GIT physiology Flashcards
Describe the anatomy of the stomach
major GI structure lying between oesophagus and dudenum and responsible for breaking down food to produce chyme.
has 4 main parts = cardia, fundus, body, antrum
lesser and greater curve.
fundus has distensible walls for food reservoir
antrum has thick walls for grinding and churning
ends in the pylorus - thick muscular funnel
inner surface has ruggae - irregular folds.
what level does the stomach sit?
T11 to L1
describe the layers of stomach - histology
mucosa = collumnar epithelium + lamina propriae + muscularis mucosa
submucosa
3 muscle layers -oblique, circular, longitundal
serosa - outermost layer
between the layers lies the myenteric plexus and the submucosal plexus
describe the structure of a gastric pit / gland
within the mucosa, the columnar epithelium invaginates into gastric pits which are openings of the gastric gland.
various cells line these and have a function in production of gastric acid and other substances for digestion.
name the main cells of the stomach and describe their action
Parietal cells = HCl + intrinsic factor. found in neck of gastric glands predominantley in fundus and body
neck cells = mucus and HCO3. found at the opening of the pits. protection
cheif cells = pepsinogen. found at the base of gastric glands. pepsinogen is precusor for pepsin which breaks down proteins (hydrolysis of peptide bond)
G cells = gastrin - found at base of the gland - stimulates acid production and gastric motility
Enterochromaffin cells = histamine - promotes acid release.
D cells = somatostatin - inhibits acid and gastrin release - in base of gastic gland.
what are the functions of gastric acid?
breakdown of proteins - denature and aid pepsins
activates pepsinogen to pepsin
kills microbes
improves absorption of Fe
what is the function of intrinsic factor?
intrinsic factor is a glycoprotein produced by parietal cells in the stomach
binds vitamin B12 = protecting it from breakdown and aiding absorption by terminal ileum
describe the innervation of the stomach…
intrinsic = myenteric plexus and submucosal plexus - pacemaker cells giving basal level of motility and sphincter control.
extrinsic = ANS
* sympathetic (coeliac plexus) (NA)- inhibits motility
* parasympathetic (ACh)- promotes motility and stimulates gastrin and histamine release hence HCL.
* inputs to ANS includ stomach distention
explain the biochemistry of HCL production..
- H20 + CO2 by carbonic anhydrase
- H/K ATPase luminal membrane
- HCO3 into blood with antiporter - chloride
- chloride channel on luminal membrane
secretion by parietal cells luminal surface
extensitve mitrochonidria, folds to increase S.A on membrane
describe the control of HCL release by parietal cells
on basolateral membrane is receptors - gastrin, histamine, M2
binding of these stimulates H/K ATPase
these 3 hormones directly stimulate acid production. others can indirectly by in turn stimulating/inhibiting these hormones
e..g ACh also stimulates gastrin and histamine as well as direct actions
e..g. S cells in duodemum secrete secretin which inhibits gastrin by G cells
e.g. D cells produce somatostatin which inhibits gastrin
e.g. acidity itself inhibits gastrin - negative feedback
describe the control of pepsin release
pepsin is an enzyme responsible for hydrolysing peptide bonds in proteins.
pepsinogen is secreted by cheif cells and then converted to active pepsin by stomach acid
pepsinogen secretion is stimulated by… low pH, gastrin, vagal stimulation
what stimulates gastic mucus production?
vagus nerve
gastrin
prostaglandins
what is the role of prostaglandins in gastric mucosa?
stimulate mucus and HCO3 production - protects stomach lining from acid
improves blood flow to mucosa
what happens if the balance between acidity and mucus is lost in the stomach?
mucosal surface irritation - gastritis
ulceration
what is the role of H.pylori?
stimulates gastrin release
produces ammonia which damages cells and reduces mucus production
what are the 3 phases of gastric secretion?
cephalic
gastric
intensitinal
cephalic
* anticipation of food - vagal nerve stimualtion - gastrin, histamine release, direct acid production, gastric motility
gastric
* presence of food, stomach distension
* i.e. stretch receptors - more vagal stimulation
* peptides stimulate gastrin production
* at pH less than 2 somatostatin released as negative feedback
intestinal
* chyme enters intestine - acidity - negative feedback by 3 main hormones.
