WEEK 5 Flashcards
(33 cards)
1
Q
GASTROINTESTINAL SYSTEM
A
- GI system responsible for breakdown of ingested food, preparing this matter for uptake by body, providing water and eliminating waste
- The organs are (in the order in which contents passes through them)
Mouth, Pharynx, Oesophagus, Stomach, Small intestine, Large intestine - Accessory organs vital to GI system function→ salivary glands, liver, gallbladder and pancreas
2
Q
DIGESTIVE FUNCTIONS
A
- Main digestive processes performed by the digestive system are:
- Ingestion of food (food enters the lumen of the GI tract, usually via the mouth)
- Propulsion of food and wastes from the mouth towards the anus
- Secretion of mucus, water and enzymes
- Mechanical digestion of food particles (physical breakdown of food into smaller particles)
- Chemical digestion of food particles (chemical breakdown of food into smaller particles)
- Absorption of digested food from the gastrointestinal tract into the bloodstream
- Elimination of waste products by defecation
3
Q
4 LAYERS OF THE GI TRACT: Serosa
A
Outermost layer of connective tissue that supports the tract
4
Q
4 LAYERS OF THE GI TRACT: Submucosa
A
Contains connective tissue and larger blood vessels as well as nerves and secretory glands
5
Q
4 LAYERS OF THE GI TRACT: Mucosa (Made up of 3 layers)
A
Mucous epithelium
- Simple columnar epithelium, lines the lumen and is therefore in direct contact with food
- Scattered amongst layer are goblet cells→ secrete mucus that lubricates during food passage
Lamina Propria
- Consists of connective tissue and provides capillaries to the epithelial layer
Muscularis Mucosae
- Contains smooth muscle and sometimes glands
6
Q
4 LAYERS OF THE GI TRACT: Muscularis (2 layers)
A
- Inner layer of muscle orientated around the circumference of the tract
- Outer layer of longitudinal muscle
7
Q
BILIRUBIN
A
- By product of broken down RBC→ haemoglobin in RBC breaks into haem and globin→ bilirubin product of haem breakdown
- Bound to albumin and transported to liver via bloodstream→ then released in bile by liver to intestine
- In intestine; processed by bacteria converting to urobilirubin (excreted in faeces; gives faeces brown colour)
- Bilirubin is a pigment; makes bile green/black, large amounts tinges skin and eyes yellow in jaundice
8
Q
COMMON SYMPTOMS OF GIS DISORDERS:
A
- Pain → location
- Loss of appetite/ vomiting
- Diarrhoea/ Constipation
- Maldigestion/ Malabsorption → malnutrition
9
Q
ACID ENVIRONMENT OF STOMACH
A
- pH = 2
- Activating pepsinogen
- Denatures proteins and kills bacteria
- Gastric mucosal barrier → Protective layer of mucus and bicarbonate
10
Q
GASTROESOPHAGEAL REFLUX (GERD) DESCRIPTION
A
- Reflux of chyme from the stomach into the oesophagus
- The oesophageal mucosa is repeatedly exposed to acids and enzymes (pepsin) in the chyme
11
Q
GASTROESOPHAGEAL REFLUX (GERD) CAUSE
A
- Increased abdominal pressure→ vomiting, coughing, lifting, bending
- Delayed gastric emptying→ peptic ulcers, narrowing of pyloric sphincter
12
Q
GASTROESOPHAGEAL REFLUX (GERD) DIAGNOSIS
A
- Heartburn→ important differentiating from other causes of chest pain (e.g. MI)
- Regurgitation of acid chyme
- Upper abdominal pain within 1 hour of eating
- Endoscopy
- Inflammatory responses
- Oedema, Tissue fragility, Erosion, Fibrosis and thickening may develop→ May develop into reflux esophagitis
13
Q
GASTROESOPHAGEAL REFLUX (GERD) TREATMENT
A
- Antacids to neutralise gastric contents (6 weeks)
- Smooth muscle stimulants to increase rate of gastric emptying
- Surgery may be necessary to narrow the gastroesophageal sphincter
14
Q
PEPTIC ULCER DISEASE
A
- Exposure to acid-pepsin secretions: a break or ulceration in the protective mucosal lining
- Superficial ulcers (erosion) erode only the mucosa
- True ulcers erode through the muscularis mucosae, or even deeper into submucosa or muscularis and can
- Damage blood vessels causing haemorrhage
- Perforate the gastrointestinal wall
- 2 common types: duodenal, gastric
Risk factors
- Long term use of NSAIDs (aspirin, ibuprofen)
- Helicobacter (H.) pylori infection of the gastric &/or duodenal mucosa- most common
- Alcohol or Smoking
- Traumatic events (e.g. burns, stroke)
15
Q
DUODENAL ULCERS: DESCRIPTION
A
- The most common type of peptic ulcer→ Most common in men and age group 20-50
- Primary defect: hypersecretion of acid & pepsin from the stomach
16
Q
DUODENAL ULCERS: CAUSES
A
- Infection with H. pylori, can be transmitted from person to person through close contact and exposure to vomit
- Long term use of NSAIDs
- Irregular meal pattern
17
Q
DUODENAL ULCERS: SYMPTOMS
A
- Chronic intermittent pain in the epigastric area
- Empty stomach pain: 2-3 hours after eating or in the middle of the night
- “Pain- food relief” pattern: ingestion of food antacids relieves the pain
- If asymptomatic, the first sign may be a haemorrhage or perforation
- Bleeding from duodenal ulcers causes haematemesis (brown) or melena (black stool)
