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GDAN year 2 nutrition > GIT tract 2 > Flashcards

GIT tract 2 Flashcards

1
Q

what does the stomach act as

A

1) reservoir
- store food
2) preparatory chamber
- breakdown ingested materials
3) emptying regulator
- responds to feedback from duodenum
- controls rate of release of calorie (energy), H+ (acid) and particles in the duodenum (1st part of intestine)

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2
Q

stomach motlilty after a meal steps

A

1) Fasting state quiescent
2) meal enters stomach
- LOS relaxes – relaxation of fundus and body
- i.e. accommodation
3) Peristalsis begins
- begins in the middle – push towards the pylorus
- mixing occurs in the antrum
4) Retropulsion
- wave pushing material in one direction
- peristaltic wave pushing the other way
- squashed in both ways – creates chyme
- push through pyloric sphincter
5) Antral systole
- peristaltic wave pushes contents back into body
- some chyme into duodenum

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3
Q

control of motility steeps

A

1) Cephalic phase
- sight, thought, smell of food
- parasympathetic activation increases motility and stimulates secretion of acids, mucus and enzymes
2) Gastric phase
- food causes peristalsis and release of gastrin in stomach
- which increases moltity and secretion
3) Interstinal phase
- arrival of food in duodenum triggers release …
- CCK, GIP, Secretin are acting to reduce the effect of gastrin to regulate amount of material entering the small intestine
- feedback loop to regulate delivery of chyme

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4
Q

rate of gastric emptying for liquids and solids

A

1) Liquids
- empty faster than solids
- 2-3m
2) solids
- lag due to time to reduce particle size 1mm diameter
- has to be broken down into smaller size intestine can accommodate
Emptying phase is the release from the stomach to intestine

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5
Q

ulcers

A

break in mucosal barrier
- exposes underlying tissue to corrosive action
can rupture if left untreated

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6
Q

symptoms of ulcers

A

abdominal pain
bloating
nausea/vomiting
bleeding

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7
Q

facotors in ulcer formation

A

1) Endogenous factors
Anxiety
- parasympathetic output (Ach, Gastric) increases acid
Stress
- sympathetic output (Ad), decrease I HCO3/mucous

2)	Exogenous factors
Diet
-	alcohol damages cells, stimulates parietal cell
-	coffee stimulates parietal cell
Non steroidal anti inflammatory drugs
-	decreased prostaglandin production
-	decrease in inhibition of acid
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8
Q

peptic ulcer

A

infectious disease
bacteria - H pylori
releases proteases and endotoxins which breaksdown tissue

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9
Q

secretion into the duodenum

A

secretion from accessory organs (gall bladder and pancreas)

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10
Q

pancrease

A 
exocrine gland (85%)
acinius
- water and ions
- bicarbonate
- enzymes (essential for normal digestion)

Endocrin 2%
islets of langerhans
Alpha cells glucagon
Beta cells insulin

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11
Q

purpose of water ions and bicarbonate from pancreas

A

neutralise duodenal contents to prevent damage and pH for enzymes to function

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12
Q

features of pancreas

A

1) acinar cells
2) centroacrinar cells
- produce biacarbonate ions
3) intercalated ducts
- made up of intercellular caniculi
4) intralobular duct
- joins to pancreatic duct
5) islets of langerhans
- lots of capillaries for hormones to secrete into

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13
Q

pancreatic enzymes and function

A

1) Trypsinogen
- makes trypsin
2) Chymotrypsinogen
- chymotrypsin
3) proelastase
- elastase
4) procarboxypeptidase
- carboxypeptidase
1) lipase and phospholipase
- fats
2) nucleases
- nucleic acids
3) alpha amylase
- carbohydrates

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14
Q

duodenal feedback

A

nutrients in chyme

  • Cholecystokinin (CCK)
  • release into blood stream in response to proteins and fats
  • pancreatic acinar cell secretion

HCL in chyme

  • secretin release into blood stream in response to pH<5
  • regualates the pH in the intestine
  • pancreatic ductal secretion (Centroacinar cells)
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15
Q

liver functions

A

protein synthesis (including albumin and clotting factors)
storage (triglycerides, glycogen, some vitamins)
gluconeogensis
toxins
bile

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16
Q

functions of bile

A

facilitate fat digestion/emilsification

excretion of waste products

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17
Q

composition of bile

A

1) water and ions
- alkali
2) bile acids
- digestion and absorption of dietary fats (micelle formation) 7)%
3) proteins
- protect against infection
4) bile pigments
- breakdown of products of haemoglobin (bilirubin)
5) organic molecules
- cholesterol 4%
- phospholipid – lecithin (20%)

