GI tract Flashcards

1
Q

List the components of GI tract

A

Mouth

Oesophagus

Stomach

Small intestine

Large intestine/colon

Rectum and anus

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2
Q

Describe the oesophagus and small intestine.

For the small intestine, mention
• Role
• Structure
• Processes involved in absorption

A

Oesophagus:
• Directs food to stomach
• Lubricates food and passageways

Small intestine:
• Principal site breaking down, digesting and absorbing food
• Numerous projections called microvilli = large surface area = maximises efficiency
• Absorption: occurs through the process of diffusion, active transport and endocytosis

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3
Q
Describe the stomach. Discuss:
• Mucus 
• HCl
• Pepsin
• Substances that interrupt the mucosal barrier
A
  • Mucus: Innermost layer or lining. It contains the glands that release digestive juices, hydrochloric acid and pepsin.
  • Secretes gastric juice to aid in the liquefaction of food
  • HCl: pH ~0.87. Kills bacteria, aids protein digestion, provides the pH for the activity of pepsin, stimulates the flow of bile and pancreatic juices
  • Pepsin: Glands in the mucous-membrane lining of the stomach make and store an inactive protein called pepsinogen. Impulses from the vagus nerveand the hormonal secretions ofgastrin stimulates the release of pepsinogen into the stomach, where it is mixed withHCl and rapidly converted to the active enzyme pepsin. Pepsin helps digest proteins
  • Substances which tend to disrupt the barrier: ethanol, bile acids and NSAIDS
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4
Q
Describe the large intestine 
Discuss: 
• The role of bacteria in the intestine 
• The roles of vitamin K, biotin/ vit B7 and vitamin B5 
• Patterns of motility
A
  • NO villi
  • Reabsorbs water and electrolytes (small intestine)
  • Here, intestinal contents are liquid but are solid (stool) by the time they reach the rectum
  • Bacteria in the large intestine can further digest some material, creatinggas
  • These bacteria also produce vitamin K (required for clotting), biotin/ vit B7 (glucose metabolism) and vitamin B5 (steroid hormones)

Motility patterns:
• Segmentation
• Antiperistalsis: reversed peristaltic action of the intestines, by which their contents are carried upward (precursor to vomiting)
• Mass movement: propels semi-solid feces into the distal colon (large intestine) and then into the rectum and anal canal

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5
Q

List the accessory organs of the GI tract

A
Involved in grinding food or providing digestive secretions. They include:
• Teeth and tongue
• Salivary glands 
• Liver
• Gallbladder
• Pancreas
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6
Q

Briefly explain the exocrine pancreas

A

• Makes digestive juices, especially HCO3 (bicarbonate)

Makes enzymes:
• Amylase: carbohydrates
• Lipase: lipids/ fats
• Phospholipase: phospholipids
• Cholesterol estarase
• Trypsin/ Chymotripsin: proteins and peptides
• Carboxypeptidase: peptides and amino acids

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7
Q

Briefly explain the role of the liver (and the bile)

A
  • Bileis a fluid that helps with digestion. It is released by the liver but stored in the gallbladder
  • The liver is also involved in protein synthesis (albumin, prothrombin, lipoprotein)
  • Clotting factors
  • Metabolises carbs, proteins and lipids
  • Responsible for hormone synthesis and metabolism
  • Help detoxify drugs and toxins
  • Provides immune defence against agents entering the portal circulation
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8
Q

Discuss bile in terms of pigments, jaundice and salts

A

• Pigments: bilirubin, which is orange or yellow (comes from dead red blood cells) and its oxidized form biliverdin, which is green

Jaundice:
• Jaundice is caused by a build- up ofbilirubin
• Caused by an inflamed liver or obstructed bile duct = excess bile

Bile salts
• Bile salts in bile increase the absorption of fats
• Bile saltshave a pH range of about 7-8. This activates lipasein the small intestine
• If bile salts are not present, then people will experience greasy stool

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9
Q

List other causes of jaundice

A
  • Haemolytic anaemia (excessive destruction of red blood cells)
  • Decreased hepatic uptake of bilirubin
  • Altered intracellular binding or conjugation
  • Decreased secretion of pigments into the bile
  • Intra or extrahepatic biliary obstruction
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10
Q

Outline the four basic processes of the GI system

A
  1. Motility: Movement and mixing of food throughout the tract
  2. Secretion: Of gastric juices that aid in digestion and absorption
  3. Digestion: Food is broken down into absorbable molecules. This can be done through enzymatic and mechanical processes
  4. Absorption: Nutrients, electrolytes and water are absorbed
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11
Q

