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Pharmacy year 2 > upper gi disorders and oesophagus > Flashcards

upper gi disorders and oesophagus Flashcards

mouth and oesophagus

1
Q

what are the main sites for therapeutic intervention in GI system

A

Mouth oesophagus stomach liver pancreas large intestine small intestine

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2
Q

can you name gastrointestinal disorders

A

oral cavity ulcers and stomatitis
gastro-oesophageal reflux disease (GORD)
Peptic ulcers disease PUD
Duodenal ulcers
nausea
emesis
IBS
diarrhoea
Constipation

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3
Q

what happens in the mouth?

A

ingestion and fragmentation of food

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4
Q

what’s in the mouth?

A

tongue, salivary glands and teeth

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5
Q

dysfunctional physiologies and diseases of mouth

A

oral ulceration, stomatitis, leukoplakia painless
dysphagia

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6
Q

oral ulceration is

A

break in the oral epithelium exposing nerve endings in the underlying connective tissue

physical or chemical injury infections drugs malignancy systemic disease

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7
Q

stomatitis

A

inflammation of the lining of any of the soft-tissues of mouth poor oral hygiene , poorly fitted dentures, heat burns drugs , allergy infections

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8
Q

leukoplakia

A

painless white patches on the side of the tongue of cheeks

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9
Q

dysphagia

A

difficulty swallowing

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10
Q

oesophagus

A

contracts rhythmically to propel food toward stomach

UOS prevents air entering oesophageal and oesophageal reflux

LOS prevents gastroesophagageal reflux. High intrluminal pressure keeps it closed until food needs to be dumped into the stomach

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11
Q

dysfunctional physiologies and diseases of oesophagus

A

GORD gastro-oesophageal reflux disorder

obesity, medication, spicy, acidic or fatty foods, smoking,

barret’s oesophagus (premalignantstate)

hiatal hernia

motility disorders
achalasia- inadequate LOS relaxation
diffuse oesophageal spasm- uncoordinated contraction hyper contraction
inaffective oesophageal motility- hypo contraction

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12
Q

GORD stands for

A

gastro-oesophageal-reflux disorder

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12
Q

what is gord?

A

exposure of unprotected oesophageal epithelium to acid

transient LOS relaxation in absence of swallowing
response to stimulation of gastric vagal mechanoreceptors and oesophageal hympomotility

potentially 3 distinct types
non-erosive reflux disease heartburn
erosive oesophagitis acute inflammatory response
Barret’s oesophagus (metaplasia of mucosa)-cancer risk

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13
Q

gastric anatomy

A

acid secreting oxyntic gland area
Mucous cells
chief cells pepsinogen
ECL cells- histamine
EnteroChromaffin-Like
parietal cells (ccl intrinsic factor)

pyloric gland area- gastrin
Mucous cells (+ pepsinogen)
G cells (gastrin)
D cella (somastatin)
no parietal cells (HCl)

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14
Q

name the gastric secretions

A

surface mucosa cells of pyloric region secrete thick, protective, alkaline-rich mucus= gastric mucosal barrier

cells stimulated by mechanical and chemical irritation and parasympathetic inputs

barrier can be damaged by bacterial, viral infection and certain drugs (eg aspirin)

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15
Q

gastric oxyntic gland

A

parietal cells
secrete 1-2L of 150-160mM HCL per day pH 0.8-1
stimulation of secretion involves translocation of H+/K+ -ATPase (proton pump) to apical membrane
resting cell H+/K+-ATPase in cytoplasmic vesicles
stimulated cell H+/K+-ATPase membrane fused
increased surface area and membrane pumps

16
Q

there are 2 types of gastric acid secretions name both?

A

positive regulator
negative regulator

17
Q

negative regulator

A

somatostatin D cells
directly inhibits parietal cell secretion
inhibits gastrin and histamine release

17
Q

name the positive regulators

A

acetylcholine (enteric neurones)
direct parietal cell stimulation

histamine (ECL) cells
direct parietal cell stimulation

gastrin (G cells)
endocrine action
stimulates histamine release - ECL cells
Directly stimulates parietal cell
proliferation

18
Q

acetylcholine

A

muscarinic (M3) receptor
cholecystokinin B (CKKB/CCK2) receptor
Histamine:H2 receptor

Ach and Gastrin act through G-coupled receptors linked to increases in Ca2+ and diacylglycerol through phospholipase -C (PLC)-inositol 1,4,5- triphosphate (IP3) pathway

histamine acts through G-coupled receptor to increase cyclic AMP (cAMP)
Most powerful stimulus for HCl secretion

19
Q

acid secretion pathways

A

Ach, Histamine and gastrin directly and indirectly induce HCl secretion

19
Q

acetylcholine

A

M3 Ca2+ dep, pathway—-PP->H+

20
Q

secretory pathways

A

gastrin
histamine
Acetylcholine

21
Gastrin
CCK Ca2+ dep, pathway->---- PP->H+
21
histamine pathway
H2 cAMP rep, pathway->PP->H+
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Pharmacy year 2 (5 decks)

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