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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ulcers

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

symptoms of ulcers

A

abdominal pain
bloating
nausea/vomiting
bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

peptic ulcer

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

secretion into the duodenum

A

secretion from accessory organs (gall bladder and pancreas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

purpose of water ions and bicarbonate from pancreas

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

liver functions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

functions of bile

A

facilitate fat digestion/emilsification

excretion of waste products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
glucose/galactose carrier
- 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
how is fructose transported
facilitated diffusion | vit GLUT2
27
protien digestion in each part of the body
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
how can amino acids enter the cell
through AT carrier mediated processes | on the surface carrier protiens
29
lipid digestion where and how
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
how is fat transported
membrane soluble diffusion
31
intracellular fat absroptio
Micelles cross via diffusion as they are fat soluble Product reconstituted into triglycerides - incorporated into chylomicrons (lipoprotein coat) - exocytosis into lateral space
32
once fat is intracellularly transported what happens
- diffusion into lacteals | - return to systemic circulation via thoracic lymph duct
33
malabsorption
- Absent or defective digestion enzymes - defects in transporter proteins - diseases or infections of small intestine
34
symptoms of malabsorption
Symptoms - steatorrhea (frothy greasy stools) - diarrhoea - weight loss – not able to get the nutrients from food
35
what is the large intestine composed of and what do they each do
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
what are the corners o the large intestine
hepatic flexure/splenic flexure
37
why is there no villi in large intestine
high conc of goblet cells | mucous secretions
38
functions of large intestine
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
gut flora
- Gut microbiome forms hours after birth - primes the gut immune system - fibre fermentation - majority in the large intestine
40
GI tract flora and in what sections of GI
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
dietary fibre effects on different aspects
1) Motility - decrease gastric emptying – stomach - increase motility of colon - intestine 2) absorption - holds water - slows absorption of nutrients 3) colonic bacterial substrate
42
sources of gastrointestinal gas
swallow air | bacterial fermentation of fibre
43
gas components
hydrogen | methane