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Food and Nutrition Module > Week 1 > Flashcards

Week 1 Flashcards

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1
Q

what does serotonin do?

A

it activates sensory afferent neurons of the myenteric plexus but 2) it also inhibits its own production from the epithelium. Otherwise we will have continuous peristaltic movements even without food.

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2
Q

Excitatory motor neurons

A

release Acetylcholine (Ach) & Substance P (P)

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3
Q

Inhibitory motor neurons

A

release Nitric Oxide (NO) & Vasoactive Intestinal peptide (VIP).

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4
Q

what happens in the propulsive segment

A

interneurons activate the excitatory neurons for the circular muscles (contraction) but inhibit the excitatory neurons for the longitudinal muscles. Interneurons also activate the inhibitory neurons for the longitudinal muscles (relaxation

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5
Q

what happens in the recieving segment

A

interneurons inhibits the excitatory neurons for the circular muscle and activate the inhibitory neurons (relaxation). Interneurons activate the excitatory neurons for the longitudinal muscles and inhibits the inhibitory neurons (contraction).

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6
Q

what are the differences in the stomach

A

mucosa does not have an epithelium organized in villi, but is made of gastric pits or gastric glands where specialized cells can be found.

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7
Q

what are the main organs

A

Mouth
Esophagus
Stomach
Small intestine: Duodenum (stomach exit); Jejunum; Ileum
Large intestine: Cecum; Ascending Colon; Transverse Colon; Descending Colon; Rectum; Anus

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8
Q

what is the anatomy of the esophaegus

A

The esophageal Muscularis propria has 2 types of muscles: striated and smooth (unlike the rest of the GI tract).

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9
Q

where is lactase located and what does it do

A

small intestine

used to digest lactose

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10
Q

what are the types of transporters involved in carbohydrate absorption

A

GLuT - 1 to 12

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11
Q

what does food intolerances cause

A

gas, bloating, cramping and diarrhoea

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12
Q

Immune Mediated examples

A

oral allergy and acute uriticaria
coeliac disease
contact dermatitis

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13
Q

Non-Medicated

A

lactose intolerance
caffieine
sulphites

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14
Q

explain how lactose intolerance works

A

Lactose transits undigested into the large intestine
Gut bacteria metabolise lactose and the resulting fermentation produces gas (carbon dioxide, hydrogen and methane) which may result in flatulence, bloating and distension pain.
The unabsorbed lactose and the fermentation products (e.g., short fatty acids) raise the osmotic pressure in the colon.
This increases the flow of water into the lumen of the colon, causing “osmotic diarrhoea” associated with lactose intolerance.

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15
Q

Congenital alactasia

A

automosal recessive mutation in the LCT gene causing the complete lack of lactase from birth. Infants with this mutation cannot be breastfed or given milk, and have to be fed with soybean-derived formulas.

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16
Q

difference between primary and secondary

A

primary is genetically inherited caused by lack of persistent allele and secondary is caused by the damage to the lining of the intestine where lactase is produced.

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17
Q

hypolactasia

A

occurs in adulthood

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18
Q

types of test

A

Hydrogen breath test

Lactose tolerance

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19
Q

Type I hypersensitivity

A

immunoglobulin E (IgE) antibody against soluble antigen, triggering mast cell degranulation.

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20
Q

Type II hypersensitivity

A

IgG and IgM antibodies directed against cellular antigens, leading to cell damage mediated by other immune system effectors.

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21
Q

Type III hypersensitivity

A

interactions of IgG, IgM, and, occasionally, IgA antibodies with antigen to form immune complexes. Accumulation of immune complexes in tissue leads to tissue damage mediated by other immune system effectors.

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22
Q

Type IV hypersensitivity

A

T-cell–mediated reactions that can involve tissue damage mediated by activated macrophages and cytotoxic T cells.

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23
Q

Imunoglobin is an antibody what happens there

A

The Fragment crystallizable (Fc) region of the antibody is formed by the two heavy chains coming together, usually linked by disulfide bonds. The Fc portion is important as many immune cells have Fc receptors. These receptors can then bind to antibody-coated pathogens.
At the other end of the Ig are two identical antigen-binding sites.