* secretin = inhibit gastrin
* gastrointestinal peptode = inhibits gastrin
* Cholecystokinin (CCK) = inhibits stomach emptying
* also promotes pancreatic enzyme release
what is the difference between reflux, aspiration and regurgitation
reflux = from stomach up oesophagus
regurgitation = into oropharynx
aspiration = into lungs
what are the functions of the stomach
main role in digesting and churning food to create chyme that can be further handled by the intestines
food storage
absorption - some drugs e.g. alcohol, aspirin
immune role - acidity kills microbes
intrinsic factor - absorption of B12
describe the function of intestinal hormones acting on the stomach
Secretin = S cells - stimulated by acidity of chyme, inhibits gastrin
CCK = I cells - stimualted by aa and fats - stimulates pancreaes and inhibits gastric emptying
gastrointestinal peptide = K cells - stimulated by fatty acids in small intestine, reduces emptying and gastric juice production. stimulates insulin
Somatostatin = D cell
what are the sphincters in GIT?
Upper oesophageal
lower oesophageal
pyloric
ileocaecal
sphinchter of oddi
anal
tell me about the oesophageal sphincters..
2 of these
upper and lower
upper - under somatic control. made up of cricopharyngeal part of inferior pharyngeal muscles
lower - under autonomic control. remains contracted at rest with a pressure of around 15-20mmHg. during swallowing the stretch of the oesophagus stimulates vagus to cause relaxation .
what is meant by the oesophageal barrier pressure?
the barrier pressure is the difference between gastric pressure and LOS pressure.
LOS = 15-20mmHg
gastric pressure normally lower at rest
hence barrier pressure is LOS - GP which is positive at rest.
if LOS reduces or gastric pressures increase the barrier pressure can drop resulting in reflux.
what factors influence reflux
barrier pressure = LOS - gastric pressure
reduced LOS = anaesthetic agents, alcohol, oestrogen/progesterone (pregnancy), antimuscarinics. physiological factors - swallowing, vagus nerve
increased gastric pressure = full stomach, pregnancy, bowel obstruction, obesity. delayed emptying (opioids, pain)
babies have low LOS and high gastric pressure hence reflux
what factors increase LOS tone?
cholinergic stimulation - neostigmine, cyclizine, succinylcholine
describe the control of gastric emptying?
stomach emptying occurs when pressure created by stomach pump exceeds pyloric pressure
in general, gastric emptying is proportional to fullness of stomach i.e. fuller, the quicker
howeveer there are a number of neural and hormal factors influencing this…
neural = enterogastric reflex
* food in duodenum - walls stretch - vagus nerve inhibited - reduces motility , slows emptying.
* gives time and control over emptying
hormonal =
* chyme + acidity in duodemum, release of CCK and secretion - reduce motility
External
* prokinetics (erythomycin, neostig, metoclop)
* opiods
* pain, fear - reduces
how does the stomach breakdown food?
mechanical - churning
chemical - pepsin, acidity
describe the process of swallowing..
both a voluntary and involuntary process
1. voluntary movement of food bolus to posterior mouth. sensory afferents via trigeminal, glossopharyngeal and vagus to swallowing centre
2. causes brainstem activation of swallowing stages. elevation of soft palate to close off nasopharynx
3. closure of vocal cords and larynx drawn down. epiglottis swings over cords. upper oesophageal spinchter widens
4. peristasis starting in upper oesophagus - coordinated by swallowing cells (medulla and pons). swallowing centre inhibits resp centre. LOS relaxes.
