Wk 19 Flashcards
Nutrition, digestion, absorption and the bowel
Which digestive enzymes are in…
Saliva (2)=
Gastric juice (2)=
Pancreatic juice (3)=
Brush border enzymes (2)=
Saliva= amylase and lipase (carbs and fat)
Gastric juice= pepsin and lipase (proteins and fat)
Pancreatic juice= amylase, trypsin and lipase (carbs, proteins and fat)
BBE= glucose enzymes (maltase, lactase, etc), protein enzymes (peptidases)
Where are carbs digested?
Where are proteins digested?
Where are fats digested?
Carbs- Starting in the mouth and then continuing in the SI (proximal duodenum)
Proteins- Stomach (pepsin and HCl) and duodenum
Fats- little in the mouth and stomach but mostly in the SI (lipase and bile salts)
Fat sol vitamins=
Water sol vitamins=
D,E,A,K
B,C
What’s absorbed in the large intestine?
Water (because it follows sodium which is also absorbed)
Also certain vitamins produced by colonic bacteria (Vit K, Vit B12, Vit B1 [thiamine], and Vit B2 [riboflavin])
Relationship between motility and absorption=
inverse (decreasing motility leads to greater absorption)
Major hormones of digestion…
Cholecystokinin:
Gastrin:
Secretin:
Somatostatin:
Substance P:
VIP:
CCK: increases enzyme secretion and contraction
Gastrin: (acts on G cells in stomach) increases H+ secretion
Secretin: (acts on S cells in SI) increases bicarb secretion and decreases gastric acid secretion
Somatostatin: decreases all secretion (gastrin, fluid, bile) and increases contractions and fluid absorption
VIP: increase contractions, increase secretions in SI and pancreas
Consequences of malabsorption on GIT:
with extra info to read
Diarrhoea
- Impaired carb and electrolyte absorption (osmotic diarrhoea)
- Unabsorbed fats lead to irritation of mucosa
- Pale, bulky, frequent stools with foul odour
What are the macronutrients broken down into?
Carbs: (3 with examples)
Protein: 2
Fat: 2
Carbs: polysaccharides (starch/ fibre), oligosaccharides, disaccharides (sucrose, lactose, maltose), monosaccharides (glucose, fructose, galactose)
Protein: peptides, AA
Fat: glycerol and fatty acids
Consequences of inadequate carb intake=
carb= tissue wasting, metabolic acidosis (from excessive fat use for energy)
What are essential fatty acids?
What are the 2 main examples?
They can not be synthesized so must get them from diet (they are all polyunsaturated fats- multiple double bonds/inks)
Linoleic acid (omega 6 FA) and linolenic (omega 3 FA)
Consequences of inadequate fat intake= 2
Consequences of inadequate essential FA intake=
weight loss and heat loss
poor growth, skin lesions (eczema like) and depression
Consequences of inadequate protein intake=
Major weight loss, tissue wasting, growth retardation in children, anemia, oedema (due to deficits of plasma proteins)
*during preg= miscarriage or premature birth
Childhood protein-energy malnutrition
- What is Marasmus?
- What is Kwashiorkor?
Marasmus= wasting due to inadequate energy intake in all forms (proteins, carbs, fat), cachexia
Kwarshiorkor= protein starvation (big swollen belly-oedema) also muscle wasting and infections, skin pigmentation, heart failure
What are coenzymes?
They are organic (non-protein) compounds that activate their specific enzymes
What are the consequences of folate deficiency?
Anemia (because need folate for red blood cell division- deficient folate= megaloblastic anaemia), GI problems, spina bifida and neural tube defect risk in babies
What are the consequences of Vit B12 deficiency?
Where do you get it from?
megaloblastic anaemia (because required for formation of RBCs), degeneration of spinal cord, GI (glossitis, angular stomatitis, jaundice)
Animal products and anaerobic bacteria in gut
Consequences of vit C deficiency?
