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GIGU Exam 1 > Secretions Of The GI Tract And The Pancreas > Flashcards

Secretions Of The GI Tract And The Pancreas Flashcards

1
Q

What does saliva digest

A

Starches and lipids initially

Dilutes and buffers and lubricates food

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2
Q

What are the 3 major salivary glands

A
  1. Parotid Glands = serous cells—-> water, ions, enzymes, AMYLASE, (25%)
  2. Submaxillary Glands and Sublingual Glands = Mixed glands —-> aqueous fluid + mucin glycoproteins to lubricate (75%)
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3
Q

Structure of the salivary gland from the bottom up

A

Acinus= secrete saliva
Myoepithelial cell = motile extensions, get neural input and contact acinus to release saliva
Intercalated Duct = has same ions as plasma
Striated Duct = columnar epithelial, modify saliva and its ions(hypotonic)

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4
Q

What enzymes are in the saliva

A
  1. Amylase - starch
  2. Lingual Lipase - begin fat breakdown
  3. Kallikrein - make bradykinin to increase BF in salivary glands (vasodilator)
    Also mucus
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5
Q

How is the saliva hypotonic

A

High K+, HCO3-

Low Na+, Cl-

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6
Q

What kind of saliva is secreted by acinar cells

A

Isotonic

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7
Q

Ducal cells do

A

Absorb Na Cl back to blood

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8
Q

Which transport is on the lumen side of the duct all cells

A
  1. Na+/H+ (Na goes into cell)
  2. Cl-/HCO3- (Cl- goes into cell)
  3. H+/K+ (H+ goes into the cell)
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9
Q

Transporters on the blood vessel side of the duct all cells

A
  1. Na+/K+ (K+ into cell)

2. Cl-/HCO3-/Na+ (both Na+ and HCO3-into the cell)

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10
Q

What is higher the amount secreted or absorbed by the duct

A

The NaCl absorbed is higher then the KHCO3 secreted

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11
Q

H2O and ductal cells

A

H2O is impermeable and is not absorbed with Na Cl

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12
Q

Innervation to Salivary Glands

Parasympathetic

A 
Presynaptic N (from CN7 + CN9) 
Postsynaptic N (go to autonomic ganglia to individual glands)
*parasympathetic is dominant
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13
Q

Innervation to Salivary Glands

Sympathetic

A 
Preganglionic N (from cervical ganglion) T1-T3
Postganglionic N (go to the glands at the periarterial spaces)
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14
Q

What are the steps when I smell food, Nausea,

A

CN 7 and 9 are stimulated ——> ACh to the mAChR located on the acinar or ductal cells
——> IP3 made = increase ICF Ca+2 = AP = release and making of saliva and contraction of myoepithelial cells

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15
Q

What turns off the Parasympathetic pathway to the salivary glands

A

Dehydration, fear, sleep

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16
Q

Steps when sypathetic N is stimulated

A

T1-T3 stimulated ——> NE —-> BAR located on the Acinar or Ductal cells
—-> cAMP released = make and release Saliva and contraction of myoepithelial cells

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17
Q

What do parasympathetic and sympathetic have in common

A

They both increase salivary secretion and myoepithelial cells contraction

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18
Q

Atropine effect

A

Blocks the mAChR so ACh can’t bind, no saliva

= also potentiation of Gastrin and Histamine is blocked

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19
Q

5 components of Gastric Juice

A
  1. HCL (H+) - with pepsin for protein digestion, kills bacteria, Pepsinogen to pepsin
  2. Pepsinogen - inactive
  3. Mucus - protection, ,lubrication, with HCO3- neutralizes acid
  4. IF - Absorb B12 in the Ileum
  5. H2O - where HCL and enzymes are active, solubilize food
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20
Q

Glands in the stomach (2 types)

A 
1. OXYNTIC GLANDS
= body and fundus (proximal 80%)
= acid (Parietal Cells)
=chief cells, D- cell (somatostatin—> acid), mucus Neck cell, enterochromaffin-like cell (histamine -> acid)
2. PYLORIC GLANDS 
=antrum (distal 20%)
=Gastrin (G-cell)
=Neck cell, D-cell, mucus cells
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21
Q