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18
Q

where is bile produced and where does it move

A

produced in liver
moves to the gall b;adder
alters bile composite and delivery

19
Q

function of gall bladder function

A

1) absorption
- NA+ Cl- H20
- concentrates bile
2) secretion
- H+ (Protons) and mucin
- neutralize alkaline bile
- protect surface epithelium
3) motor
- interdigestive – storage of bile
- digestive, contraction and delivery of bile

20
Q

control of bile delivery

A

secretin
- stimulates secretion
CCK
- stimulates release of bile

21
Q

how does CCK stimulate release of bile

A

1) relaxing sphincter of Oddi (where the bile and pancreatic duct meet enter the intestine)
2) Contracting gall bladder

22
Q

what are gallstones

A

Calcified stones

  • cholesterol
  • bilirubin
  • calcium
23
Q

causes of gall stones

A

1) genetics
2) body weight
3) decreases mobility of gall bladder
4) diet
5) other diseases (cirrhosis, sickle cell)

24
Q

microivill brush border layers

A
  • glycocalyx (unstirred layer) – sugar layer
  • brush border enzymes
    Addditonal surface for absorption
  • maltase, lactase sucrase, dipeptidases
    Absorbed pancreatic enzymes
25
Q

glucose/galactose carrier

A
  • co transport Na+ dependent, secondary AT
  • energy required to maintain Na+ gradient
  • sodium potassium ATP ase, pumping sodium out of cell to maintain gradient
  • sodium falls down gradient, glucose comes in viat SGLT1
  • once in cell then goes through into the blood via GLUT2, facilitated diffusion as it is higher in cell compared to blood stream
26
Q

how is fructose transported

A

facilitated diffusion

vit GLUT2

27
Q

protien digestion in each part of the body

A

1) Stomach
- gastric pepsin
- protein – polypeptides, small peptides
2) duodenum
- pancreatic proteases secreted
- protein – polypeptide, small peptides and amino acids
3) jejunum (brush border)
- peptidases in the border
- large peptides – small peptides and amino acids

28
Q

how can amino acids enter the cell

A

through AT carrier mediated processes

on the surface carrier protiens

29
Q

lipid digestion where and how

A

1) Lipase
- pancreas
- broken into monoglycerides, fatty acids, glycerol
2) Bile salts
- emulsifyed (smaller droplets) into micelles
3) Micelles
- transport across unstirred layer sat on the surface of epithelial cells

30
Q

how is fat transported

A

membrane soluble diffusion

31
Q

intracellular fat absroptio

A

Micelles cross via diffusion as they are fat soluble
Product reconstituted into triglycerides
- incorporated into chylomicrons (lipoprotein coat)
- exocytosis into lateral space

32
Q

once fat is intracellularly transported what happens

A
  • diffusion into lacteals

- return to systemic circulation via thoracic lymph duct

33
Q

malabsorption

A
  • Absent or defective digestion enzymes
  • defects in transporter proteins
  • diseases or infections of small intestine
34
Q

symptoms of malabsorption

A

Symptoms

  • steatorrhea (frothy greasy stools)
  • diarrhoea
  • weight loss – not able to get the nutrients from food
35
Q

what is the large intestine composed of and what do they each do

A

1) Tenia coli
- 3 bands longitudinal muscle
2) haustra
- pockets undergoing segmentation
- slow movements of contents
- regulates movement through
- allowing remaining absorption and fermentation
3) sphincters
- internal and external
- regulate movement of feses

36
Q

what are the corners o the large intestine

A

hepatic flexure/splenic flexure

37
Q

why is there no villi in large intestine

A

high conc of goblet cells

mucous secretions

38
Q

functions of large intestine

A

1) high mucous secretion – goblet cell
2) efficient water reabsorption
- aided by Cl- absorption in exchange for HCO3-
3) HCO3- buffer acids
- produced by bacterial fermentation

39
Q

gut flora

A
  • Gut microbiome forms hours after birth
  • primes the gut immune system
  • fibre fermentation
  • majority in the large intestine
40
Q

GI tract flora and in what sections of GI

A

1) oral
- commensal bacteria
- pathogens
- eg porphyromonas gingivalis
2) stomach
- H pylori
3) large intestine
- bacterial fermentation indigestbale materials eg fibre
- they benefit from the food, we benefit from what they do
- short chain fatty acids
- synthesise essential nutrients (folic acid, vit K)
- aid absorption of vit B12

41
Q

dietary fibre effects on different aspects

A

1) Motility
- decrease gastric emptying – stomach
- increase motility of colon - intestine
2) absorption
- holds water
- slows absorption of nutrients
3) colonic bacterial substrate

42
Q

sources of gastrointestinal gas

A

swallow air

bacterial fermentation of fibre

43
Q

gas components

A

hydrogen

methane

GDAN year 2 nutrition (14 decks)

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