control of digestion and absorption Flashcards
what are the 2 hormones involved in regulating appetite
ghrelin
leptin
what is ghrelin main fuction and where is it made
hunger hormone, tells ur brain ur hungry
- produced by stomach
besides signalling hunger, what other functions does ghrelin have
- Increases food intake and helps your body store fat.
- Helps trigger your pituitary gland to release growth hormones.
- Plays a role in controlling sugars and how your body releases insulin, the hormone responsible for processing sugar.
- Has a role in protecting your muscles from weakness and bone formation and metabolism.
what is the main function of leptin and where is it made
- regulating hunger by providing the sensation of satiety (feeling full).
- help regulate the long-term balance between your body’s food intake and energy use (expenditure)
- leptin is released by the bodies adipose tissue
Leptin mainly acts on your brainstem and hypothalamus to regulate hunger and energy balance, though you have leptin receptors in other areas of your body.
Leptin doesn’t affect your hunger levels and food intake from meal to meal but rather acts to alter food intake and control energy expenditure over a longer period of time to help maintain your normal weight.
what area does leptin and ghrelin act on
hypothalamus
why is it when you lose weight or have less fat, you tend to get hungry faster
Leptin has a more profound effect when you lose weight. As your body fat (adipose tissue) decreases, your leptin levels decrease, which signals your body to think that it’s starving. This stimulates intense hunger and appetite and can lead to increased food consumption.
what 3 components make up slaive
- amylase
- mucous/mucin
- lysossome
what system does salivary release use
parasympathetic
explain how the parasympathetic system works to release saliva
trigger:
- pressure or chemoreceptors in mouth OR
- thing/see/smell food in cerebral cortex
- these trigger the salivary center in medulla
- autonomic nerve stimulater
- activating salivary glands leading to saliva secretion
oesophageal secretions are mucous as it is lined with simple mucous glands
describe the reflex of swallowing
all or none reflux
what motion does the oesophagus use
peristalsis
which nerves is connected to the swallowing centre
vagus nerve
glossopharyngeal nerve
what is dysphasia
difficulty swallowing
what is dysepepsia
indigestion
what are the 3 phases of gastric secretion
cephalic phase (via vagus)
gastric phase
intestinal phase
what is gastric secretion
The stomach secretes water, electrolytes, hydrochloric acid, and glycoproteins, including mucin, intrinsic factor, and enzymes
- The process of gastric secretion can be divided into three phases (cephalic, gastric, and intestinal) that depend upon the primary mechanisms that cause the gastric mucosa to secrete gastric juice.
what produces gastric juice and where is it found
gastric glands found in the mucosa layer of the fundus/body of stomach
what are 5 components found in the gastric gland
- chief cells
- parietal cells
- ECL cells (histamine)
- G cells (gastrin)
- D cells
what cells are the gastric pit formed of
mucous cells
what is the role of chief cells in gastric gland
- Pepsinogen secretion
what is the role of parietal cellist gastric gland
Hydrochloric acid (HCl) secretion
- intrinsic factor secretion ( glycoprotein)
what is role of ECL/histamine cells
- enterochromatic cell
- produce, store and secrete histamine
what is the role of histamine
- stimulates parietal cells
what are G cells/ its role
neuroendocrine cells responsible for the synthesis and secretion of gastrin
what are D cells nd its role
- delta cells
- somatostatin-producing cells
what is the role of somatostatin
inhibits parietal, G and ECL cells
what do mucous cells sevrete
mucous
what does gastrin do
stimulate parietal, chief and ECL cells
what happens in gastritis
achlorhydria and pernicious anemia
what is achlorhydria and how does it lead to pernicious anemia
- a condition in which the stomach does not produce hydrochloric acid
- lack of production of intrinsic factor from the stomach prevents absorption of vitamin B12 from the terminal ileum (pernicious anemia)
what 4 things do the pyloric glands secrete
- pepsinogen (small amount)
- mucous
- gastrin
- somatostatin
describe how protein digestion occurs in the stomach and how it is stopped
- protein found in food in stomach
- Acetylecholine released by nervous system, stimulating gastrin and histamine release
- gastrin and histamine stimulate the parietal cells to release HCL
- HCL activates the pepsinogen released by chief cells
- activated pepsinogen digests proteins into pepsin
- the release of HCL also stimulates release of somatostatin which inhibits parietal, g and ECL cells
how much gastric juice is released a day
2 litres
what is the pH range for pepsin proteolytic activity and inactivity
pH 1.8 - 4.5 = active
pH 5 = inactive
what is a peptic ulcer
open sores that develop on the inside lining of your stomach
what are the 2 main causes of peptic ulders
- Helicobacter pylori
- Over use of non steroidal anti-inflammatory drugs (damages the mucous layer)
what are 3 tests that can be done for peptic ulcers
- upper endoscopy
- upper GI xrays
- test for H.pylori
what is gastric emptying
the process by which the contents of the stomach are moved into the duodenum.