What do mucus neck cells make

A

Pepsinogen, Mucus, HCO-3

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22
Q

What do chief cells make

A

Pepsinogen

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23
Q

What do parietal cells make

A

IF and HCL

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24
Q

What do G cells make

A

Gastrin into the blood

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25
Q

Where and how in HCL made in the parietal cells

A

In the villus-like membranes of the canaliculi

CO2+ H2O—> H2CO3—> H+ and HCO3-
H2O —> OH- and H+
* CARBONIC ANHYDRASE does these reactions

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26
Q

What determines the secretory rate of the stomach

A

The number of parietal cells present

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27
Q

Special thing about OXYNTIC cells

A

High mitochondria to make ATP for making a lot of acid HCL

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28
Q

Transporters present on the lumen side of the gastric parietal cells

A
  1. K+/H+ (K goes into cell)

2. Cl- follows H+ out of the cell into lumen

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29
Q

Transporters present on the blood vessel side of the gastric parietal cells

A
  1. Na+/K+ ( K into the cell)
  2. HCO3/Cl- (Cl- into the cell)
    = HCO3- absorbed (*ALKALINE TIDE)
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30
Q

Omeprazole function

A

Inhibits the K+/H+ channel on the lumen side
So H+ cant leave cell, and K+ cant go into the cell
= no HCL

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31
Q

What is gastric juice there are 2 types

A
  1. Non-Parietal = Alkaline constant flow and volume
    (Na+, Cl-) (HCO3- secreted)
  2. Parietal = hyperosmotic , after a meal
    (Cl-) (H+)
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32
Q

Which things bind to parietal cell to stimulate HCL secretion

A
  1. ACh——> M3 receptor (VAGUS), simulate IP3
  2. Gastrin ——> CCK(B) receptor (G CELLS), stimulate IP3
  3. Histamine ——> H2 receptor (ECL CELLS), stimulate cAMP
  • all go and stimulate the H+/K+ transporter
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33
Q

ACh and Gastrin also

A

Go a stimulate ECL cells to secrete Histamine

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34
Q

What inhibits the parietal cell from secreting HCL

A
  1. Somatostatin——I cAMP (D CELLS)

2. Prostaglandins ——I cAMP (protects the mucosa of GI)

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35
Q

What inhibits Gastrin release

A

HCL (negative feedback)
Somatostatin and prostaglandins
GASTRIN——> increase HCL from parietal cell + SOMATOSTATIN from D cell——I G-cells

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36
Q

Cimethidine function

A

Inhibits the H2 receptor so Histamine cant bind to it = can’t stimulate HLC secretions

= in potentiation effect : also blocked Ach and Gastrin potentiation

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37
Q

What inhibit the ECL cells

A

Somatostatin and Prostaglandins

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38
Q

Direct pathway of VagusN to secrete HCL

A

Vagus nerve goes to stomach and releases ACH on the parietal cells = HCL

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39
Q

Indirect Pathway of Vagus N on stimulating release of HCL

A

Vagus nerve comes to stomach and released GRP ——> on the G-cells = secretes Gastrin—-> BLOOD——> Parietal cell for secretin of HCL

40
Q

What other 2 things stimulate g-cells

A
  1. Dissension of the stomach —-> ACH on G -cells

2. AA —-> stimulate G-cells

41
Q

Atropine blocks what

A

Only the DIRECT vagus N pathway (only blocks mAChR)

42
Q

What are 2 effects of GRP released by indirect vagal n

A

1 G-cell stimulation

2 inhibit somatostatin

43
Q

2 things that stimulate somatostatin release

A

Gastrin and H+

44
Q

PROTIENS in the stomach stimulates

A

G-cells

45
Q

Potentiation (requires separate receptors on target cell) so two stimuli can make a double effect
Name 2

A
  1. Histamine increases effect of ACH (HCL) and Gastrin (HCL +Somatostatin)
  2. ACh increases the effect of Histamine (HCL) and Gastrin (HCL +somatostatin)
46
Q

Effect of using Atropine

A

Health defect since we have so many ACH receptors in our bodies

47
Q

Effect of using Cimetidine

A

Treat duodenal and gastric ulcers, and GERD

48
Q

Effect of using omeprazole

A

Inhibits the H+/K+ pump on lumen side

Treat ulcers (reduce H+ secretion)

49
Q

3 phases of Gastric HCL secretion

A

Phase 1 : Cephalic Phase - chewing,sight smell taste of food, make Gastrin and HCL (CNX)
Phase 2 : Gastric Phase. - DISTENTION make Gastrin,HCL and histamine, (CN X + local neural plexus reflexes)
Phase 3 : Intestinal Phase - AA cause Gastrin secretin in G-cell and GI, from hormones and neurons

