Phy & Pharm Mouth & Stomach

Front 1

What are fats (mostly triglycerides) broken down into

Back 1

monoglycerides and free fatty acids (FFAs)

Front 2

4 accessory organs of the GI tract

Back 2

salivary glands
pancreas
liver
gallbladder

Front 3

role and difference of endo and exocrine pancreas functions

Back 3

EXOcrine (acinar cells): secrete dig juices & enzymes important in hormonal secretion...coordinate digestion....via DUCTS

ENDOcrine (islets of Langerhan's): secrete hormones directly into BLOOD (endo-no ducts!)

Front 4

which 2 enteric plexuses lie within the GI tract

in which layers of the GI tract wall

Back 4

SUBMUCOSAL plexus

MYENTERIC plexus- between walls of muscularis externa (mediates shortening)

Front 5

whats the myenteric & digastric reflexes

Back 5

mastication stiulates salive, taste buds --> increases gastric, pancreatic & bile secretions

Front 6

3 main salivary glands, which responsible for most of the salivary secretions

Back 6

★SUBMANDIBULAR 70%★
Sublingual
parotid

Front 7

primary & secondary secretions by salivary glands are via which cells

Back 7

primary secretions- ACINUS
secondary- DUCT cels

Front 8

how is the saliva from acinus cells modified by duct cells

is saliva or plasma more diluted

Back 8

ACINUS secretes Na, K, Cl, HCO3 fluid

DUCT cells remove Na & Cl= dulited, ↓ NaCl than plasma

Front 9

6 functions of saliva

Back 9

lubrication
solvent (taste)
antibacterial
digestion (amylase - carbs)
neutralisation (HCO3)
sucking

Front 10

what substrate is digested my saliva

by what enzyme

Back 10

carbohydrates

amylase

Front 11

control of saliva secretions can be due to simple unconditioned and acquired conditioned reflexes

differentiate the 2 & their signalling pathways

Back 11

SIMPLE: chemo/ pressure RECEPTORSin mouth --> afferents --> medulla (salivary centre)

ACQUIRED: think/ smell/ see/ hear--> cerebral CORTEX --> medulla

---> both impulses via extrinsic autonomic nerves (symp & parasym)

Front 12

control of saliva if due to 1)reflexes (simple & acquired) & 2) ANS

describe 2) para and symp ANS control of saliva secretions:
- which nerves
- receptors
- type of saliva secreted

Back 12

PARA: dominant role---> facial CN VII & glossopharyngeal CN IX --> M3 - Gq - phospholiapse C ---> large watery, enzyme-rich

SYMP: stress---> superior cervical postganglionic fibres --> B1- Gs - adenylyl cyclase ---> small thick, mucus-rich

Front 13

what stimulates the upper oesophageal (cricopharyngeal) sphincter to open in swallowing

Back 13

pressure stimulates PHARYNGEAL PERSSURE RECEPTORS ---> afferents to medulla ---> efferents

Front 14

wheres the swallowing centre loc

Back 14

medulla oblongata

Front 15

what does oesophagus secrete
from which layer in wall
function

Back 15

MUCUS from submucosal glands
- lubrication
- protect epithelium from acid & enzyme attack

Front 16

stomach is the starting point for which substrate digestion

by which substances/ enzymes

Back 16

PROTEIN

by pepsin & HCl

Front 17

areas of the stomach

Back 17

Front 18

what substance does stomach produce

how much gastric juice secreted per day, where from

Back 18

CHYME

~2L/day from gastric PITs & GLANDs

Front 19

how does the stomach contraction come about

Back 19

PACEMAKER cells of CAJAL in FUNDUS establish basal electrical rhythm (BER)

ALL or nothing
spreads
continuous 3/min

Front 20

stomach emptying controlled by 1) gastric & 2) duodenal factors

what factors are these

Back 20

1) GASTRIC: distension ----thick consistency

2) DUODENAL: neuronal---hormonal

Front 21

duodenal factors control gastric emptying via hormonal and neuronal control. Which stimuli within the duodenum drive these responses?

