-out any harmful material

66
Q

Pancreatic secretion percentages

A
  • 98% exocrine to intestine
  • 2% endocrine to blood
67
Q

Daily Pancreas secretion

A

700 - 900 ml / Day

68
Q

Fat-Soluble vitamins

69
Q

Daily Bile production

A

200 - 1200 ml / Day

70
Q

What makes Bile acids more water soluble

A

Conjugation with:
- Glycine
- Taurine

71
Q

2 Pathways for entry of solutes into Bile

A
  • Active Secretion (trans.c)
  • Passive permeation (para.c)
72
Q

Bile acid-dependent flow

A
  • Hepatocytes pump bile acids into canaliculi
  • Pulls water with it creating a flow
  • Gradient maintained by Na+
73
Q

Bile acid-independent flow

A
  • Carbonic anhydrase in Hepatocytes forms bicarbonate
  • HCO3 to canaliculi using Cl exchanger
  • Pulls water creating flow
74
Q

How is Bilirubin removed

A

Conjugated with Glucuronic acid in Hepatocytes to make it water-soluble
- Goes to canaliculi
- Converted to Urobilinogen & Stercobilin (color)
- Excreted via feces & urine

75
Q

Fate of bile produced by Hepatocytes

A
  • 450ml as Hepatic Bile to intestines
  • 450ml stored in Gallbladder
76
Q

Daily production of Bile acids in Liver

A

0.6 g / Day

77
Q

Entire pool of Bile acids in the body

78
Q

Total Bile acid usage per day

A

20g Bile acid / Day

79
Q

Enterohepatic Circulation of Bile

A

Where one bile acid molecule is used several times

80
Q

Loss of Bile acids + Salts

A

0.6 g / Day
Equal to what is produced

81
Q

Neurohormonal control of Gallbladder Contraction

A
  • NO + VIP relax sphincter of Oddi
  • ACh SM contraction of gallbladder
  • CCK Enhances effects