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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
Where and how in HCL made in the parietal cells
In the villus-like membranes of the canaliculi CO2+ H2O—> H2CO3—> H+ and HCO3- H2O —> OH- and H+ * CARBONIC ANHYDRASE does these reactions
26
What determines the secretory rate of the stomach
The number of parietal cells present
27
Special thing about OXYNTIC cells
High mitochondria to make ATP for making a lot of acid HCL
28
Transporters present on the lumen side of the gastric parietal cells
1. K+/H+ (K goes into cell) | 2. Cl- follows H+ out of the cell into lumen
29
Transporters present on the blood vessel side of the gastric parietal cells
1. Na+/K+ ( K into the cell) 2. HCO3/Cl- (Cl- into the cell) = HCO3- absorbed (*ALKALINE TIDE)
30
Omeprazole function
Inhibits the K+/H+ channel on the lumen side So H+ cant leave cell, and K+ cant go into the cell = no HCL
31
What is gastric juice there are 2 types
1. Non-Parietal = Alkaline constant flow and volume (Na+, Cl-) (HCO3- secreted) 2. Parietal = hyperosmotic , after a meal (Cl-) (H+)
32
Which things bind to parietal cell to stimulate HCL secretion
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
33
ACh and Gastrin also
Go a stimulate ECL cells to secrete Histamine
34
What inhibits the parietal cell from secreting HCL
1. Somatostatin——I cAMP (D CELLS) | 2. Prostaglandins ——I cAMP (protects the mucosa of GI)
35
What inhibits Gastrin release
HCL (negative feedback) Somatostatin and prostaglandins GASTRIN——> increase HCL from parietal cell + SOMATOSTATIN from D cell——I G-cells
36
Cimethidine function
Inhibits the H2 receptor so Histamine cant bind to it = can’t stimulate HLC secretions = in potentiation effect : also blocked Ach and Gastrin potentiation
37
What inhibit the ECL cells
Somatostatin and Prostaglandins
38
Direct pathway of VagusN to secrete HCL
Vagus nerve goes to stomach and releases ACH on the parietal cells = HCL
39
Indirect Pathway of Vagus N on stimulating release of HCL
Vagus nerve comes to stomach and released GRP ——> on the G-cells = secretes Gastrin—-> BLOOD——> Parietal cell for secretin of HCL
40
What other 2 things stimulate g-cells
1. Dissension of the stomach —-> ACH on G -cells | 2. AA —-> stimulate G-cells
41
Atropine blocks what
Only the DIRECT vagus N pathway (only blocks mAChR)
42
What are 2 effects of GRP released by indirect vagal n
1 G-cell stimulation | 2 inhibit somatostatin
43
2 things that stimulate somatostatin release
Gastrin and H+
44
PROTIENS in the stomach stimulates
G-cells
45
Potentiation (requires separate receptors on target cell) so two stimuli can make a double effect Name 2
1. Histamine increases effect of ACH (HCL) and Gastrin (HCL +Somatostatin) 2. ACh increases the effect of Histamine (HCL) and Gastrin (HCL +somatostatin)
46
Effect of using Atropine
Health defect since we have so many ACH receptors in our bodies
47
Effect of using Cimetidine
Treat duodenal and gastric ulcers, and GERD
48
Effect of using omeprazole
Inhibits the H+/K+ pump on lumen side Treat ulcers (reduce H+ secretion)
49
3 phases of Gastric HCL secretion
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
DISTENTION causes
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
Cephalic Phase
30%of HCL secretion (chew, swallow, smell, taste) Vagus ach ——> Parietal Cell (HCL) Vagus grp ——> G- cell (Gastrin)
52
Vagotomy
X INDIRECT VAGUS N and DIRECT VAGUS N | = NO CEPHALC PATHWAY
53
Gastric Phase
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
Coffee stimulation
Stimulates the gastric HCL secretion
55
High H+ in lumen causes
Selection of SECRETIN (*Duodenum) into BLOOD ——> block Gastrin and stimulate Pepsinogen to be made
56
Intestinal Phases
10%-5%, DISTENTION of SI ——> HCL in stomach | Proteins sensed ——> SI G-cells ——> HCL in stomach
57
What signals chief cells to secrete Pepsinogen
DISTENTION ——-> VAGUS N | Pepsin can convert other pepsinogen to pepsin
58
+ feedback