Back 21

- FAT - delay requried
- ACID- delay for neutralising
- HYPERTONICITY- osmotically active chyme reduces plasma vol in intestine
- DISTENSION

Front 22

how do the gastric glands differ in the oxnytic mucosa (fundus & body) compared with the pyloric gland area (antrum)- i.e which cells present

Back 22

1) oxnytic mucosa (fundus & body): parietal & enterochromaffin-like (ELC) cells

2) pyloric gland area (antrum): G & D cells
NB: both contain Cheif cells

Front 23

what do these cells secrete:
- cheif cells
- parietal cells
- enterochromaffin-like cells
- G cells
- D cell

Back 23

chief- dig enzymes (pepsinogen)
parietal- HCl & intrinsic factor
ECL- histamine
G- gastrin
D- somatostatin

Front 24

what are the functions of chief cell secretions

Back 24

pepsinogen digests protein (when activated by HCl from parietal cells)

Front 25

whats the function of parietal cell secretions (oxnytic mucosa - fundus & body)

Back 25

HCl- activates pepsinogen (from chief cells)

intrinsic factor- binds vitB12 (allows absorption in the terminal ileum)

Front 26

whats the function of the ECL cell secretions (oxyntic mucosa- fundus & body)

via which receptor

Back 26

HISTAMINE- stimulates HCl secretions
via H2 receptors on parietal cells

Front 27

whats the function of gastrin secretions (pyloric gland area- antrum)

via which receptors & where

Back 27

GASTRIN- stimulates HCl secretion from parietal & histamine from ECL cells
via Gastrin receptors on ECL and parietal cells

Front 28

whats the function of D cell secretions (from pyloric gland area of antrum)

Back 28

SOMATOSTATIN: INHIBITS HCl secretion from parietal & histamine from ECL cells
via Gastrin receptors on both cells- BETWEEN meals

Front 29

which 5 pumps are present in parietal cells for HCl secretion (& production)

Back 29

Front 30

which enzyme present in parietal cells makes hydrogen bicarbonate

how does it exit paritel cells

Back 30

carbonic anhydrase --> HCO3- --> Cl-/HCO3- antiporter

Front 31

which direction does the Na/K ATPase pump ions at the basal side of parietal cells

Back 31

Na+ --> OUT to basal side
K+ --> IN (then --> lumenal side via K + channels--> back in via H/K ATPase)

Front 32

which ion is recycled by parietal cells, the gradient of which is used to power H/K ATPase

Back 32

K+

Front 33

which receptors are present on parietal cells- for what substrates (oxyntic mucosa- fundus & body)

Back 33

M3- Ach; G- gastrin/ somatostatin; H2- histamine; P- PGE2

Front 34

what receptors are on ECL cells (oxyntic mucosa- fundus & body)

Back 34

M1- Ach; G-gastrin

Front 35

what produces PDE2 & what effect does it have

Back 35

loacally by COX --> PGE2 receptor parietal cell--> INHIBITs acid ................powerful!

Front 36

what does it mean by trafficking of H/K ATPase in parietal cells of oxyntic mucosa (fundus & body)

Back 36

resting parietal cells:
- H/K ATPase largely within cell

stimulated parietal cell:
- H/K ATPase trafficks to apical membrane
- extends microvilli

Front 37

what are the 3 phases of gastric secretion

Back 37

1) cephalic
2) gastric
3) intestinal

Front 38

how is gastric secretion stimulated in the 1) CEPHALIC phase of gastric secretion

Back 38

Front 39

in the 2) GASTRIC phase of gastric secretions (instead of conditioned reflexes activating vagal stimulation in cephalic phase,) what sitmuli activate secretions?

where do they act to cause secretion

Back 39

DISTENTION --> mechanoreceptors--> G cells
PROTEIN---> G cells

Front 40

what role does the 3) INTESTINAL phase have on gastric secretions

Back 40

switch OFF secretions
stomach empties--> ↓G cell activation
SOMATOSTATIN prod continues (low pH between meals- proteins act as buffer)

