control of digestion and absorption Flashcards
1
Q
what are the 2 hormones involved in regulating appetite
A
ghrelin
leptin
2
Q
what is ghrelin main fuction and where is it made
A
hunger hormone, tells ur brain ur hungry
- produced by stomach
3
Q
besides signalling hunger, what other functions does ghrelin have
A
- 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.
4
Q
what is the main function of leptin and where is it made
A
- 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
5
Q
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.
A
6
Q
what area does leptin and ghrelin act on
A
hypothalamus
7
Q
why is it when you lose weight or have less fat, you tend to get hungry faster
A
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.
8
Q
what 3 components make up slaive
A
- amylase
- mucous/mucin
- lysossome
9
Q
what system does salivary release use
A
parasympathetic
10
Q
explain how the parasympathetic system works to release saliva
A
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
11
Q
oesophageal secretions are mucous as it is lined with simple mucous glands
A
12
Q
describe the reflex of swallowing
A
all or none reflux
13
Q
what motion does the oesophagus use
A
peristalsis
14
Q
which nerves is connected to the swallowing centre
A
vagus nerve
glossopharyngeal nerve
15
Q
what is dysphasia
A
difficulty swallowing
16
Q
what is dysepepsia
A
indigestion
17
Q
what are the 3 phases of gastric secretion
A
cephalic phase (via vagus)
gastric phase
intestinal phase
18
Q
what is gastric secretion
A
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.
19
Q
what produces gastric juice and where is it found
A
gastric glands found in the mucosa layer of the fundus/body of stomach
20
Q
what are 5 components found in the gastric gland
A
- chief cells
- parietal cells
- ECL cells (histamine)
- G cells (gastrin)
- D cells
21
Q
what cells are the gastric pit formed of
A
mucous cells
22
Q
what is the role of chief cells in gastric gland
A
- Pepsinogen secretion
23
Q
what is the role of parietal cellist gastric gland
A
Hydrochloric acid (HCl) secretion
- intrinsic factor secretion ( glycoprotein)
24
Q
what is role of ECL/histamine cells
A
- enterochromatic cell
- produce, store and secrete histamine
25
what is the role of histamine
- stimulates parietal cells
26
what are G cells/ its role
neuroendocrine cells responsible for the synthesis and secretion of gastrin
27
what are D cells nd its role
- delta cells
- somatostatin-producing cells
28
what is the role of somatostatin
inhibits parietal, G and ECL cells
29
what do mucous cells sevrete
mucous
30
what does gastrin do
stimulate parietal, chief and ECL cells
31
what happens in gastritis
achlorhydria and pernicious anemia
32
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)
33
what 4 things do the pyloric glands secrete
- pepsinogen (small amount)
- mucous
- gastrin
- somatostatin
34
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
35
how much gastric juice is released a day
2 litres
36
what is the pH range for pepsin proteolytic activity and inactivity
pH 1.8 - 4.5 = active
pH 5 = inactive
37
what is a peptic ulcer
open sores that develop on the inside lining of your stomach
38
what are the 2 main causes of peptic ulders
1. Helicobacter pylori
2. Over use of non steroidal anti-inflammatory drugs (damages the mucous layer)
39
what are 3 tests that can be done for peptic ulcers
- upper endoscopy
- upper GI xrays
- test for H.pylori
40
what is gastric emptying
the process by which the contents of the stomach are moved into the duodenum.
41
what 4 factors of the duodenum affect gastric emptying
- fat
- acid
- hypertonicity
- distention
42
why does fat effect gastric emptying
-effective in delaying gastric empyting
- digestion and absorption of fat takes longer
43
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
44
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
45
how does distention (enlargement) affect gastric emptying
too much chyme in duodenum inhibits emptying and gives time for digestion (linked to hypertonicity)
46
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
47
what are the 3 enterogastrons released by duodenum
- secretin (S cells)
- CCK (I cells)
- GLP-1 (L cells)
48
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
49
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
50
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
51
what 2 pancreatic enzymes are released into the duodenum already active
- pancreatic amylase
- pancreatic lipase
52
what pancreatic enzyme is released into duodenum inactive and what enzyme is required to active ti
- trypsinogen
- activated by enterokinase
53
what are the 4 activated forms of trypsinogen
trypsin
chymotripsin
carboxypeptidase
elastase
(all digest proteins)
54
what physical pain is felt with pancreatitis
- epigastric pain radiating to the back
- tender upper abdomen
55
what 2 blood tests are done to identify pancreatitis
blood lipase and amylase
56
what 5 things are found in bile
- bile salts
- cholesteral
- lecithin
- bilirubin
- alkaline fluid
57
what is the role of bile salts
- detergent action in emulsification of fat
(increase SA available for pancreatic lipase)
58
what 4 things regulate bile secrretion
- choleretic (bile salts)
- secretin (stimulates alkaline bile secretion)
- vagus nerve
- CCK
59
what is a hepatic lobule
the anatomic unit of the liver.
- hexagonal shaped/ arrangement
60
what structure is found in the middle of every hepatic lobule
central vein
61
what is the major cell type involved in liver fibrosis (formation of scar tissue) in response to liver damage / cirrhosis
kupffer cells (specialised macrophages )
62
cirrhosis causes:
- viral infection
- fatty liver
- autoimmune disease
- iron overload
- inflammation
- thrombosis of proton veins/hepatic arteries/central veins
63
find an image and understand the structure of hepatic lobule e.g central vein et
64
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
65
what are 2 types of gall stone
- cholesterol
- pigment (bilirubin calcium salts)
66
causes of cholesterol stones:
- age
- race
- female / female sex hormone
- oral contraceptive
- obesity, insulin resistance
67
causes of pigment stones :
- race
- sick cell anemia
- GIT disorder e.g chrons
- pancreatic insufficiency
68
biliary colic - RUQ pain, colicky
cholecystitis- RUQ pain constant, mild jaundice
cholangitis - RUQ pain, jaundice, fever
69
what is crypts of lieberkuhn in the small intestine and its role
pits between villi
- secretion of water and salt, place of stem cells
70
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
71
what is malabsorption
body does not fully absorb nutrients) can lead to a deficiency of vitamins and minerals
72
what breaks down carbs, proteins, fat
carbs = amylase
protein = pepsin
fat = lipase, bile salts
73
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
74
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
75
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
76
what is coeliac disease
immune reaction to gluten in small intestine
- plasma cells produce anti-bodies (IgA) on exposure to gluten
77
how much chyme is received by the large intestine a day and how much is actually absorbd
500ml recieved
350ml absorbed
78
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+
79
bacteria can convert vitamin K1 into vitamin K2 and other isoforms of vitamin K
80
What are the 2 types of inflammatory bowel disease
crohns and ulcerative colitis
81
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
82
