The upper GI tract Flashcards

1
Q

Regulation of saliva secretion

A

-Regulated by ANS
-Small amount continuously secreted, increased due to ANS stimulation

  • Food chemicals stimulate taste receptors
  • sensory impulse sent to brainstem salivary nuclei
  • parasympathetic activity activity initiated
  • parasympathetic fibres terminate on the smooth muscle fibre that surrounded the salivary nuclei
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2
Q

Pathophysiology of the oesophagus - dysphagia

A

Defined as difficulty, discomfort or pain in swallowing

Commonly a consequence of a neuromuscular disease

Difficult to treat with pharmacotherapy

mechanical obstruction = majority of cases

motor disorders = minority of cases

Functional dysphagia

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3
Q

Oesophageal spasm pharmacotherapy

A

Long acting nitrates - causes inhibition of contraction

Calcium channel blockers - reduced calcium entry into smooth muscle cells and reduces contraction amplitude

Injection of type A botulinum toxin - contains a protease that targets a protein involved in the CA2+ exocytosis of ach from presynaptic membrane

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4
Q

Stomach structure

A

Functions are - reservoir, partial digestion, limited absorption and regulated release of chyme into duodenum

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5
Q

Regulation of parietal cell HCL secretion

A
  • Regulated process
  • Ach, Gastrin and Histamine stimulate HCL secretion
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6
Q

Gastritis

A

Inflammation of the gastric mucosa leading to discomfort and tenderness.

Acute gastritis is the injury of the protective mucosal barrier by drugs, chemicals or infection

Chronic gastritis commonly occurs in the elderly and is usually due to the thinning or breakdown of the stomach wall. Leads to chronic fundal or anstral gastritis

Treatment = remover trigger or decrease acid

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7
Q

Prokinetic drugs

A

Enhance coordinated GI motility without purgation (cleansing)

Aim is to increase ACH without pattern interference to enhance stomach motility

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8
Q

Ulcer formation

A

Located in the stomach

Normally the mucus cells in the neck of the gastric glands secrete and bicarbonate ions to create a chemical barrier to protect the stomach from digesting itself

Acid and pepsin can destroy mucosa and form holes through submucosa into the muscularis forming ulcers

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9
Q

Triggers of ulcer formation

A

Smoking
High alcohol intake
Bacterial infection

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10
Q

Aims of therapy

A

healing of ulcer
Prevention of recurrence
Avoidance by a combination of drug therapy and lifestyle modifications

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11
Q

Proton pump inhibitors

A

Irrervirsible inhibition of the H+ / k+ ATPase
- binds covalently to enzyme
- marked inhibiton of basic acid secretion, stimulated acid secretion
- NO EFFECT on release of pepsin

TREAT WITH PPI FOR 4-8 WEEKS

Due to adverse drug reactions, it is recommended that PPIS are prescribed for the shortest possible duration

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12
Q

Bismuth subsalicylate

A

is a medicine that relieves diarrhoea, nausea, heartburn, and other stomach problems

strongly adheres to proteins

forms a complex gel with mucus

promotes increases mucus production and bicarbonate release

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13
Q

Antacids

A

Neutralise gastric acid
Aim to keep PH rise more less than 4

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14
Q

Aluminium compounds

A
  • Reacts slowly with HLC
  • gradual and prolonged action
  • forms a protective coat over ulcer
  • adsorbs pepsin
  • constipating
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15
Q

Magnesium compounds

A

-very little absorbed
- gut stimulant and provides a laxative effect
- can cause phosphate depletion

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16
Q

Sodium bicarbonate

A
  • Rapid reaction with gastric acid
  • causes rapid pH rise
  • Causes CO2 generation in stomach
17
Q

Alginates - active ingredient = alginic acid

A
  • Taken after meals
    -Forms a raft on the surface of gastric contents - preventing reflux and protects the oesophageal mucosa
  • Commonly available as compound preparations also including antacids
18
Q

GORD

A
  • Common disorders
  • exposure of oesophageal mucosa to gastric acid or bile leads to heartburn
  • lack of effective barrier to acid / bile reflux from stomach due to an ineffective LOS ( lower oesophageal sphincter )

long term effects
- chronic ulceration
- fibrosis/stenosis = causes progressive dysphagia

Treatment
- lifestyle modifications
- antacids to neutralise acids
- PPI
- alginates to prevent acid or bile reflux into the oesophagus