50
Q

DISTENTION causes

A

Stimulation of local neural reflex to make ACH to stimulate HCL

Stimulate CN X to release GRP to stimulate G-cell - Gastrin

Stimulate CN X to release ACH on Chief cells - pepsinogen

51
Q

Cephalic Phase

A

30%of HCL secretion (chew, swallow, smell, taste)
Vagus ach ——> Parietal Cell (HCL)
Vagus grp ——> G- cell (Gastrin)

52
Q

Vagotomy

A

X INDIRECT VAGUS N and DIRECT VAGUS N

= NO CEPHALC PATHWAY

53
Q

Gastric Phase

A

60% of HCL , distention, AA + small peptides present,
Activates mechanoreceptors on OXYNTIC and PYLORIC glands
1. Directly stimulate G- cell (local neural plexus)
2. Vagus——> Direct + Indirect

54
Q

Coffee stimulation

A

Stimulates the gastric HCL secretion

55
Q

High H+ in lumen causes

A

Selection of SECRETIN (*Duodenum) into BLOOD ——> block Gastrin and stimulate Pepsinogen to be made

56
Q

Intestinal Phases

A

10%-5%, DISTENTION of SI ——> HCL in stomach

Proteins sensed ——> SI G-cells ——> HCL in stomach

57
Q

What signals chief cells to secrete Pepsinogen

A

DISTENTION ——-> VAGUS N

Pepsin can convert other pepsinogen to pepsin

58
Q

+ feedback

A

HCL —> Pepsin—> AA—> Gastrin—> more HCL

59
Q

Pepsin is active at what pH

A

1.8-3.5

60
Q

IF

A

Secreted by parietal cells only in stomach

Absorbs B12

61
Q

Achlorhydria

A

Damaged parietal cells = no HCL no IF no B12 absorption

62
Q

R-Protein

A

Transports B12 to the duodenum
Where the pancreatic protease releases B12
= IF from stomach also in duodenum transports B12 to ileum and absorbs it at the IF receptor (B12+ TC11 absorbed together)

63
Q

Pernicious Anemia

A

Parietal cells don’t produce enough IF
Difficult to understand since SX seen much later due to huge B12 storage in Liver
CAUSES:
Atrophic gastritis - chronic inflammation of stomach mucosa-> kills parietal cells
Autoimmune meta plastic atrophic gastritis -> immune cells attack IF protein or the parietal cells

64
Q

Disruption in the VIT B12 can be caused by what surgeries

A
  1. Gastrectomy : loss of parietal cells (source of IF)

2. Gastric Bypass : Exclusion of stomach, duodenum, and proximal jejunum which alters B12 absorption

65
Q

Growth of Gastric Mucosa what is this

A

Gastric Epithelial cells secrete HCO3- (epithelial cells) and mucus (mucus cells) for a barrier
Protect against pepsin and HCL

66
Q

What can protect and what can damage the growth of the gastric mucosa

A

Protect: HCO-3, Mucus, prostaglandins, mucosal BF, Gastrin, GFs
Damage :H-pylori, alcohol, bile, stress, NSAIDS, pepsin’s, acid
*Gastrin can be a GF for mucosa

67
Q

CASE 1: LLQ pain, N, V, D weight loss from 3 weeks, T2D, HTN, Brest cancer, erosive esophagitis, chronic peptic ulcer disease, takes B-blocker drugs,
CT : mass over pancreas head
LABS : high Gastrin, low hematocrit, high acid

A

DX:
Tumor in pancreas causes oversecretion of Gastrin which goes to stomach to increase secretion of HCL = Gastrinoma
Gastrin has no response to 1 red back control

Ulcer usually in proximal jejunum + Melena

68
Q

Gastrinoma are associated with

A

Zollinger - Ellison Syndrome

69
Q

CASE 2 : 55yo m hematemesis, 8X higher Gastrin
Many duodenal ulcers, MEN1 suspected,
How do you confirm this Dx:

A

Administer Secretin (secretin stimulating test)

70
Q

Zollinger-Ellison Syndrome

A

Gastrinoma - large Gastrin secretion by duodenal or pancreatic tumor
HIGH : acid, parietal cells can grow
LOW : NA+ and H2O absorption, by SI (diarrhea)
SX: ulcer, low SI pH= inactivates pancreatic enzymes, fat absorption by bile ——-> Steatorrhea (maldigestion, malabsorption)

