physiology Flashcards
what is the alimentary canal
serious of hollow tubes running from mouth to anus (oral to aboral) separated by sphincters
what are the components of the GI tract
mouth and oropharynx, oesophagus, stomach, small intestine, large intestine, rectum and anus
where is the principle site of digestion and absorption
small intestine
what happens in the large instestine
holds the colon where fluids and electrolytes are reabsorbed and stored as faeces
what are the assessory features of the alimentary canal
salivary glands, pancreas, liver and gall bladder
how long is the GI tract
7-10m
what are the components of the digestive tract wall
mucosa, submucosa, muscularis externa, serosa
what is the function of the mucosa
fat absorption
what dies the muscularis externa do
changes shape to facillitate absorption
what are the 4 major functions of the alimentary canal
motility, secretion, digestion, absorption
what is the main type of muscle in the GI tract and what are the exceptions
mostly smooth, skeletal in mouth, pharynx, upper oesophagus and external anal sphincter
when does secretion occur and what does it do
in response to food, hormones or nerves, needed for digestion, protection and lubrication
what happens during digestion
chemical breakdown by hydrolysis of complex food to absorbable units
what happens during absorption
transfer from digestive tract to blood
when circular muscles contract what happens to the lumen
narrower and longer
when longitudinal muscles contract what happens to the lumen
shorter and fatter
adjacent cells are coupled by?
gap junctions
when the cells depolarise in a synchronous wave what is this called
single unit smooth muscle
what type of wave occurs in stomach, small and larger intestines
slow wave
what type of cells cause slow wave depolarisation
interstitial cells of Cajal (ICC’s), these are pacemakers
where are ICCs found
between circular and longitudinal muscle
when does depolarisation of slow waves result in contraction
when there are frequent enough AP’s to get to the threshold. (AP’s increase force not speed)
the upstroke is due to an influx of what
Ca++
what are short waves also known as
basic electrical rhythm
what type of outflow is involved in the PARASYMPATHETIC autonomic innervation and which nerves are involved
cranio-sacral, vagus and pelvic nerves
where to preganglionic fibres synapse with ganglion cells in parasympathetic.
enteric nervous system.
what are the excitatory influences of parasympathetic outflow
increased gastric, pancreatic and small intestinal secretion, increased blood flow and increased muscle contraction
what are the inhibitory influences of parasympathetic outflow
relaxation of sphincters, relaxation of stomach
what is more significant in the GI tract parasympathetic or sympathetic
parasympathetic
where to preganglionic fibres synapse in SYMPATHETIC outflow
prevertebral ganglia, (post release NA)
what are excitatory influences of sympathetic outflow
increased sphincter tone
what are inhibitory influences of sympathetic outflow
decreased motility, decreased secretion, decreased blood flow
what does the enteric nervous system act on
the gut
give an example of local, short and long nerve reflexes
local: peristalsis, short: intestino-intestinal inhibitory reflex, long: gastroileal
what is peristalsis
wave of relaxation followed by a contraction, usually over short distances and oral–>aboral
in the oral section, what muscle relaxes and what contracts
longitudinal relaxes and circular contracts
in the aboral section, what muscle relaxes and what contracts
longitudinal contracts and circular relaxes
what causes relaxation of longitudinal/ circular muscle
NO and VIP
what causes contraction of longitudinal/ circular muscle
ACh and substance P
what are the 5 major motility functions of the GI tract
peristalsis, segmentation, colonic mass movement, migrating motor complex (MMC), tonic contractions
what happens in segmentation, what is it called in large intestine
rhythmic contractions of circular muscle for mixing/ churning. Occurs in small and large intestine (haustration)
what are the 6 sphincters
upper oesophageal, lower oesophageal, pyloric, illeocacal, internal anus, external anus
which sphincters are controlled by skeletal
upper oesophageal and external anus
food entering the oesophagus does what to stomach
relaxes receptively to prepare, vagus activity
What are the 4 main anatomical areas of the stomach?