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24
Q

difference between IgE and IgG

A

IgE is typically the least abundant isotype whilst IgG is the most abundant isotype.
IgE is associated with type I allergic reactions and binds to Fc receptors on mast cells and basophils.

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25
Q

what does histamine do

A

Histamine stimulates mucus secretion in nasal passages and tear formation from lacrimal glands, promoting the runny nose and watery eyes of allergies.

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26
Q

food allergy and intolerance difference

A

allergy is in the GI tract and the immune system and the symptoms will appear on the skin
intolerances are more internal so like stools gas wheezing

27
Q

when activated what are ig e cells made up of

A

b cells

28
Q

ige cells are created in what

A

type 1 allergic reaction

29
Q

primary exposure for example peanuts

A 
the food is incorrectly ingested 
the allergen is taken in 
proccesed by antigen presenting cells 
presents the antigen to TH2 lymphocytes
TH2 releases cytokines IL4 and IL3 which activates the B cells 
B cells undergo clonial expression
IgE specific is produced
Fragment crystalizable regions of IGE bind s to the receptors 
presented on mast cells
30
Q

secondary exposure how does it work

A

allergen binds to the igE molecules binds to many mast cells which cross linking the IgE molecules
Mast cells activates and triggers degranulation where histamine seratonin which are tumour necrosis factors are released, can cause anaphylaxis

31
Q

cross activity

A

those allergic to radweed may be sensitive and could possibly react to honeydew peach and apples

32
Q

what does fodmap stand for and what are they

A

Fermentable, Oligo-, Di-, Mono-saccharides and Polyols (FODMAPs) are short chain carbohydrates that are poorly absorbed in the small intestine.
Oligo-saccharides: e.g. fructans (found in wheat, rye and some vegetables) and galacto-oligosaccharides (found in pulses and legumes)
Di-saccharides: e.g. lactose (found in mammalian milk)
Mono-saccharides: e.g. free fructose (found in honey, some fruit and fruit juices)
Polyols: e.g. sorbitol and mannitol (found in some fruits and vegetables)

33
Q

stages of fodmap

A

3

34
Q

stage 1 of fodmap

A

an individual reduces their FODMAP intake by avoiding foods that are high in FODMAPs for 4 to 8 weeks as this period is considered long enough to identify if symptoms will respond to a low FODMAP diet.

35
Q

stage 2 of fodmap

A

If the individual’s symptoms have improved following FODMAP restriction, it is important to reintroduce some high FODMAP foods. This will enable them to identify which FODMAPs they are most sensitive to, as well as how much of a high FODMAP food triggers their symptoms.

36
Q

stage 3 of fodmap

A

Stage 3 Personalisation : The long term aim of a low FODMAP diet is to personalise their diet so they only avoid foods that trigger their symptoms and enable them return to as normal a diet as possible.

37
Q

irritable bowl syndrome what can help it

A

low fodmap

38
Q

food intolerance tests

A

IgG tested

39
Q

bile salts are what

A

both hydrophilic and hydrophobic

40
Q

where is bile made

A

in the gall bladder and is released into the duodenum

41
Q

what is emulsification

A

fat globules broken down into little droplets to make digestion easier

42
Q

what is micelles

A

small droplets of fat surrounding the bile

43
Q

what doesn’t need to be enzymatically digested

A

cholesterol and fat-soluble vitamins

44
Q

types of lipase

A

lingual lipase
gastrial lipase made in the stomach
lingual lipase made as food is chewed and swallowed.

45
Q

what happens in the digestion phase

A

pancreatic lipase is a water soluble molecule
synthesised by pancreatic acinar cells
intestinal lumen breaks down the bonds between the 1- 3 triglycerides
leaving 2 monoglyceride and two free fatty acids
the emulsification of lipids by the bile anions create a large surface
for lipids to act on
fatty acids 2 monoglycerides with phospoholipids and cholestrol make micelles
bile salts emulsify to make more micelles

46
Q

SCFA’s what are they and what do they produce

A

used by the liver and colonial cells

and acetate, propionate, and butyrate are produced

47
Q

what is butyrate

A

it is the main source of energy for human colonocytes

intestinal production of glucose

48
Q

what is butyrate essential for

A

its essential for epithelial cells to get oxidation through b oxidation which is when fatty acids can get to atp
which allows more atp production
prevents gut microbiota dysbiosis.