Scurvy (degeneration of skin, teeth, blood vessels- vit c is critical cofactor in collagen formation and without collagen= scurvy), weakness, delayed wound healing, impaired immunity, GI upset, kidney stone formation, gout
Consequences of vit A deficiency?
Night blindness, dry/ scaling skin, reproductive failure, increased infection (because immune disruption)
Vitamin D deficiency
Rickets (bone deformities) in kids, (osteomalacia) bone softening in adults, poor muscle tone, joint pain, more infections, cancer risk
Iron deficiency
anaemia, weakness, impaired immunity
Iodine deficiency
Goiter (enlarged thyroid), hypothyroidism (iodine essential for production of thyroid hormone)
Digestion of starch polysaccharides
First:
Halted:
2nd:
Last:
First salivary amylase- polysaccharides into short polysaccharides
Then amylase is inactivated by acid in stomach
Pancreatic amylase- digests polysaccharides into oligosaccharides (3-6 monosaccharides)
Small intstine- Oligosaccharides hydrolysed by disaccharidases into simple sugars
Glucose transport from intestinal lumen to inside intestinal cell to blood
What is the type of transporter that takes glucose from lumen into cell?
Lumen-> Cell= Symport (seconday active transport), the Na+ glucose cotransporter brings 2 Na and 1 glucose into the cell
(uses energy from electrochemical gradient of Na to transport glucose into cell against conc gradient)
Cell-> Blood= Uniport (facilitated diffusion)
(follows conc gradient (high to low) so no energy required)
Where are galactose ad fructose (both monosaccharides) converted to glucose?
Liver
Where does digestion of proteins begin? (how)
What are the pancreatic and intestinal enzymes in the SI that break down protein? (what do they do?)
Stomach (HCl denatures [uncoils] protein and Pepsin cleaves protein into smaller polypeptides)
Peptidases (cleave small polypeptides into AA, dipeptides and tripeptides)
AA absorption in the small intestine…
Into cell from lumen=
Into blood from cell=
How are peptides absorbed in SI?
(same as glucose)
Symport (secondary active transport) brings Na and AA into cell (uses conc gradient of Na)
Uniport (facilitated diffusion) exports AA from cell into blood (down AA conc grad so no energy required)
Peptides: (Has to be 4 AA or less to be absorbed and then converted to AA by peptidses inside cell)
- Get into cell from lumen via secondary active transport (co transport with H+, brings 1 H+ and 1 peptide inside cell)
- When converted to AA in cell, it leave cell and goes into blood via the uniport (facilitated diffusion)
Digestion of lipids…
Mouth:
Stomach:
SI:
Mouth: little bit from lipase
Stomach: little bit from lipase
SI: arival of lipids in duodenum promotes bile secretion from the gall bladder, this allows pancreatic and SI lipases to hydrolyze triglycerides into free FAs and monoglycerides (1 glycerol linked to 1 FA)
Process of triglycerides in lumen to chylomicrons in lymph:
Triglycerides–> bile salts and lipase convert TGs to FAs and monoglycerides
FAs and MGs enter cell and form triglycerides again
These triglycerides combine with cholesterol and apolipoproteins to form chylomicrons, which enter lymph
What is a chylomicron?
Biggest lipoprotein with the lowest density (due to high triglyceride count and low protein count)
Order of time it takes to digest proteins, fats and carbs:
Carbs are usually quickest to digest, followed by proteins and fat takes the longest
Absorption of fat sol vs water sol vitamins
Fat sol:
- what are they
- how are they absorbed
Water sol:
Fat sol:
- D,E,A,K
- require lipids in diet to be absorbed, carried by micelles, once in cell, packaged into chylomicrons and get into lymph and then blood
Water sol:
- B and C
- absorbed in the upper part of the SI (diffusion) directly into blood (except B12 because it is large and charged)
Absorption of B12:
Vit B12 binds to intrinsic factor (released by stomach parietal cells), forming a complex that resists digestion by GIT enzymes
Vit B12 intrinsic factor complex is absorbed (endocytosis) at the terminal ileum
Vit B12 transported around body by transcobalamin II
Stored mainly in liver (2-5 mg, 3 yrs)
Role of vit D in absorption of calcium in small intestine
Vit D (calcitriol) promotes synthesis of calbindin (Ca carrier protein) and Ca channels and extrusion pumps (active transport of calcium out of cell into blood)
Where in the SI is iron absorbed and by what cells
What form is the iron absorbed in?
