CCP: Digestion and Absorption of Biomolecules Flashcards
1
Q
pneumatosis intestinalis
A
- accumulation of gas in intestinal mucosa from bacteria production as a biproduct of metabolism.
- in some cases the gas can perforate the intestines and move into body cavity
2
Q
Clinical presentation: necrotizing enterocolitis (NEC)
A
- necrotize = dirty form of cell death
- enterocolitis = inflammation of colon
Clinical presentation:
- bloody stool
- distended abdomen
- radiograph of pneumatosis intestinalis
- high mortality
3
Q
risk factors of NEC
A
- Prematurity (low birth weight)
- Diseases that would cause intestinal ischemia
- Bacterial Colonization
- Enteral feeding (Milk and Formula)
4
Q
Pathology of NEC
A
- Typically involves terminal illeum, cecum and right colon
- Involved segments can be distended, congested or gangrenous
- Microscopically there is mucosal or transmural coagulative necrosis, ulceration and/or submucosal gas bubbles
- Toll Like Receptors perhaps are involved in the pathophysiology: likely that this disease is an accumulation of many factors
5
Q
Necrosis
A
- result of an irreversible cell injury
- due to ischemia: ischemia could be due to immaturity of cardiovascular system.
- decreased ox phos = decreased ATP = increased lactic acid and decreased pH and protein synthesis = ultimately inhibits cellular functions of Na+/K+ ATPase and results in cellular swelling, resulting in necrosis.
- consequences of mitochondrial dysfunction can be necrosis and apoptosis
6
Q
What occurs in NEC? Pathogenesis
A
- insult like ischemia and hypoxia along with bacterial invasion of gut. result should be lymph stimulation within gut, however this response does not occur properly b/c infant is preterm.
- They have decreased ability to produce gastric acid, mucous (mucin is produced which forms barrier), have decreased peristalsis, decreased IgA in this area, decreased T cell immunity response, tight junctions are not fully mature.
- All of these together with increased inflammation due to existing immune response and macrophage infiltration will result in NO synthase and free radical production, which leads to enterocyte apoptosis or necrosis
7
Q
Tight junctions
A
- important intestinal barriers. should not be permeable to bacteria, however in preterm infant, it is not mature and bacteria can pass through.
- inflammation can make tight junctions more permeable to bacteria.
8
Q
Crypt Paneth cells
A
- specialized enterocytes which secrete intestinal defensins such as lysozymes and antimicrobial peptides.
- these cells aren’t as active in preterm infants
- the unstirred water layer is penetrated with bacteria, they adhere to cells and inflammatory responses will ensue
9
Q
MAMPs(microbial-associated molecular patterns) and TLRs (Toll-like receptors)
A
- TLR expression is inducible and is thought that some are expressed on apical side of enterocytes. most are expressed on the basolateral side to show if bacteria have penetrated monolayer.
- these receptors may play a role in NEC. The TLR’s detect microbial patterns (MAMPs) and can ultimately leading to apoptosis of the cell when bound.
10
Q
what are consequences of markedly decreased amount of small bowel?
A
secretion decreased: pancreatic secretion, bile, bicarb.
absorption decreased: water, na, k, cl
- these profiles would be changed…..
10
Q
Duodenum/Proximal Jejunum: ions absorbed?
A
- Na+ absorption:
1. via nutrient coupled Na+ transport (most important after meal, electrogenic, cause Cl- transport)
2. Na-H exchanger - Passive Cl- Absorption driven by voltage dependent manner
- Cl- secretion occurs through CFTR throughout entire small and large intestine
10
Q
Duodenum/Proximal Jejunum: food/nutrients?
A
- duodenum is VERY important in biomolecule absorption
- Carbs, proteins, lipids absorption greates in duodenum
- Ca2+ throughout entire small intesine
- Iron and Folate exclusively absorbed in duodenum
- A, D, K (fat soluble) vitamins absorbed here
- lipid digestion
- Duodenum also plays role in mixing and receiving of bile and pancreatic enzymes. Allows for micellar solubilization via pancreatic secretions of Pancreatic Lipase. If don’t have duodenum, would have limited fat absorption.
- gastrointestinal hormones are also released here
10
Q
Consequences of Loss of Duodenum and Proximal Jejunum?
A
- Absence of micellar solubilization may affect normal digestion.
Patient must be closely monitored for:
Na+, H2O, Fat-soluble vitamins, Ca2+, Mg2+, PO4-, Fe3+
- effects lipids: will see lipids in stool, will see bacterial fermentation of these products in intestines.
10
Q
Ileum: ions?
A
- Na+ absorption: via Parallel Na-H and Cl-HCO3- exchangers
- Cl- absorptions: via Cl-HCO3- exchanger (electroneutral) and parallel exchangers
- Passive K+ absorption
10
Q
Ileum: foods?
A
- Little carbs, proteins, lipids absorbed here
- Ca2+ is absorbed throughout entirety of small intesine
- iron and folate, not absortbed here
- bile salts active abosrption occurs here. WOULD HAVE LIMITED BILE SALT ABSORPTION
- COBALAMIN ABSORPTION HAPPENS HERE