Describe the different patterns of GI motility

A

Peristalsis
• Occurs in oesophagus, stomach, small intestine and large intestine
• Propels GI contents in one direction towards the anus
• Movements occur through muscle contractions behind the bolus, pushing it anally

Segmentation
• Occurs mainly in small intestine
• Cyclic contractions of the muscle which force the chyme (food bolus) to slosh back and forth for short distances

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12
Q

Describe the three phases of digestion and absorption

A
  1. Cephalic phase: Occurs before food enters the stomach, especially while food is being eaten. It results from the sight, smell, thought, or taste of food, stimulating the vagus nerve -> releases some stomach chemicals like pepsin and HCl
  2. Gastric phase: The gastric phase is a period in which swallowed food activates gastric activity in the stomach.
    Ingested food stimulates gastric activity in two ways: stretching the stomach and by raising the pH of its contents.
    Mechanical and chemoreceptors are prompted to release more gastrin, pepsin and HCl. This process is very fast.
  3. Intestinal phase: Begins when chyme enters the small intestine. This phase controls the rate of gastric emptying and it moderates gastric activity via hormones and nervous reflexes. The duodenum initially enhances gastric secretion, but soon inhibits it.
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13
Q

Understand the integrated mechanisms that regulate GI function

A

Extrinsic (long pathway):
• Sympathetic and parasympathetic innervation (vagus nerve for stomach)
• When a stimulus is present, chemoreceptors, mechanoreceptors will send signals in the form of emotions, sight, taste and smell to the CNS -> ANS -> ENS -> Informs endocrine cells to release hormones -> effect on smooth muscles cells -> response = changes in motility or secretory activity

Intrinsic: Enteric Nervous system (ENS)
• The GI system has it’s own nervous system
• The GI tract can act on its own without having to send information to the spinal cord or brain
• Contained within the walls of the GI
• When a stimulus is present, chemoreceptors, mechanoreceptors will send signals to the ENS -> Informs endocrine cells to release hormones -> effect on smooth muscles cells -> response = changes in motility or secretory activity

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14
Q

Describe a peptic ulcer, it’s cause and its Tx

A
  • Peptic ulcersare sores that develop in the lining of thestomach, lower esophagus, or small intestine
  • Is an inflammatory reaction to the bacteria H. pylori OR from erosion fromstomachacids
  • Tx: antibiotics + gastric histamine H2 receptor blocker / cholinergic M1 receptors blocker/ H-K-ATPase inhibitors (work by blocking histamine, a signalling chemical for the stomach to produce acid)
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15
Q

Define bowel cancer and risk factors for it

A
  • A malignant growth that develops most commonly in the lining of the large bowel
  • Risk factors: Age, genetics, smoking, obesity
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16
Q

Define inflammatory bowel disease and symptoms

A
  • Ulcerative colitis: Affect large intestine
  • Crohn’s disease: Any part of the intestines
  • Symptoms: Abdominal cramps and pain, frequent watery diarrhoea, weight loss, tiredness, fatigue
17
Q

Describe Gastroesophageal Reflux disease and its risk factors

A
  • Gastroesophageal reflux GER: when stomach contents come back up into the esophagus causing heartburn
  • Gastroesophageal Reflux Disease GERD. A condition that develops when the reflux of stomach contents causes troublesome symptoms/complications

Risk factors:
• Lower oesophageal sphincter incompetence (alcohol, nicotine, caffeine, medication)
• Increased intra-abdominal pressure (obesity, pregnancy)
• Increased gastric volume (heavy meals, intestinal obstruction)

18
Q

List oral manifestations of malabsorption

A
  • Prone to infections
  • Angular cheilitis
  • Poor wound healing
  • Atrophic glossitis
  • Burning mouth syndrome
  • Aphthous ulceration
19
Q

List oral manifestations of IBD

A
  • Cobblestone appearance with hyperplastic mucosal folds
  • Swelling
  • Fissured tongue
  • Angular cheilitis
  • Glossitis
  • Peripheral erythema
20
Q

List oral manifestations of GERD

A
  • Dental erosion
  • Chalky/frosted enamel
  • Dentin hypersensitivity
  • Slight rounded cusps – flattening of occlusal surface morphology

DDX: chronic alcoholism, eating disorders (vomiting) etc