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61 Cards in this Set
- Front
- Back
What are fats (mostly triglycerides) broken down into
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monoglycerides and free fatty acids (FFAs)
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4 accessory organs of the GI tract
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salivary glands
pancreas liver gallbladder |
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role and difference of endo and exocrine pancreas functions
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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!) |
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which 2 enteric plexuses lie within the GI tract
in which layers of the GI tract wall |
SUBMUCOSAL plexus
MYENTERIC plexus- between walls of muscularis externa (mediates shortening) |
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whats the myenteric & digastric reflexes
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mastication stiulates salive, taste buds --> increases gastric, pancreatic & bile secretions
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3 main salivary glands, which responsible for most of the salivary secretions
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★SUBMANDIBULAR 70%★
Sublingual parotid |
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primary & secondary secretions by salivary glands are via which cells
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primary secretions- ACINUS
secondary- DUCT cels |
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how is the saliva from acinus cells modified by duct cells
is saliva or plasma more diluted |
ACINUS secretes Na, K, Cl, HCO3 fluid
DUCT cells remove Na & Cl= dulited, ↓ NaCl than plasma |
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6 functions of saliva
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lubrication
solvent (taste) antibacterial digestion (amylase - carbs) neutralisation (HCO3) sucking |
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what substrate is digested my saliva
by what enzyme |
carbohydrates
amylase |
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control of saliva secretions can be due to simple unconditioned and acquired conditioned reflexes
differentiate the 2 & their signalling pathways |
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) |
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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 |
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 |
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what stimulates the upper oesophageal (cricopharyngeal) sphincter to open in swallowing
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pressure stimulates PHARYNGEAL PERSSURE RECEPTORS ---> afferents to medulla ---> efferents
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wheres the swallowing centre loc
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medulla oblongata
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what does oesophagus secrete
from which layer in wall function |
MUCUS from submucosal glands
- lubrication - protect epithelium from acid & enzyme attack |
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stomach is the starting point for which substrate digestion
by which substances/ enzymes |
PROTEIN
by pepsin & HCl |
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areas of the stomach
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what substance does stomach produce
how much gastric juice secreted per day, where from |
CHYME
~2L/day from gastric PITs & GLANDs |
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how does the stomach contraction come about
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PACEMAKER cells of CAJAL in FUNDUS establish basal electrical rhythm (BER)
ALL or nothing spreads continuous 3/min |
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stomach emptying controlled by 1) gastric & 2) duodenal factors
what factors are these |
1) GASTRIC: distension ----thick consistency
2) DUODENAL: neuronal---hormonal |
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duodenal factors control gastric emptying via hormonal and neuronal control. Which stimuli within the duodenum drive these responses?
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- FAT - delay requried
- ACID- delay for neutralising - HYPERTONICITY- osmotically active chyme reduces plasma vol in intestine - DISTENSION |
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how do the gastric glands differ in the oxnytic mucosa (fundus & body) compared with the pyloric gland area (antrum)- i.e which cells present
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1) oxnytic mucosa (fundus & body): parietal & enterochromaffin-like (ELC) cells
2) pyloric gland area (antrum): G & D cells NB: both contain Cheif cells |
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what do these cells secrete:
- cheif cells - parietal cells - enterochromaffin-like cells - G cells - D cell |
chief- dig enzymes (pepsinogen)
parietal- HCl & intrinsic factor ECL- histamine G- gastrin D- somatostatin |
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what are the functions of chief cell secretions
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pepsinogen digests protein (when activated by HCl from parietal cells)
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whats the function of parietal cell secretions (oxnytic mucosa - fundus & body)
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HCl- activates pepsinogen (from chief cells)
intrinsic factor- binds vitB12 (allows absorption in the terminal ileum) |
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whats the function of the ECL cell secretions (oxyntic mucosa- fundus & body)
via which receptor |
HISTAMINE- stimulates HCl secretions
via H2 receptors on parietal cells |
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whats the function of gastrin secretions (pyloric gland area- antrum)
via which receptors & where |
GASTRIN- stimulates HCl secretion from parietal & histamine from ECL cells
via Gastrin receptors on ECL and parietal cells |
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whats the function of D cell secretions (from pyloric gland area of antrum)
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SOMATOSTATIN: INHIBITS HCl secretion from parietal & histamine from ECL cells
via Gastrin receptors on both cells- BETWEEN meals |
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which 5 pumps are present in parietal cells for HCl secretion (& production)
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which enzyme present in parietal cells makes hydrogen bicarbonate
how does it exit paritel cells |
carbonic anhydrase --> HCO3- --> Cl-/HCO3- antiporter
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which direction does the Na/K ATPase pump ions at the basal side of parietal cells
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Na+ --> OUT to basal side
K+ --> IN (then --> lumenal side via K + channels--> back in via H/K ATPase) |
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which ion is recycled by parietal cells, the gradient of which is used to power H/K ATPase
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K+
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which receptors are present on parietal cells- for what substrates (oxyntic mucosa- fundus & body)
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M3- Ach; G- gastrin/ somatostatin; H2- histamine; P- PGE2
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what receptors are on ECL cells (oxyntic mucosa- fundus & body)
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M1- Ach; G-gastrin
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what produces PDE2 & what effect does it have
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loacally by COX --> PGE2 receptor parietal cell--> INHIBITs acid ................powerful!