describe the breakdown of macromolecules
carbohydrates - amylase in saliva and pancreatic juices. makes oligosaccharides and disaraccharides. further broken down by lactase, sucrase and maltase into glucose which can be absorbed.
proteins = pepsin and aa are absorbed
fats = lipase and emulsification
describe the breakdown and absorption of fats by intestines..
lipids are emulsified by bile salts
increases S.A for lipase to breakdown triglycerides to FFA and glycerol
FFA, cholesterol, fat soluble vitamins and other molecules form micelles
at the luminal membrane, FFA and monoglycerides leave the micelle and are absorbed into intestinal cell.
within intestinal cell, they reform to form chylomicrons
chylomicrons enter lymphatics via exocytosis
enter blood at thoracic duct
capillary endothelium has lipoprotein lipase which further digests and allows uptake of FFA to cells.
chylomicrons with removed FFA return to hepatocytes
how is glucose absorbed from GIT?
secondary ATP
Na/K ATPase on basolateral membrane
gradient for NA into the cell
SGLT 2 = cotransport for Na and glucose - luminal
GLUT 2 = basolateral
define nausea
define vomitting
nausea - unpleasant experience / senation of the need to vomit
vomitting - physical involuntary forceful expulsion of gastric content via the mouth
describe the physiology of vomiting..
complex process involving many afferent and efferent pathways
Thought to be coordinated by the vomitting centre - an area within the medulla oblongata made of multiple neural connections.
This recieves 3 main inputs
* chemoreceptor trigger zone - lies at base of 4th ventricle, area postrema and lies outside of BBB allowing it to sense toxins within the blood and input into vomitting centre
* nucleus tractus solitarus - lies within medulla - recieves inputs from various areas (vestibular apparatus, GIT, pain afferents)
* higher centres - pain, emotion, fear, raised ICP
various neurotransmitters and receptors are involved including dopamine, serotonin, acetylcholine, histamine and mu opioid receptors.
once threshold reached, central pattern generator activated and vomitting initiated.
describe the vomitting reflex..
pre-ejection - nausea, activation of sympathetic NS - sweating, tachycardia. also parasymp - salivation, relaxation of oesophageal sphincters and retrograde peristalsis
retching - respiration caeses, glottis closes, larynx rises, soft palate elevates - protect airway
ejection phase - coordinated contraction of diaphragm and abdominal muscles.
can you tell me some stimuli for vomitting?
toxins in blood - CTZ - many receptors D2, 5HT3, u opioid, neurokinin (sub P)
vesticular apparatus - motion sickness - via H1 and M3 reecptors
GIT - toxins in gut lumen, gut visceral pathology - 5HT3, dopamine receptors and substance P all implicated. e.g. 5HT3 receptors on end of vagal afferents which transmit impulses to vomitting centre.
raised ICP
complications of vomitting
electrolyte disturbance
dehydration
aspiration
poor absorption/ malnutrion
increase ICP
wound dehiscence
what are the risk factors for PONV?
patient factors - anxiety, female, previous PONV or motion sickness, non smoker, dehydration
anaesthetic factors - inhalation agents, N20, opioids . over use of bag/ mask ventilation and stomach inflation
surgical factors - obsteric, cholecystectomy, middle ear , laparoscopic
how does PONV in children compare to adults?
increases with age - more likely than adults
rare under 2
no sex differences before puberty
do you know any scoring systems for PONV?