Fundus
Body
Antrum
Pylorus
what are the 2 mechinal sections of stomach
orad and caudad
what happens in orad section
relaxes in preparation for food, tonic contractions
what happens in caudad section
slow waves (3/min) when threshold met, peristalsis i antrum, propels chyme towards pylorus. also retropulsion of chyme
where does mixing occur
antrum
What is the substance produced when food mixes with gastric secretions
chyme
Name a substance which can be absorbed by the stomach
ethanol
What occurs in Retropulsion?
Peristaltic wave forces chyme against closed pyloric sphincter, so chyme bounces back and undergoes more mixing
what are some gastric factors promoting gastric emptying
volume of chyme, consistency of chyme, muscle strength, increases vagus nerve and gastrin release
Which 2 duodenal factors delay gastric emptying?
Enterogastric reflex (decreases antral activity) Release of enterogastrones (inhibit stomach contractions eg CKK)
What is the enterogastric reflex?
Duodenum signals to stomach that it has enough chyme so slow down emptying/peristaltic contraction
which stimuli in duedendum can decrease stomach emptying
fat, acid, hypertoncity, osmotically active, distension
Where is the oxyntic mucosa area located?
fundus and body
Where is the pyloric gland area located?
antram
Which cells are contained in the oxyntic mucosa amd what do they secrete?
Parietal cells: HCL
Enterochromaffin-like cells (ELC): histamine
Chief cells: pepsinogen
Which cells are contained in the pyloric gland area and what do they secrete?
D cells: somatostatin
G cells: gastrin
What does autocatalytic mean with regards to pepsinogen and pepsin?
Pepsin formation triggers further pepsin formation from pepsinogen
what does HCL do (oxyntic mucosa)
converts pepsinogen to pepsin, denatures enzymes and kills bacteria (parietal cell)
what does histamine do (oxyntic mucosa)
stimulates HCL release (ECL cell)
what does pepsinogen do (oxyntic mucosa)
converted to pepsin which breaks down proteins (chief cells)
What is the role of intrinsic factor and in the oxyntic mucosa?
Binds vitamin B12
What is the role of gastrin in the pyloric gland area?
Stimulates HCl secretion (G cell)
What is the role of somatostatin in the pyloric gland area?
Inhibits HCl secretion (D cell)
in the parietal cell, which enzyme forms H2CO3 from which to substrates
carbonic anhydrase, Co2 and H2O
what does H2CO3 dissociate to
HCO3 (bicarbonate) and H+
what does H/KATPase do
actively pumps K in and H+ out at apical end to canaliculus
How does bicarbonate exit cell, what enters in the exchanger
antiporter into plasma, chlorine enters
what channel does Cl exit to canaliculus
CFTR
CL and H then form to make acid true/false
true :)
What are Secretagogues?
Substances promoting secretion of HCl (gastrin, ACh, histamine)
What are the 3 phases of gastric secretion?
Cephalic
Gastric
Intestinal
What is involved in the cephalic phase?
Stomach is prepared to receive food by conditioned reflex, chewing or swallowing, leading to gastric secretion through ACh and GRP
What is involved in the gastric phase?
Distension of stomach causes G cells to be activates and D cells to be inhibited
what inhibits gastric secretion in cephalic stage
vagal nerve activity once you’ve stopped eating
what inhibits gastric secretion in gastric stage
fall in antral pH after eating, prostaglandin E2 removing histamine
what inhibits gastric secretion in intestinal stage
Gastric secretion is halted through secretin, CCK and somatostatin as the stomach empties
What is the importance of the mucus gel layer on the surface of mucous secreting cells?
Prevents pepsin/HCl reaching the apical surface of the cells and damaging the cells
how does the mucus gel layer prevent damage
produces PGE2 and PGL2 to reduce acid, increases mucous and bicarbonate secretion, increased mucous blood flow
Place the parts of the small intestine in order from shortest to longest
Duodenum (0.25m)
Jejunum (2.5m)
Ileum (3m)
what does the small intestine recieve
chyme, pancreatic juices, bile from gallbladder
Which 3 components increase the SA of the small intestine?