Front 41

what role does PROTEIN have on (pH &) gastric secretions

Back 41

protein = buffer of stomach acid
↑gastric pH = turn off somatostatin (inhibitory)

Front 42

how do mucosal protecting mechanisms prevent against ulcers

Back 42

hydrophobic monolayer repels H+
HCO3- in surface mucus gel layer
high mucosal blood flow to clear H+

Front 43

what role do NSAIDs have in predisposing to peptic ulcers

Back 43

reduce PGE2 formation by INHIBITing COX
(PGE2 is powerful inhibitor of acid secretion)

damage mucus layer & HCO3- prod

Front 44

how are peptic ulcers prevented in long-term NSAID use (e.g aspirin)

Back 44

stable PGE1 analogue (e.g misoprostol)
acts like PGE2 to inhibit acid secretion
maintains mucus & HCO3-

Front 45

what role does H.pylori have in causing ulcers

Back 45

CHRONIC infection : lies in mucus layer
secretes inflammatory agents
weaken mucosal barrier --> breakdown --> HCl & pepsin attack

Front 46

3 ways drug treatment aims to promote ulcer healing

Back 46

- reduce acid
- promote mucosal resistance
- eradicate H.pylori

Front 47

3 types of drugs used in treating peptic ulcers

Back 47

PPIs
H2-antagonists
muscarinic antagonists (M1 on ECL & M3 on parietal)

Front 48

how do PPIs work to reduce acid secretion in treating peptic ulcers

eg

Back 48

OMEPRAZOLE:
- covalently modifies ACTIVE H/K ATPase
- irreversible
- prodrug
- active in acid

Front 49

how to H2-antagonists work in treating peptic ulcers

eg

Back 49

RANITIDINE:
- comp inhib H2 receptor on ECL cells
(competes with Ach & gastrin)
- ↓histamine
- indirectly ↓H/K ATPase activity (acid prod)

Front 50

how do muscarinic antagonists work in treatment of peptic ulcers

eg
NB: now obselete

Back 50

PIRENZEPINE:
- competes with ACh
- blocks M1 = ↓histamine
- blocks M3= ↓proton pump activation (H/K ATPase)

Front 51

what's SUCRALFATE & how does it act to strengthen mucosal barriers

administration

Back 51

mucosal strengthener (Al hydroxide & sulphated sucrose)
- acid-activated
- Al- binds to ulcer base & gels with mucus
- ↑mucosal blood flow

ORAL

Front 52

how does bismuth chealate work in treating peptic ulcers

administration

Back 52

MUCOSAL STRENGTHENER:
- acid-activated
- ↑mucosal blood flow
- eradiates H.PYLORI (+ ranitidine)

ORAL

Front 53

what are PPIs used to treat (e.g. omeprazole)

Back 53

peptic ulcers
GORD
1st line Zollinger-Elison syndrome

Front 54

what's Zollinger-Ellison syndrome

Back 54

acid HYPERSECRETION due to GASTRIN-producing tumour

Front 55

what are H2-antagonists (ranitidine) used to treat

Back 55

peptic ulcers
GORD

Front 56

what are antacids used for

Back 56

symptomatic relief of peptic ulcers & dyspepsia

Front 57

3 types of antacids and complexes they form in the stomach

Back 57

MgOH --> MgCl
Mg trisilicate --> MgCl
AlOH --> AlCl (causes diarrhoea)

Front 58

2 sets of PPI & abx combinations used in treatment of peptic ulcers

Back 58

1) omeprazole + clarythromycin + amox
2) omeprazole + clarythromycin + metranidazole

Front 59

2 drugs used to increase gastric MOTILITY

clinical indications for:
- GORD
- disorders of gastric emptying

Back 59

DOMPERIDONE
METPROCLAMIDE

Front 60

what are the effects of domperidone

clinical uses

Back 60

↑gastric MOTILITY: ↑tone LOS, gastric emptying & peristalsis

GORD
gastric emptying disorders

Front 61

what are the effects of metoproclamide

clinical uses

Back 61

↑gastric emptying

- GORD
- disorders of gastric emptying