GI Physiology Flashcards

1
Q

What is Ludwig’s angina?

A

A serious, potentially life-threatening cellulitis, of the floor of the mouth, usually occurring in adults with concomitant dental infections and if left untreated, may obstruct the airways, necessitating tracheostomy.

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2
Q

What are the 3 salivary glands?

A

1) Submandibular. 2)Sublingual. 3)Parotid.

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3
Q

What does mastication do?

A

1) Reduces particle size within the food bolus.
2) Mixes food with salvia (lubrication and enzymes).
3) Increases surface area.

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4
Q

What is achalasia?

A

The lower esophageal sphincter (LES) is a muscular ring that closes off the esophagus from the stomach. If you have achalasia, your LES fails to open up during swallowing, which it’s supposed to do. This leads to a backup of food within your esophagus.

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5
Q

What are oesophageal varices?

A

Oesophageal varices are extremely dilated sub-mucosal veins in the lower third of the esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding.

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6
Q

What is a Sengstaken tube and what is it used for?

A

It is a 3 lumen tube (1- inflate gastric balloon, 2-inflate oesophageal balloon, 3-aspirate gastric contents) that is used to buy time in life-threatening upper GI bleeds caused by ruptured oesophageal varices. Used when other treatments haven’t worked.

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7
Q

What is Cimetidine?

A

A histamine H2 receptor antagonist that inhibits stomach acid production.

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8
Q

What are the 3 phases of gastric secretion?

A

1) Cephalic 2) Gastric 3)Intestinal

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9
Q

What foods directly stimulate gastrin release?

A
  • Protein/peptides
  • Coffee
  • Calcium rich
  • Alcohol oddly doesn’t appear to
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10
Q

Where is enteropeptidase found and what does it do?

A

It is found in the small intestine and it activates trypsinogen.

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11
Q

What are Kupffer cells?

A

Specialised macrophages located in the liver.

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12
Q

What is enteral feeding?

A

Nutritionally complete feeding directly into stomach, duodenum or jejunum.

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13
Q

What is parenteral feeding?

A

IV feeding, bypassing normal process of eating and digestion.

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14
Q

What is Loperamide?

A

A gut selective opiate Mu receptor agonist. It decreases tone and activity of myenteric plexus and slows colonic transit leading to increased water absorption.

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15
Q

What is Prucalopride?

A

Gut selective 5HT4 receptor agonist, increase colonic (and other gut) motility. Licensed or use of chronic constipation in UK.

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16
Q

What is ferritin?

A

A soluble cellular iron store. Iron safe and it is readily available from the reticuloendothelial system.

17
Q

What is haemosiderin?

A

Insoluble conglomerates of ferritin as a cellular iron store. Iron only slowly available.

18
Q

What is hepcidin?

A

Central regulatory hormone of systemic iron homeostasis, Hepcidin deficiency is the cause of iron overload in hereditary haemochromatosis, iron-loading anaemias and hepatitis C. Hepcidin works by binding to ferroportin and degrading it.

19
Q

What is non-haem iron absorbed?

A

Non-haem iron must be reduced from the ferric to the ferrous form by duodenal cytochrome b1 (dCytb1). This process is influences by vitamin C.

20
Q

What is DMT1?

A

Divalent metal transporter 1. An electrogenic pump that allows iron (Fe2+) to be taken into the enterocyte. Its expression is unregulated in iron deficiency. Iron is exported from the enterocyte to the circulating plasma through ferroportin and hepcidin.

21
Q

What is Ferroportin?

A

A transmembrane protein that allows iron to move from enterocyte to circulating plasma. Also essential for the release of iron from macrophages. Interaction between ferroportin and hepcidin is the single most important regulator of GI iron absorption (and RES iron release).

22
Q

What is transferrin?

A

A glycoprotein, synthesised in the liver, involved in plasma iron transport. Synthesised in hepatocytes. 2 iron binding domains. 30% saturated with Fe.

23
Q

What is hereditary haemochromatosis?

A

An autosomal recessive disorder of iron metabolism causing iron overload. Abnormalities in the HFE gene are responsible for the vast majority of cases. Though to principally reduce hepicidin production. Homozygous mutation of C282Y mutation of the HFE gene is most common.

24
Q

What is the percentage saturation of transferrin in normal, iron deficiency anaemia and hereditary haemochromatosis cases?

A

1) Normal 30%
2) IDA 15%
3) HHC 100%

25
Q

What is restrictive cardiomyopathy?

A

The walls of the ventricles become stuff, but not necessarily thickened.

26
Q

What is sideroblastic anaemia?

A

When erthrocytes take in iron but don’t transfer it into haem.