Circular folds
Villi
Microvilli
Where is gastrin secreted from?
G cells of stomach + duodenum
Where is secretin secreted from?
S cells of duodenum
Where is CCK secreted from?
I cells of duodenum + jejunum
Where is motilin secreted from?
M cells of duodenum + jejunum
Where is ghrelin secreted from?
Gr cells of stomach, small intestine + pancreas
what factors increases small intestine secretion
gastrin, CCKm distension and parasympathetic stimulation
does segmentation occur in small intestine
yes, to mix chyme,
what is the migrating motor complex
strong peristaltic contraction between meals, clears stuff from stomach to ileum, activated by motilin
what does the endocrine pancreas secrete
insulin and glucagon
what does the exocrine pancreas secrete and from which cells
anicar cells: digestive enzymes
duct cells: aqueous salts (NaHCO3)
where do exocrine secretions go
duodenum
explain neutralisation in small intestine (involving pancreas)
duodenum has high acid which causes S cells to release secretin. Secretin travels in blood to pancreas, it then releases aqueous salts from duct cells (NaHCO3) to duodenum lumen
explain digestion in small intestine (involving pancreas)
fat and protein in duodenum causes I cells to release CKK in blood to pancreas, it then releases digestive enzymes from anicar cells to duodenum lumen
name some forms of carbs
starch, cellulose, disaccharides, glycogen
name some types of lipids
triglycerides, free fatty acids, cholesterol, phospholipids
what is luminal digestion
digestion by pancreatic enzymes secreted into duodenum
what is membrane digestion
by enzymes at brush of epithelial cells
what is the combined term for digestion and absorption
assimilation
Name two polysaccharides
starch glycogen
what are 2 forms of starch
amylose, amylopeptin
what bonds does amylose have
alpha 1,4
what bonds does amylopeptin have
alpha 1,4 and 1,6 in branches
Name two disaccharides (oligosaccharides)
Sucrose
Lactose
Name three monosaccharides
Glucose
Fructose
Galactose
what do carbs have to be broken into for absorption
monosaccharides
what happens in intraluminal hydrolysis
eg starch –> ogliosaccharides by alpha amylase
what happens in membrane hydrolysis
ogliosaccharides –> monosaccharides by ogliosaccharidases
what does lactase do
breaks down lactase to glucose and galactose
what does maltase do
degrades alpha 1,4 bonds
what does isomaltase do
only enzyme that breaks down alpha 1,6
what does sucrose hydrolyse
sucrose + glucose –> fructose
What is lactose intolerance?
Inability to digest lactose, caused by lactase insufficiency
what side of enterocytes are monosaccharides absorbed
apical
how doe glucose and galactose enter enterocytes
secondary transport, by SGLT1
how does fructose enter enterocytes
facilitated diffusion by GLUT 5
how do all monosaccherides exit monocytes
GLUT 2
What denatures proteins in the stomach?
HCl
Which enzyme cleaves protein into peptides in the stomach and is it essential for digestion
pepsin, no.
What are the active enzymes that digest protein in the duodenum from the pancreas
Trypsin Chymotrypsin Elastase Procaroxypeptidase A Procaroxypeptidase B
What are the ranges for normal BMI?
18.5-25
What are the ranges for BMI classed as overweight?
25-29.9
What are the ranges for BMI classed as obese?
30-39.9
What are the ranges for BMI classed as morbidly obese?
> 40
How is obesity “a disease of the brain”?