APFEL
* adult scoring system
* 1 point for each = female, non smoker, opioids, prev PONV
* each point = 20%
POVOC
* paediatric tool
* 1 point = op more than 30mins, stradbidmus surgery, prev PONV, FHx PONV
describe the anatomy of the liver..
major organ within body
sits in RUQ
consisting of 2 anatomical lobes divided by falciform ligament.
also 2 smaller accessory lobes = caudate and quadrate lobe.
what is the difference between physiological and anatomical liver lobes?
anatomical - 2 unequal lobes divided by falciform ligament
physiological - 2 more equal size lobes, determined by their bilary drainage and blood supply. can be further divided into 8 functional units 4 on each side.
do you know any ligaments holding the liver in place
falciform - between R and L lobe. also attaches anterior surface to anterior abdo wall.
coronary - attaches superior surface to diaphragm
triangular ligaments - attach left and right lobe to diaphragm
describe the microscopic structure of the liver…
made up of millions of lobules
Whereby there is a branch of the hepatic vein at the centre of a hexagonal structure
at each corner of the hexagon is the portal triad = hepatic artery, portal vein, bile duct
30% of blood flow is via hepatic artery and 70% via the portal vein
however hepatic artery and portal vein supply around 50:50 of O2 content to the hepatocytes - they drain into sinusoids which lie between the hepatocytes. these sinusoids eventually meet and drain into the hepatic vein.
bile duct cannuli also line the hepatocytes, which make bile which is drained via bile duct
the liver can also be divided into zones 1,2,3 - this is a functional division (acinus) - zone 1 is closest to arteries and zone 3 closest to hepatic vein.
what is the difference between hepatic lobule, acinus and portal lobule
liver acinus = functional unit
describe the structure of hepatic sinusoids
hepatic artery and portal vein empty into the sinusoids - capillaries which pentrate hepatocytes and drain into hepatic vein.
large gaps (sinusoidal cap) to allow passage of proteins and sometimes cells
close association with kupffer cells
what are the different hepatic zones responsible for?
zone 1 = metabolism - most oxygenated region, rich in mitochondria. glycogen synthesis etc
zone 3 - drug detox , CYP450 - poorest blood supply. at risk of ischaemia. anaerobic.
describe blood supply to liver
extremely vascular organ, recieves 25% of CO (1500ml/min).
30:70 hepatic artery: portal vein
but 50:50 O2 supply
both enter at the hilum and divide to eventually supply portal triad
portal vein goes to liver after draining and supply GIT, pancreas, spleen. (from superior mesenteric plexus)
hepatic artery comes from coeliac trunch which arises from aorta
hepatic vein - drains into IVC
what factors affect the blood flow to the liver..
hepatic blood flow alters throughout the day with reduces with sleep, exercise, increases after a meal. hence needs regulation.
mostly controlled via hepatic artery (rather than portal vein).
intrinsic
* myogenic response - up to MAP 60mmHg- 150mmHg
* hepatic arterial buffer response - if portal vein flow is reduced, hepatic artery is increased and vice versa to help maintain flow. this occurs via adenosine. adenosine is constantly being produced around portal triad, if flow is reduced, it builds up and causes vasodilation of hepatic artery to increase flow.
extrinsic
- neural - sympathetic NS - A1
- humeral - catecholamines, angiotensin II, ADH. also nitric oxide (vasodilation), and secretin, glucagon and CCK all cause vasodilation and improved flow
- drugs - volatiles reduce flow
describe biliary drainage..
bile is made by hepatocytes
drained via bile caniculi in lobules
into bile duct within liver follows series of bile ducts e.g. interlobular, septal.
eventually ends in left and right hepatic duct
which join to fom common hepatic bile duct
then common bile duct
which enters duodenum at sphincter of oddi.
pancreatic duct also drains into common bile duct
how are hepatocytes adapted to function..
depends on which
zone 1 = many mitochondria and glycogen synthesis enzymes, more RER for protein synthesis.
zone 3 = rich in SER and CYP450
describe the production and recycling of bile…
bile is composed of bile pigments (bilirubin, biliverdin), cholesterol, phospholipids, bile acids and electrolytes.
it is produced by hepatocytes and enters the biliary system and is secreted into the small intestine to aid with digestion.
prior to secretion it is stored in the gall bladder where it is concentrated by primary and secondary AT. released from gall bladder by CCK (causes contraction) when fatty acids are present in duodenum. also vagal stimulus causes contraction.
primary bile salts include cholic acid and chenodeoxycholic acid
in the colon bacteria modify these to produce secondary bile acids = deoxycholic acid and lithocholic acid.
these are absorbed by terminal ileum and trasnported by portal vein to liver and resecreted by hepatocytes.
what are the functions of bile?
emulsification of fats and aid digestion - increase S.A
absorption of fat soluble vitamins - ADEK
elimination of cholesterol and bilirubin
how much bile can the gall bladder store?
