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rad414 pt 2 > control of digestion and absorption > Flashcards

control of digestion and absorption Flashcards

1
Q

what are the 2 hormones involved in regulating appetite

A

ghrelin
leptin

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2
Q

what is ghrelin main fuction and where is it made

A

hunger hormone, tells ur brain ur hungry

  • produced by stomach
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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.
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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
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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
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6
Q

what area does leptin and ghrelin act on

A

hypothalamus

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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.

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8
Q

what 3 components make up slaive

A
  • amylase
  • mucous/mucin
  • lysossome
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9
Q

what system does salivary release use

A

parasympathetic

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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
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11
Q

oesophageal secretions are mucous as it is lined with simple mucous glands

A
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12
Q

describe the reflex of swallowing

A

all or none reflux

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13
Q

what motion does the oesophagus use

A

peristalsis

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14
Q

which nerves is connected to the swallowing centre

A

vagus nerve
glossopharyngeal nerve

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15
Q

what is dysphasia

A

difficulty swallowing

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16
Q

what is dysepepsia

A

indigestion

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17
Q

what are the 3 phases of gastric secretion

A

cephalic phase (via vagus)

gastric phase

intestinal phase

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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.
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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

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20
Q

what are 5 components found in the gastric gland

A
  • chief cells
  • parietal cells
  • ECL cells (histamine)
  • G cells (gastrin)
  • D cells
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21
Q

what cells are the gastric pit formed of

A

mucous cells

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22
Q

what is the role of chief cells in gastric gland

A
  • Pepsinogen secretion
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23
Q

what is the role of parietal cellist gastric gland

A

Hydrochloric acid (HCl) secretion

  • intrinsic factor secretion ( glycoprotein)
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24
Q

what is role of ECL/histamine cells

A
  • enterochromatic cell
  • produce, store and secrete histamine
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25
Q

what is the role of histamine

A
  • stimulates parietal cells
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26
Q

what are G cells/ its role

A

neuroendocrine cells responsible for the synthesis and secretion of gastrin

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27
Q

what are D cells nd its role

A
  • delta cells
  • somatostatin-producing cells
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28
Q

what is the role of somatostatin

A

inhibits parietal, G and ECL cells

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29
Q

what do mucous cells sevrete

A

mucous

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30
Q

what does gastrin do

A

stimulate parietal, chief and ECL cells

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31
Q

what happens in gastritis

A

achlorhydria and pernicious anemia

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32
Q

what is achlorhydria and how does it lead to pernicious anemia

A
  • 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)
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33
Q

what 4 things do the pyloric glands secrete

A
  • pepsinogen (small amount)
  • mucous
  • gastrin
  • somatostatin
34
Q

describe how protein digestion occurs in the stomach and how it is stopped

A
  • 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
Q

how much gastric juice is released a day

A

2 litres

36
Q

what is the pH range for pepsin proteolytic activity and inactivity

A

pH 1.8 - 4.5 = active

pH 5 = inactive

37
Q

what is a peptic ulcer

A

open sores that develop on the inside lining of your stomach

38
Q

what are the 2 main causes of peptic ulders

A
  1. Helicobacter pylori
  2. Over use of non steroidal anti-inflammatory drugs (damages the mucous layer)
39
Q

what are 3 tests that can be done for peptic ulcers

A
  • upper endoscopy
  • upper GI xrays
  • test for H.pylori
40
Q

what is gastric emptying

A

the process by which the contents of the stomach are moved into the duodenum.

41
Q

what 4 factors of the duodenum affect gastric emptying

A
  • fat
  • acid
  • hypertonicity
  • distention
42
Q

why does fat effect gastric emptying

A

-effective in delaying gastric empyting

  • digestion and absorption of fat takes longer
43
Q

why does acid effect gastric emptying

A

high acidic chyme is neutralised by bicarbonates in duodenum

  • acid induces release of secretin that slows gastric emptying until full neutralisation is achieved
44
Q

why does hypertonicity affect gastric emptying

A

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
Q

how does distention (enlargement) affect gastric emptying

A

too much chyme in duodenum inhibits emptying and gives time for digestion (linked to hypertonicity)

46
Q

what are enterogastrons

A

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
Q

what are the 3 enterogastrons released by duodenum

A
  • secretin (S cells)
  • CCK (I cells)
  • GLP-1 (L cells)
48
Q

why is GLP-1/ glucagon like peptide released, what are its 3 main functions

A

in response to food intake

  • stimulate insulin secretion
  • inhibits glucagon secretion (lowers blood glucose)
  • inhibits gastrointestinal motility and gastric secretion
49
Q

explain the process of how chyme gets neutralised

A
  • 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
Q

explain the process of how fats and peptides get digested in the duodenum

A
  • 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
Q

what 2 pancreatic enzymes are released into the duodenum already active

A
  • pancreatic amylase
  • pancreatic lipase
52
Q

what pancreatic enzyme is released into duodenum inactive and what enzyme is required to active ti