The brain sees new fat/weight as normal, and attempts to lose weight are seen as a threat to survival, so the new weight is defended
what part of the brain regulates body weight
hypothalamus
Which lesioning part of the hypothalamus causes leanness?
lateral
Which lesioning part of the hypothalamus causes obesity
ventromedial
define satiation
feeling full during/ end of a meal
define satiety
fasting between means
when do satiation signals increase and why
when you are eating, Increased signals limit meal size, i.e. you can’t eat anymore
name some satiation singals
CKK, peptide YY, GLP1, OXM, obestatin
What is ghrelin?
a hunger signal
what are adiposity signals, give examples
signal fat stores to the brain, leptin and insulin, higher levels = more fat
how can obesity affectin leptin and insulin
alter transduction, damage receptors
what is the ‘food reward’
hedonistic affect, releases dopamine
name some ways to tackle obesity
drugs: orlistat
gastric bypass
heat therapy
name some types of lipids
Fats/ oils, phospholipids, fatt acids, cholesterol
what is emulsion
creating droplets suspending lipids in water to increase surface area.
what are the stages of lipid digestion
lingual phase –> gastric phase (gastric lipase in stomach) –> intestinal (small intestine, most important)
what is released to the duodenum from the gall bladder in lipid digestion
bile salts
what are bile salts released in response to and what do they do
CCK, emulsify lipids
what cofactor is needed for pancreatic lipase so it can access triglycerides
colipase
how is colipase activated
procolipase –> colipase by trypsin
what is a mixed micelle
product of digestion, emulsified globule containing TAGs, esterified cholesterol, bile salts, phospholipids and fatty acids
where do short/ medium exit enterocytes to capillaries and how do they do this
basolateral membrane by passive diffusion and membrane fatty-acid translocase
how are long fatty acid chains and monoglycerides digested
resnythesized to triglcyerides in the ER and made to chylomicrons
how are chylomicrons formed
triglycerides synthesised to cholesterol esters –> chylomicrons and coated with apolipoproteins
where are chylomicrons released to
lymphatic system by exocytosis
how is cholesterol absorbed
NPC1L1
how does NPC1L1 move around the cell
by myosin
how is Ca absorbed
passive diffusion in small intestine, is regulated by calcitrol
what does Vit D do in relation to Ca absorption
increased expression for Ca channels when Ca conc is low
what binds to Fe2+ in the stomach
gastroferrin
how does Fe2+ enter cells
contransporter iron
which acid is absorbable ferric or ferrous
ferrous (Fe2+) is bit ferric (Fe3+) is not, must be converted
how does haem increase iron levels in the blood
degradation of haem oxidase
what is the storage form of iron
ferratin
what are the fat soluble vitamins
ADEK
how is vit B12 absorbed
haptocorin binds to vitB12 in stomach, stomach parietal cells release intrinsic factor and in small intestine the intrinsic factor binds to it. It is then absorbed by endocytosis
what diet can lead to vit B12 deficiency
vegans, only present in animal produce
what is the large intestine made up of
caecum and appendix, ascending, transverse, descending and sigmoid colon, rectum, anal canal and anus
what type of muscle is in the caecum and colon
longitudunal smooth muscle that divides into 3 strands called taeniae coli
what surrounds the internal anal sphincter
the external skeletal sphincter
what does the colon mainly absorb
Na, Cl and H2O, also short chain fatty acids
what does the colon mainly secrete
K, HCO3 and mucus
what are the 4 functions of the colon
absorption, secretion, storing faeces and eliminating faeces
what does the colon have instead of villi
colonic folds, crypts and microvilli
what do epithelial cells (colonocytes) mediate in the colon
electrolyte absorption
what do crypt cells mediate
ion secretion
what do goblet cells secrete
mucous
what are haustra
saccule in colon from haustration
what is the mass movement of the colon, what reflex causes it
contraction of large sections of the colon at the same time towards the rectum, gastrocolic response
describe the defaecation reflex
reflex stretch receptors activate pelvic nerve, activates parasympathetic efferents causing internal sphincter to relax (rectum not normally filled with faeces)
which nerves control the external anal sphincter
pudenal nerve (S2,3,4)
why are colonic flora important