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what does it mean by trafficking of H/K ATPase in parietal cells of oxyntic mucosa (fundus & body)
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resting parietal cells:
- H/K ATPase largely within cell stimulated parietal cell: - H/K ATPase trafficks to apical membrane - extends microvilli |
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what are the 3 phases of gastric secretion
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1) cephalic
2) gastric 3) intestinal |
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how is gastric secretion stimulated in the 1) CEPHALIC phase of gastric secretion
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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 |
DISTENTION --> mechanoreceptors--> G cells
PROTEIN---> G cells |
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what role does the 3) INTESTINAL phase have on gastric secretions
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switch OFF secretions
stomach empties--> ↓G cell activation SOMATOSTATIN prod continues (low pH between meals- proteins act as buffer) |
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what role does PROTEIN have on (pH &) gastric secretions
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protein = buffer of stomach acid
↑gastric pH = turn off somatostatin (inhibitory) |
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how do mucosal protecting mechanisms prevent against ulcers
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hydrophobic monolayer repels H+
HCO3- in surface mucus gel layer high mucosal blood flow to clear H+ |
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what role do NSAIDs have in predisposing to peptic ulcers
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reduce PGE2 formation by INHIBITing COX
(PGE2 is powerful inhibitor of acid secretion) damage mucus layer & HCO3- prod |
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how are peptic ulcers prevented in long-term NSAID use (e.g aspirin)
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stable PGE1 analogue (e.g misoprostol)
acts like PGE2 to inhibit acid secretion maintains mucus & HCO3- |
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what role does H.pylori have in causing ulcers
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CHRONIC infection : lies in mucus layer
secretes inflammatory agents weaken mucosal barrier --> breakdown --> HCl & pepsin attack |
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3 ways drug treatment aims to promote ulcer healing
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- reduce acid
- promote mucosal resistance - eradicate H.pylori |
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3 types of drugs used in treating peptic ulcers
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PPIs
H2-antagonists muscarinic antagonists (M1 on ECL & M3 on parietal) |
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how do PPIs work to reduce acid secretion in treating peptic ulcers
eg |
OMEPRAZOLE:
- covalently modifies ACTIVE H/K ATPase - irreversible - prodrug - active in acid |
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how to H2-antagonists work in treating peptic ulcers
eg |
RANITIDINE:
- comp inhib H2 receptor on ECL cells (competes with Ach & gastrin) - ↓histamine - indirectly ↓H/K ATPase activity (acid prod) |
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how do muscarinic antagonists work in treatment of peptic ulcers
eg NB: now obselete |
PIRENZEPINE:
- competes with ACh - blocks M1 = ↓histamine - blocks M3= ↓proton pump activation (H/K ATPase) |
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what's SUCRALFATE & how does it act to strengthen mucosal barriers
administration |
mucosal strengthener (Al hydroxide & sulphated sucrose)
- acid-activated - Al- binds to ulcer base & gels with mucus - ↑mucosal blood flow ORAL |
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how does bismuth chealate work in treating peptic ulcers
administration |
MUCOSAL STRENGTHENER:
- acid-activated - ↑mucosal blood flow - eradiates H.PYLORI (+ ranitidine) ORAL |
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what are PPIs used to treat (e.g. omeprazole)
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peptic ulcers
GORD 1st line Zollinger-Elison syndrome |
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what's Zollinger-Ellison syndrome
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acid HYPERSECRETION due to GASTRIN-producing tumour
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what are H2-antagonists (ranitidine) used to treat
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peptic ulcers
GORD |
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what are antacids used for
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symptomatic relief of peptic ulcers & dyspepsia
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3 types of antacids and complexes they form in the stomach
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MgOH --> MgCl
Mg trisilicate --> MgCl AlOH --> AlCl (causes diarrhoea) |
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2 sets of PPI & abx combinations used in treatment of peptic ulcers
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1) omeprazole + clarythromycin + amox
2) omeprazole + clarythromycin + metranidazole |
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2 drugs used to increase gastric MOTILITY
clinical indications for: - GORD - disorders of gastric emptying |
DOMPERIDONE
METPROCLAMIDE |
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what are the effects of domperidone
clinical uses |
↑gastric MOTILITY: ↑tone LOS, gastric emptying & peristalsis
GORD gastric emptying disorders |
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what are the effects of metoproclamide
clinical uses |
↑gastric emptying
- GORD - disorders of gastric emptying |