- Often periods of remission followed by exacerbation
18
Q
DUODENAL ULCERS: TREATMENT
A
- Triple therapy
- Antibiotics to kill H. pylori
- Acid suppressors- proton inhibitors
- Stomach protectors
- H. pylori can be transmitted from person to person through close contact and exposure to vomit
19
Q
GASTRIC ULCERS (STOMACH ULCERS)
A
- Primary defect is the increased permeability of the gastric mucosa to hydrogen ions
- Occurs equally in males and females between 55-65
- Major causes are the same as duodenal ulcers
Symptoms
- Epigastric pain occurs immediately after eating
- Usually chronic
- Can progress to cancer
20
Q
THE PANCREAS
A
- Exocrine pancreas→ releases digestive juices through a duct→ to the duodenum
- Endocrine pancreas→ releases hormones into the blood
21
Q
ACUTE PANCREATITIS: DESCRIPTION
A
- Life threatening
- Common cause→ gallstone or beer BBQ (alcohol and fatty food)
- Sudden and severe inflammatory reaction
- Escape of activated pancreatic enzymes: autodigestion of the pancreas
22
Q
ACUTE PANCREATITIS: SYMPTOMS
A
- Severe pain: Upper left abdominal pain ; radiates to the back
- Inflammation→
- Fever, nausea and vomiting,
- Produces large volumes of exudate into abdominal cavity→ hypovolemia→ decreased BP
- Bleeding
- Damage to other organs: acute respiratory distress syndrome, acute renal failure, myocardial insufficiency→ multiple organ failure→ death
23
Q
ACUTE PANCREATITIS: TREATMENT
A
- ICU
- Pain relief (i.e. opiods, epidural analgesia)
- Fasting (including fluids) - putting the pancreas to rest
- IV fluids, electrolytes, colloid solutions, nutrition
- Antibiotics
24
Q
CHOLELITHIASIS (GALLSTONES)
A
- Formation of gallstones
- Abnormality in bile composition
- Cholesterol - most common
- Bile supersaturated with cholesterol forms microstones which aggregate
- Risk factors→ Obesity, middle age, female, starvation, skipping breakfast, rapid weight loss
25
CHOLECYSTITIS
- Inflammation of the gallbladder: cholecystitis- changed absorption characteristics→ excessive water absorption
Symptoms
- Asymptomatic
- Abdominal pain: upper right quadrant or epigastric area
- Radiates to the right shoulder, midscapular region, and upper back
- Often occurs after a fatty meal: intolerant to fatty food
- Belching
26
MALABSORPTION SYNDROMES: DESCRIPTION
- The failure of intestinal mucosa to absorb digested nutrients
- Most are a result of maldigestion rather than malabsorption
27
MALABSORPTION SYNDROMES: CAUSE
- Pancreatic insufficiency → Deficiency of pancreatic enzymes which are required for digestion of proteins, carbohydrates and fats
28
MALABSORPTION SYNDROMES: BILE SALT DEFICIENCY
- Bile salts are necessary for emulsification of fats
- Conditions that decrease production and secretion of bile result in fat malabsorption
- Advanced liver disease
- Obstruction of the common bile duct
- Intestinal stasis that prevents bile reabsorption
29
MALABSORPTION SYNDROMES: STEATORRHOEA; INCREASED FAT IN THE STOOL
- Excess fat drags fluids, electrolytes and proteins with it into the stool
- Bulky extremely foul smelling stools as colon bacteria digest the extra food source
30
MALABSORPTION SYNDROMES: DECREASED LIPID ABSORPTION
- Decreased absorption of fat soluble vitamins and cholesterol
- Vit A deficiency- night blindness
- Vit D deficiency→ decreased Ca++ absorption (osteoporosis, bone pain)
- Vit E deficiency→ slow healing, nerve damage
- Vit K deficiency→ easy bruising, decreased clotting
- Decreased cholesterol, decreased steroid hormone synthesis
31
VOMITING
- Protective mechanism
- A net blood loss of H20: dehydration
- Hypovolemia (low plasma in blood volume)
- A decrease in BP and blood perfusion in the tissues
- A decrease in O2 and other nutrient delivery to cells
- A decrease in the removal of CO2 and other wastes from cells
- Nerve cells first to be affected by the lack of O2 and the build up of wastes→ Inattention, drowsiness, coma
- Eventually all cells are affected
A net blood loss of acid (H+)
A blood accumulation of HCO3→ acidosis
- Nerve function is the first affected
- Decrease in enzyme function
- Eventually all cell function is compromised leading to death
32
CONSTIPATION
- The GIT flow rate decreases
- Increased contact time of the contents with the lumen of the colon→ increased absorption of water and ions→ hard stools
- Insufficient intake of fibre or water retaining substances
- Weakness of the abdominal muscles: inactivity and bed rest, pregnancy
- Decreased parasympathetic nervous system stimulation
- Treatment→ relieving the cause→ laxatives and enemas (should not be used at a regular base)
33
DIARRHOEA
- Excessively frequent passage of stools- acute or chronic (>3 weeks in children, 4 weeks in adults)
- Large volumes→ painless, water type
- Small volume→ colicky pain, urgency
- GIT mobility may be increased by:
- Osmotic effect of luminal contents (i.e. increased water- retaining substances→ excess fats, salts, dried fruits etc)
- Irritants in food, inflammation, microbial growth, or toxins from bacteria