compete with pathogenic microbes, promote motility,, synthesise vit K2 and free fatty acids
what is flatus
intestinal gas, from swallowed air, bacteria and gases
what can cause constipation
enhances absorption of H20, suppressing the need, decreases motility obstruction, hirschprung disease
what can hardened calcified matter cause
appendicitis
how does chyme enter the caecum
through ileocal valve by gastroileal reflex in response to gastrin and CCK
what does the caecum relax in response to
distension of the duodenum
where is the appendix attached to the caecum
distal via appendiceal orifice
what can happen if appendiceal orifice is obstructed by faecalith
appendicitis
when should laxatives and purgatives not be used
bowel obstruction
what can laxatives be used for
to increase peristalsis and soften faeces, clean bowel before surgery, when pooing is sore
name 2 chronic bowel disease
irritable (IBS) and inflammatory (IBD)
what causes vomiting and nausea
reverse peristlasis from upper
where is the vomiting centre (VC)
medulla oblongata
describe how the mediator is released in the vomiting pathway
toxic materials in gut lumen stimulate enterchromaffin cells in mucosa to release mediates (5-HT)
describe how the nerves cause vomiting in pathway
sensory afferent terminals in mucosa depolarise, AP discharge in vagal nerve afferents to brainstem, VC causes you to throw up
what are the events of vomiting
sphincters relax and retrograde contractions from ileum to stomach. proceeded by lack of saliva, sweating, high BP and nausea
what are some consequences of severe vomiting
dehydration, loss of protons and chloride (met alkalosis), raised pH, hypokalaemia
how much water is lost on faeces, what else does it contain
100ml, cellulose, bilirubin and bacteria
what is the main solute that drives absorption of water
Na
what are the major mechanisms in postorandiral period in jejunum
Na/glucose co-transport and Na/ amino acid co-transport
do cAMP and cGMP increase or decrease NaCl absorption
decrease
what is the definition of diarrhoea
loss of fluid and solutes in excess of 500ml a day
what can cause diarrhoe
infectious agents, chronic disease, toxins, impaired absorption of NaCl, excession secretion of Cl and Na (cholera), poorly absorbable intestinal lumen
what are some consequences of diarrhoea
dehydration (Na+H2O loss), metabolic acidosis (HC03 loss), hypokalaemia
how does rehydration therapy work
Na and glucose translocate from extracellular to intracellular and water follows
how do opiods act as anti-diarrhoeal
increase fluid absorption, contrict pyloric, iliocaecal and anal sphincters and decrease peristalsis
name some opiods
codeine, diphenoxylate (least abuse potential), loperamide
what 3 things does the liver metabolise
carbs, fat and protein
describe carb metabolism in the liver
gluconeogenesis, glycogenesis, glycogenolysis
describe fat metabolism in the liver
processes chylomicron remains and synthesises lipoproteins and cholesterol, ketogenesis
what does the liver degrade
insulin, glucagon, ADH, steroid hormones
what does the liver activate
thyroid –> throxine, vit D
what does the liver store
fat soluble vitamens (ADEK), water soluble vit b12, iron copper, glycogen
what does the liver synthesis
coagulation factors (II, VII, IX, X), albumin, apoliproteins
what does the liver do for protection
kupffer cells digest and destroy old and bad stuff. produce immune cells
what does the liver detoxify
bilirubin, drugs and ethanol
where is bile stores and concentrated between meals
gall bladder
how is bile released during a meal
chyme stimulates gall bladder to contract (via CCK and vagal impulses), sphincter of Oddi opens via CCK and bile exits
where is primary bile secreted and what does it contain
hepatocytes: cholic + chenodeoxycholic acids
what is the most common bilary system problems
cholelithiasis (gall stones), happens when bile crystallises
what is best treatment for gall stones
laparoscopic cholectystectomy
how are bile salts recycled
enterohepatic recycling
how are some primary bile acids converted to secondary
dehydroxylated by bacteria and returned to liver
what does the liver do to drugs
converts them to less pharmacologically active metabolites
where does phase 1 happen and what does it do
right side, makes drugs more polar eg oxidation, reduction, hydrolysis
where does phase 2 happen and what does it do
conjugation, adding something. glucuronidation is common
what mediates oxidation reactions in phase I
CYP450