A
  • trypsinogen
  • activated by enterokinase
53
Q

what are the 4 activated forms of trypsinogen

A

trypsin
chymotripsin
carboxypeptidase
elastase

(all digest proteins)

54
Q

what physical pain is felt with pancreatitis

A
  • epigastric pain radiating to the back
  • tender upper abdomen
55
Q

what 2 blood tests are done to identify pancreatitis

A

blood lipase and amylase

56
Q

what 5 things are found in bile

A
  • bile salts
  • cholesteral
  • lecithin
  • bilirubin
  • alkaline fluid
57
Q

what is the role of bile salts

A
  • detergent action in emulsification of fat

(increase SA available for pancreatic lipase)

58
Q

what 4 things regulate bile secrretion

A
  • choleretic (bile salts)
  • secretin (stimulates alkaline bile secretion)
  • vagus nerve
  • CCK
59
Q

what is a hepatic lobule

A

the anatomic unit of the liver.

  • hexagonal shaped/ arrangement
60
Q

what structure is found in the middle of every hepatic lobule

A

central vein

61
Q

what is the major cell type involved in liver fibrosis (formation of scar tissue) in response to liver damage / cirrhosis

A

kupffer cells (specialised macrophages )

62
Q

cirrhosis causes:

  • viral infection
  • fatty liver
  • autoimmune disease
  • iron overload
  • inflammation
  • thrombosis of proton veins/hepatic arteries/central veins
A
63
Q

find an image and understand the structure of hepatic lobule e.g central vein et

A
64
Q

explain how fats are digested

A
  • 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
Q

what are 2 types of gall stone

A
  • cholesterol
  • pigment (bilirubin calcium salts)
66
Q

causes of cholesterol stones:

  • age
  • race
  • female / female sex hormone
  • oral contraceptive
  • obesity, insulin resistance
A
67
Q

causes of pigment stones :
- race
- sick cell anemia
- GIT disorder e.g chrons
- pancreatic insufficiency

A
68
Q

biliary colic - RUQ pain, colicky

cholecystitis- RUQ pain constant, mild jaundice

cholangitis - RUQ pain, jaundice, fever

A
69
Q

what is crypts of lieberkuhn in the small intestine and its role

A

pits between villi

  • secretion of water and salt, place of stem cells
70
Q

what are paneth cells, where are they found and what do they do

A
  • reside in the base of the crypts
  • secrete lysozyme (antimicrobial factors) and defensins
71
Q

what is malabsorption

A

body does not fully absorb nutrients) can lead to a deficiency of vitamins and minerals

72
Q

what breaks down carbs, proteins, fat

A

carbs = amylase
protein = pepsin
fat = lipase, bile salts

73
Q

what 3 areas are carbs broken down in and by what and into what

A

saliva
- amylase into disaccharide dextran

small intestine lumen
- pancreatic amylase into disaccharides

small intestine brush border
- maltase, sucrase, lactase, isomaltase into mono-sachyrides

74
Q

what 3 areas are proteins broken down in and by what and into what

A

stomach
- pepsin into peptides

small intestine lumen
- trypsin, chymotrypsin, carboxypeptidase into peptide fragments

small intestine brush border
- amino peptidases into amino acids

75
Q

what singular area are fats/triglycerides broken down in and by what into what

A

small intestinal lime
- lipase and bile salts from triglycerides into fatty acids and monoglycerides

76
Q

what is coeliac disease

A

immune reaction to gluten in small intestine

  • plasma cells produce anti-bodies (IgA) on exposure to gluten
77
Q

how much chyme is received by the large intestine a day and how much is actually absorbd

A

500ml recieved

350ml absorbed

78
Q

what is the 4 purpose of the hundreds/thousands of bacteria in the colon

A
  • enhance intestinal immuity
  • promote colonic motility
  • synthesise vitamin K
  • rise colonic acidity thus promoting absorption of Ca2+, Mg2+, Zn2+
79
Q

bacteria can convert vitamin K1 into vitamin K2 and other isoforms of vitamin K

A
80
Q

What are the 2 types of inflammatory bowel disease

A

crohns and ulcerative colitis

81
Q

compare the symptoms of crohns and ulcerative colitis

A

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
Q
A

rad414 pt 2 (33 decks)

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