71
Q

Secretin stimulating test

A

Normal : you inject secretin and Gastrin levels are normal (working - feedback loop)
Gastrinoma : you inject secretin and Gastrin levels increase even more

72
Q

Peptic Ulcer Disease
Cause
What happens
2 types

A

H-pylori and NSAIDS
Loss of mucosal layer, excessive H+ and pepsin, or both
Gastric ulcer and Duodenal Ulcer

73
Q

H-Pylori how they survive and how they break down gastric mucosa

A

They release cytotoxins that break down the mucosa and underlying cells ,
adhesion factors that helps it bind
It releases Urease an enzyme that allows bacteria to convert urea to ammonium for alkaline effects so it doesn’t die and it can keep digesting

74
Q

Gastric Ulcer cause

A

In stomach , due to defected mucosal barrier

Increased Gastrin

75
Q

Duodenal Ulcers due to

A

In SI , due to increased H+
Not malignant usually
Most common
Increased Gastrin + parietal cells grow

76
Q

You can test for H-Pylori by looking for

A

Urease activity

Ammonium

77
Q

Pancreatic Lipase

A

Converts TAGS to monoglycerides and FreeFAs

78
Q

Exocrine Pancreas what does it release

A

Acinars secrete pancreatic juice : HCO-3 and enzymes to break down carbs, lipids, proteins

79
Q

Secretin function

A

Stimulate HCO3- serration from pancreas and inhibit Gastrin release in stomach

80
Q

Pancreatic enzymes are stored in

A

Zymogens

If protease they are secreted in inactive form (activated in duodenum

81
Q

What does CCK and parasympathetic innervation to pancreas do

A

ENZYMES and HCO3-

82
Q

Parasympathetic innervation to pancreas

A

Postganglionic from celiac and superior mesenteric plexus

*STIMULATE PANCREATIC SECRETION

83
Q

Sympathetic innervation to pancreas

A

Preganglionic ——> CN X vagus synapse in the ENS
Postganglionic ——> CN X synapse on exocrine pancreas
*INHIBIT PANCREATIC SECTRETION

84
Q

Papancreatic juice

A

Isotonic and high in HCO3-
Secreted by the centroacinar cell that is in the center of the acinus and connected to the duct

enzymes present secreted by acinar cells

85
Q

Trypsin inhibitor

A

Causes inhibition of proteases to become active (in the pancreatic duct) so they can only be activated in the duodenum

86
Q

Transporters on the lumen side of the pancreas

A

Cl-/HCO3- (Cl- into the cell)

87
Q

Transporters in the blood vessel side on pancreas ductal cells

A

NA+/K+ (K into the cell) Na leaves

H+/Na+ (NA into the cell) H+ leaves

88
Q

How does the HCO-3 come into the lumen

A

Cl-/HCO-3 or CFTR cl channel

Aldo Na+ is moved into the lumen (between the cells)

89
Q

pancreatic cells absorb

A

H+

Secrete HCO-3

90
Q

Cystic Fibrosis and pancreas

A

Defected CFTR Cl- channel which allows the Cl-/HCO-3 to work on the lumen apical side
= no HCO-3 can be secreted
= enzymes are not flushed out from duct, chronic and acute pancreatitis

91
Q

Cephalic Phase of pancreas

A

Smell taste
CN X
Make enzymatic secretion

92
Q

Gastric Phase

A

DISTENTION of stomach
CN X
Make enzymatic secretion

93
Q

Intestinal Phase of pancreas

A

80% of pancreatic secetion
Enzymes + Aqueous secretions
* AA and FA and try, met, phn ——> I-cell——> CCK——> acinar cells (ACH can potentiate) = enzymes
*H+ ——> S-cells ——> Secretin ——> Ductal cells (potentiated by CCK and ACH) = HCO-3 and NA+

94
Q

CCK causes secretion of

Secretin causes secretion of

A

Enzymes (Trypsinogen….)

HCO-3 aqueous solution

95
Q

what is essential for protein digestion

A

Enterokinase which cleave trypsinogen to Trypsin and other zygomogens from the pancreas ——> SI
Trypsin activates colipase = activates lipase from pancreas

GIGU Exam 1 (19 decks)

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