what 4 factors of the duodenum affect gastric emptying
- fat
- acid
- hypertonicity
- distention
why does fat effect gastric emptying
-effective in delaying gastric empyting
- digestion and absorption of fat takes longer
why does acid effect gastric emptying
high acidic chyme is neutralised by bicarbonates in duodenum
- acid induces release of secretin that slows gastric emptying until full neutralisation is achieved
why does hypertonicity affect gastric emptying
gastric emptying gets inhibited when osmolarity of duodenal content increases ( lots of protein and carb molecules)
- high osmolarity causes lots of water entering duodenum affecting distention and plasma volume so gastric emptying limited to prevent this
how does distention (enlargement) affect gastric emptying
too much chyme in duodenum inhibits emptying and gives time for digestion (linked to hypertonicity)
what are enterogastrons
Enterogastrone hormone is released from duodenum and it slows gastric contraction to delay emptying of stomach and stops secretion of gastric juice
- hormones that delay gastric emptying
what are the 3 enterogastrons released by duodenum
- secretin (S cells)
- CCK (I cells)
- GLP-1 (L cells)
why is GLP-1/ glucagon like peptide released, what are its 3 main functions
in response to food intake
- stimulate insulin secretion
- inhibits glucagon secretion (lowers blood glucose)
- inhibits gastrointestinal motility and gastric secretion
explain the process of how chyme gets neutralised
- acid detected in duodenum
- secretin hormone is released by duodenum into blood
- this stimulates pancreatic duct cells to release sodium bicarbonate into the duodenum and neutralise
explain the process of how fats and peptides get digested in the duodenum
- fat and peptides in duodenum
- CCK hormone released by duodenum into blood stream
- acinar cells (functional unit of exocrine pancreas) in pancreas detect
- enzymes released into duodenum from pancreas and digest fat and peptides
what 2 pancreatic enzymes are released into the duodenum already active
- pancreatic amylase
- pancreatic lipase
what pancreatic enzyme is released into duodenum inactive and what enzyme is required to active ti
- trypsinogen
- activated by enterokinase
what are the 4 activated forms of trypsinogen
trypsin
chymotripsin
carboxypeptidase
elastase
(all digest proteins)
what physical pain is felt with pancreatitis
- epigastric pain radiating to the back
- tender upper abdomen
what 2 blood tests are done to identify pancreatitis
blood lipase and amylase
what 5 things are found in bile
- bile salts
- cholesteral
- lecithin
- bilirubin
- alkaline fluid
what is the role of bile salts
- detergent action in emulsification of fat
(increase SA available for pancreatic lipase)
what 4 things regulate bile secrretion
- choleretic (bile salts)
- secretin (stimulates alkaline bile secretion)
- vagus nerve
- CCK
what is a hepatic lobule
the anatomic unit of the liver.
- hexagonal shaped/ arrangement
what structure is found in the middle of every hepatic lobule
central vein
what is the major cell type involved in liver fibrosis (formation of scar tissue) in response to liver damage / cirrhosis
kupffer cells (specialised macrophages )
cirrhosis causes:
- viral infection
- fatty liver
- autoimmune disease
- iron overload
- inflammation
- thrombosis of proton veins/hepatic arteries/central veins
find an image and understand the structure of hepatic lobule e.g central vein et
explain how fats are digested
- triglycerides - large structure
- bile salts added to emulsify triglycerides
- pancreatic lipase acts on lipid emulsions to form monoglycerides and free fatty acids
- bile salts used again to emulsify monoglycerides and free fatty acids
to form micelles - micelles are smaller and more easily diffuse through semi permeable membrane
- monoglycerides and free fattty acids reform triglycerides inside cell
- triglycerides moderated by Golgi apparatus to form chylomicrons
- exocytosis of chylomicrons and enters central lacteal which enters venous circulation at level of subclavian and jugular vein
what are 2 types of gall stone
- cholesterol
- pigment (bilirubin calcium salts)
causes of cholesterol stones:
- age
- race
- female / female sex hormone
- oral contraceptive
- obesity, insulin resistance
causes of pigment stones :
- race
- sick cell anemia
- GIT disorder e.g chrons
- pancreatic insufficiency
biliary colic - RUQ pain, colicky
cholecystitis- RUQ pain constant, mild jaundice
cholangitis - RUQ pain, jaundice, fever
what is crypts of lieberkuhn in the small intestine and its role
pits between villi
- secretion of water and salt, place of stem cells
what are paneth cells, where are they found and what do they do
- reside in the base of the crypts
- secrete lysozyme (antimicrobial factors) and defensins
what is malabsorption
body does not fully absorb nutrients) can lead to a deficiency of vitamins and minerals
what breaks down carbs, proteins, fat
carbs = amylase
protein = pepsin
fat = lipase, bile salts
what 3 areas are carbs broken down in and by what and into what
saliva
- amylase into disaccharide dextran
small intestine lumen
- pancreatic amylase into disaccharides
small intestine brush border
- maltase, sucrase, lactase, isomaltase into mono-sachyrides
what 3 areas are proteins broken down in and by what and into what
stomach
- pepsin into peptides
small intestine lumen
- trypsin, chymotrypsin, carboxypeptidase into peptide fragments
small intestine brush border
- amino peptidases into amino acids
what singular area are fats/triglycerides broken down in and by what into what
small intestinal lime
- lipase and bile salts from triglycerides into fatty acids and monoglycerides
what is coeliac disease
immune reaction to gluten in small intestine
- plasma cells produce anti-bodies (IgA) on exposure to gluten
how much chyme is received by the large intestine a day and how much is actually absorbd
500ml recieved
350ml absorbed
what is the 4 purpose of the hundreds/thousands of bacteria in the colon
- enhance intestinal immuity
- promote colonic motility
- synthesise vitamin K
- rise colonic acidity thus promoting absorption of Ca2+, Mg2+, Zn2+
bacteria can convert vitamin K1 into vitamin K2 and other isoforms of vitamin K
What are the 2 types of inflammatory bowel disease
crohns and ulcerative colitis
compare the symptoms of crohns and ulcerative colitis
crohns:
- ulcers penetrate fully
- no blood in stool
- anywhere in GI tract
- patches of inflammation
ulcerative colitis:
- ulcers only penetrate inner lining
- blood in stool
- limited to large intestine
- continuous inflamed areas
BOTH typically in lower left abdomen