HCL —> Pepsin—> AA—> Gastrin—> more HCL
59
Pepsin is active at what pH
1.8-3.5
60
IF
Secreted by parietal cells only in stomach | Absorbs B12
61
Achlorhydria
Damaged parietal cells = no HCL no IF no B12 absorption
62
R-Protein
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
Pernicious Anemia
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
Disruption in the VIT B12 can be caused by what surgeries
1. Gastrectomy : loss of parietal cells (source of IF) | 2. Gastric Bypass : Exclusion of stomach, duodenum, and proximal jejunum which alters B12 absorption
65
Growth of Gastric Mucosa what is this
Gastric Epithelial cells secrete HCO3- (epithelial cells) and mucus (mucus cells) for a barrier Protect against pepsin and HCL
66
What can protect and what can damage the growth of the gastric mucosa
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
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
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
Gastrinoma are associated with
Zollinger - Ellison Syndrome
69
CASE 2 : 55yo m hematemesis, 8X higher Gastrin Many duodenal ulcers, MEN1 suspected, How do you confirm this Dx:
Administer Secretin (secretin stimulating test)
70
Zollinger-Ellison Syndrome
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
Secretin stimulating test
Normal : you inject secretin and Gastrin levels are normal (working - feedback loop) Gastrinoma : you inject secretin and Gastrin levels increase even more
72
Peptic Ulcer Disease Cause What happens 2 types
H-pylori and NSAIDS Loss of mucosal layer, excessive H+ and pepsin, or both Gastric ulcer and Duodenal Ulcer
73
H-Pylori how they survive and how they break down gastric mucosa
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
Gastric Ulcer cause
In stomach , due to defected mucosal barrier | Increased Gastrin
75
Duodenal Ulcers due to
In SI , due to increased H+ Not malignant usually Most common Increased Gastrin + parietal cells grow
76
You can test for H-Pylori by looking for
Urease activity | Ammonium
77
Pancreatic Lipase
Converts TAGS to monoglycerides and FreeFAs
78
Exocrine Pancreas what does it release
Acinars secrete pancreatic juice : HCO-3 and enzymes to break down carbs, lipids, proteins
79
Secretin function
Stimulate HCO3- serration from pancreas and inhibit Gastrin release in stomach
80
Pancreatic enzymes are stored in
Zymogens | If protease they are secreted in inactive form (activated in duodenum
81
What does CCK and parasympathetic innervation to pancreas do
ENZYMES and HCO3-
82
Parasympathetic innervation to pancreas
Postganglionic from celiac and superior mesenteric plexus | *STIMULATE PANCREATIC SECRETION
83
Sympathetic innervation to pancreas
Preganglionic ——> CN X vagus synapse in the ENS Postganglionic ——> CN X synapse on exocrine pancreas *INHIBIT PANCREATIC SECTRETION
84
Papancreatic juice
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
Trypsin inhibitor
Causes inhibition of proteases to become active (in the pancreatic duct) so they can only be activated in the duodenum
86
Transporters on the lumen side of the pancreas
Cl-/HCO3- (Cl- into the cell)
87
Transporters in the blood vessel side on pancreas ductal cells
NA+/K+ (K into the cell) Na leaves | H+/Na+ (NA into the cell) H+ leaves
88
How does the HCO-3 come into the lumen
Cl-/HCO-3 or CFTR cl channel Aldo Na+ is moved into the lumen (between the cells)
89
pancreatic cells absorb
H+ | Secrete HCO-3
90
Cystic Fibrosis and pancreas
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
Cephalic Phase of pancreas
Smell taste CN X Make enzymatic secretion
92
Gastric Phase
DISTENTION of stomach CN X Make enzymatic secretion
93
Intestinal Phase of pancreas
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
CCK causes secretion of | Secretin causes secretion of
Enzymes (Trypsinogen....) | HCO-3 aqueous solution
95
what is essential for protein digestion
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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