49
Q

what does propionate do

A

regulates gluconeogenesis and satiety signalling through interaction with the gut fatty acid receptors.

50
Q

what does acetate do

A

reaches the peripheral tissues where it is used in cholesterol metabolism and lipogenesis, and may play a role in central appetite regulation.

51
Q

how is glucose absorbed

A

Glucose is co-transported with Na+ ions
into the cells on a co-transporter SGLUT1.
Once in the cell, glucose exits to the interstitial fluid down its concentration gradient via GLUT2 one of the family of glucose transporters.
GLUT2 transports glucose out of the cell into the portal circulation, going to the liver.
The Na+ that entered with the glucose is actively pumped out of the cell into the interstitial fluid by Na+/K+ATPase, thus maintaining the Na+ gradient (which is necessary for Na+ to enter the enterocyte in the first place).

52
Q

how is fructose and galactose absorbed

A

Galactose is transported into the enterocytes via SGLT1

Fructose is transported into the enterocytes by facilitated diffusion via GLUT5, another member of the glucose transporters.

Both Galactose and Fructose exit the enterocytes via GLUT2.

53
Q

what do gut microbials do

A

Gut microbial enzymes leads to contribute to bile acid metabolism, generating unconjugated and secondary bile acids that act as signalling molecules and metabolic regulators to influence important host pathways.

54
Q

what is a chylomicron

A

large lipoprotein that enters the lymphatic system before being released into the bloodstream which transport them to various destinations including the liver

55
Q

what is an VLDL

A

Very low-density lipoproteins are made in the liver from remnants of chylomicrons and transport triglycerides from the liver to various tissues in the body.

56
Q

how is cholesterol absorbed

A

poorly absorbed when compared to phospholipids and triglycerides. Cholesterol absorption is aided by an increase in dietary fat components and is hindered by high fiber content. This is the reason that a high intake of fiber is recommended to decrease blood cholesterol. Foods high in fiber such as fresh fruits, vegetables, and oats can bind bile salts and cholesterol, preventing their absorption and carrying them out of the colon

57
Q

how is protein absorbed

A

Gastric and pancreatic enzymes hydrolyze protein to short-chain peptides (up to 6 residues long), which are further hydrolyzed at the brush border to free amino acids or to di-or tri-peptides.
The different amino acids resulting from protein digestion are absorbed by different types of carriers coupled to the active transport of Na+.
Dipeptides or tripeptides are also actively absorbed and then digested to their amino acids within the epithelial cells.
Amino acids leave the cell across the basolateral membrane either by simple diffusion or by carrier-mediated processes.

58
Q

functions of the urinary tract

A

excrete wastes
regulating water absorbpion
regualting sodium consumption
vitamin synthesis

59
Q

what does the kidney do

A

they get rid of waste products
they keep the electrolytes
they secrete hormones

60
Q

examples of hormones in the kidney

A

renin which keep blood pressure

61
Q

what is the anatomy of kidneys

A

The structure of the kidney is divided into two principle regions: the peripheral rim of cortex and the central
medulla
The two kidneys receive about 20 percent of cardiac output.
The renal arteries arise directly from the aorta, and the renal veins drain directly into the inferior vena cava.
Kidney function is derived from the actions of about 1 million nephrons per kidney; these are the “functional units.”
A capillary bed called the glomerulus, filters blood and the filtrate is captured by Bowman’s capsule.
A portal system is formed when the blood flows through a second capillary bed surrounding the proximal and
distal convoluted tubules and the loop of Henle. Most water and solutes are recovered by this second capillary bed.
This filtrate is processed and finally gathered by collecting ducts that drain into the minor calyces, which merge to
form major calyces; the filtrate then proceeds to the renal pelvis and finally the ureters.

62
Q

what are LDLs , how are they produced and what do they do

aka bad cholesterol

A

low density lipoproteins

carry cholesterol and other lipids from the liver to tissue throughout the body.

63
Q

what are LDLs , how are they produced and what do they do

aka bad cholesterol

A

low density lipoproteins

carry cholesterol and other lipids from the liver to tissue throughout the body.

64
Q

what is steaorrheoa

A

when lipids arent absorbed

Food and Nutrition Module (5 decks)

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