13. Gut flux and motility Flashcards
primary peristaltic wave
forces the bolus down the esophagus and into the stomach
wave lasts about 8–9 seconds
secondary peristaltic wave
In the event that the bolus gets stuck
a secondary peristaltic wave occurs
forces the bolus further down the esophagus
waves continues until the bolus enters the stomach
What part of the brain controls the process of peristalsis?
medulla oblongata
5 Functions of the Fundus (Proximal stomach)
1) Gastro duodenal flow
2) Intragastric pressure
3) Temporary storage
4) Tonic motor activity
3) Stimulates propulsion
What % of body weight does the pancreas represent
0.1%
How may enzymes does the pancreas release?
15 digestive enzymes
4 Functions of the small bowel
Lymphoid tissue
Absorption
Immune function
Digestion
Where is Lymphoid Tissue concentrated
Terminal ileum
Tonsils
3 Functions of the large bowel
Salvage of water and electrolytes
Absorption of undigested carbohydrates
Secretion of mucus
How is the small bowel adapted for Immune function?
MALT (GALT) made up of B and T cells
Peyer’s patches (discrete clusters of immune cells)
Secretory IgA
How is the small bowel adapted for Absorption
Microvilli = large S.A
Motility = allows contact of contents with absorptive surfaces
Where is majority of iron absorbed?
Duodenum
Where is majority of folate absorbed?
Jejunum
Where is majority of B12 absorbed?
Ileum
Where does majority of water absorption occur?
ascending and transverse colon
What 4 factors determine Fluid Absorption?
Luminal Osmolarity
Motility
Mucosal Integrity
S.A
Oral intake of fluid a day
2L
Biliary fluid entering a day
0.5L
Pancreatic fluid entering a day
1L
Intestinal fluid entering a day
1L
Gastric fluid entering a day
2.5L
Salivary fluid entering a day
1.5L
Fluid reabsorbed in to small intestine a day
7L
Fluid reabsorbed in to large intestine a day
1.4L
Treatment of FH (Familial Hypercholesterolaemia)
statins
Classification of hyperlipidaemias
Fredrickson/WHO (1970)
Type I Increased CMs
Type IIa Increased LDL
Type IIb Increased LDL and VLDL
Type III Increased Remnants and IDL
Type IV Increased VLDL
Type V Increased Chylomicrons and VLDL
Familial Type III Hyperlipidaemia
Mechanism: defective remnant clearance
Prevalence: 1 in 5000
Inheritance: autosomal recessive
Physical Signs: striate palmar and tuberoeruptive xanthomata
Familial Hypercholesterolaemia
Mechanism: LDL Receptor defect
Prevalence: 1 in 500
Inheritance: Autosomal dominant
Physical Signs: Tendon Xanthomata, corneal arcus
Familial Combined Hyperlipidaemia
Mechanism: overproduction of VLDL and apoB
Physical Signs: variable, Xanthelasmata
Prevalence: 1 in 100
Inheritance: variable, some autosomal dominant
Familial Hypertriglyceridaemia
Physical Signs: prone to pancreatitis and diabetes mellitus
Prevalence: 1 in 300
Inheritance: variable
post MI treatment
atorvastatin 80mg
Statins mode of action
inhibit cholesterol synthesis
increase hepatic LDL receptor activity
Fibrates mode of action
activate PPAR alpha
↑ LPL activity
↑ biliary cholesterol secretion
Bile Acid Binding Resins mode of action
divert cholesterol into bile acid synthesis
interrupt enterohepatic circulation of bile acids
↑ hepatic LDL receptor activity
Cholesterol Absorption Inhibitors mode of action
reduce enterohepatic cholesterol recycling
PCSK9 Inhibitors mode of action
antibodies to PCSK9
advantages of statins
potent
mostly well tolerated
single (nightly) dose
disadvantages of statins
muscle toxicity
hepatic toxicity
may aggravate liver disorder
advantages of fibrates
potent
mostly well tolerated
quite cheap
disadvantages of fibrates
muscle toxicity
↑ incidence of gallstones
potential for toxic interactions
ezetimibe
used to treat hypercholesterolaemia
used for patients intolerant to statins
management of abdominal pain
NG tube
Oxygen therapy
Proton pump inhibitors
IV fluids
Likelihood of colorectal cancer in Ascending colon
30%
Colorectal cancer
Right Sided Lesion
Present later
Less likely to cause diarrhoea
May give rise to iron deficiency anaemia
Colorectal cancer
Left Sided Lesion
Present earlier
More likely to cause a change in bowel habit
More likely to obstruct
How do you diagnose colorectal cancers?
Blood tests
Examination and History
Radiology
Tissue diagnosis
Pancreas protein producing capacity
13x protein producing capacity of liver
Likelihood of colorectal cancer in Transverse colon
10%
Likelihood of colorectal cancer in Descending colon
15%
Likelihood of colorectal cancer in Sigmoid colon
25%
Likelihood of colorectal cancer in Rectum
20%