What is the intracellular iron storage protein?
Duodenum
SI mucosal cells
ferrous Fe form
Ferritin
What is the difference between Autoimmunity vs Allergy?
Autoimmunity= results from an exaggerated (hypersensitive) response to ‘self’ antigen
Allergy= results from exaggerated (hypersensitive) response to harmless food allergen/ antigen
Define food allergy vs food intolerance…
Food allergy= occurs when an immune response is activated by otherwise harmless food antigen/ allergen
Food intolerance (non-allergic hypersensitivity)= occurs when the body has a non-immune response to eating a particular food or drink (does not cause anaphylaxis) - not detected by allergy testing
Difference between lactose intolerance and milk allergy…
Lactose intolerance= non-immune response to lactase (a sensitivity)
Milk allergy= immune response to milk protein (allergy)
How does food allergy occur?
milk protein allergy
Food allergens contact the intestinal mucosa (normally processed by GALT tissue and no allergy occurs) and if there are weakened tight junctions between epithelial cells, the allergen bypasses GALT tissue and leads to loss of tolerance, immune activation and ongoing tissue damage
(tight junctions are weakened by imaturity [babies], alcohol ingestion and inflammation in the gut epithelium from infection etc)
How does lactose intolerance occur?
If someone doesn’t have lactase, they can’t convert lactose into glucose and galactose so it travels further down the intestine and pulls water into the lumen (osmosis) and arrives in the large intestine still as lactose so colonic microbes try and break it down, producing FAs and gas (causes bloating, abdominal pain and gas)
What are DAMPs and what are PAMPs?
DAMPs= damage associated molecular patterns (tissue damage [penetrating trauma, blunt trauma, thermal injury and tissue damage] causes DAMPs to be released which triggers inflammatory response
PAMPs= infection triggers immune response when PAMPs are released
How does the immune system cause tissue damage?
DAMPs and PAMPs:
Pathogens:
DAMPs and PAMPs activate cells (complement–> neutrophils and monocytes) which activate pro-inflammatory cytokines
Pathogens cause tissue damage by direct mechanisms (endo/exotoxins and direct cytopathic effect) and indirect mechanisms (immune complexes, anti-host antibodyand cell-mediated immunity)
How does Coeliac Disease occur?
When gluten is partially digested, it forms gliadin, gliadin absorbed across mucosa, gliadin cross-links with tissue transglutaminase and this complex is detected as being antigenic, CD4 T cells are activated and anti transglutaminase antibodies (IgG) are formed
Immune reaction causes an inflammatory process, the mucosal villi become blunt/ flattered leading to malabsorption
What type of disease is Coeliac Disease?
TH1 Autoimmune disease (does NOT involve IgE or allergic response)
Definition of autoimmunity:
A misdirected immune response against host tissue
- Complex interaction between genetic susceptibility and environmental exposure (triggers)
Where are T cells ‘educated’?
Thymocytes (T cells) are positively and negatively (destroyed) selected in the thymus
-Negative T cells are those which strongly bind to MHC+ self peptides and are likely to trigger an autoimmune response
What is anergy?
Absence of the normal immune response without killing the immune cell (just inactivates it)
What does central tolerance do (B cells)
What does peripheral tolerance do (B cells)
Removes B cells that react to self antigens (receptor editing or decreased receptor expression and signalling [anergy] or apoptosis)
‘Somatic hypermutation’ which modifies their antigen receptor, also B cells that bind to self antigen are removed by apoptosis
What is the hygiene hypothesis?
States that the lack of early childhood exposure to
- Infectious agents
- Symbiotic microorganisms (such as gut microbes or probiotics)
Increases susceptibility to allergic and autoimmune diseases by interfering with the natural development of the immune system