30-60ml
what happens to bile production in terminal ileum resection?
not reabsorbed and recycled
hepatocytes cant make enough bile
so fat indegesiton and poor fat soluble vitamin absorptoon
describe the metabolism of haem
when erythrocytes are digested by macrophages in the spleen they release haemoglobin
broken down to haem and globin
globin reused
haem broken down to biliverdin which is converted to unconjugated bilirubin.
unconjugated bilirubin binds to albumin
taken up by liver and conjugated
conjugated bilirubin excreted in bile
conjugated bilirubin –> urobilinogen by intestinal bacteria.
excreted and some reabsorbed and excreted in urine.
what is jaundice and what are the causes?
Jaundice is a condition characterized by the yellowing of the skin, mucous membranes, and the whites of the eyes (sclerae) due to elevated levels of bilirubin in the blood, a condition known as hyperbilirubinemia.
pre hepatic = heamolysis (haemolytic anaemias - spherocytosis, autoimmune, ABO incompatibiltiy)
hepatic = cirrhosis ,hepatitis, gilberts
post hepatic = gall stones , tumours
in general pre-hepatic - rise in unconjugated
hepatic - both increase
post hepatic - conjugated increases
how can hypoalbumin affect jaundice?
unconjugated binds albumin in blood
low albumin can result in increase of unconjugated bilirubin
what is the cori cycle?
the metabolic pathway of conversion of lactate back to glucose during aerobic conditions
during anaerobic exercise, lactate can build up from glycolysis. (produced by lactate dehydrogenase). this also occurs in ischaemia or all the time by RBC (no nucleus)
the lactate is transported to the liver in the blood and converted back to pyruvate and then glucose - for further glycolysis, glycogen storage or production of aa.
certain lactate dehydrogenase isoenzymes can catalyse the reverse reaction
describe the metabolism of ammonia ..
amino acid breakdown produces ammonia from amine group
also nucleic acid metabolism
urea cycle removes ammonia from blood
urea cycle occurs in zone 1 of hepatocytes where ammonia is converted to urea for excretion in kidneys.
what are the functions of the liver
metabolic
* glycogenesis
* gluconeogeneiss
* glycogenolysis
* urea cycle
* cori cycle
drug detox
* cyp 450 - phase 1
* phase 2 - conjugation
* protects body from toxins ingested
haematological
* clotting factors
* albumin
immunological
* acute phase proteins - CRP
* kuppfer cells
digestion
* bile - fat sol vitamins
how can liver function be assessed?
transaminase blood levels - suggests inflammation of liver e.g. ALT , AST
synthetic function - clotting factors, INR , albumin levels
indicators of biliary disease - bilirubin, ALP
where is energy derived from?
glucose in blood
macromolecules - glycogen, proteins, fats (break down and gluconeogenesis / B oxidation)
define metabolism
chemical processes that occur within cells encompassing anabolic and catabolic reactions.
regulated by complex pathways and second messengers and enzymes
2 main pathways = catabolism (exothermic) and anabolism (endothermic)
what is the basal metabolic rate?
the amount of energy used by an individual in times of rest to maintain basic physiological functions.. 12 hours after a meal, in normothermia
usually around 70-100 cals/ hr
varies depending on gender, age, muscle mass etc
overall in women around 1500cals/day and 2000 in men.
what factors influence BMR?
patient - age, sex, muscle mass, ethnicity, pregnancy
situation - stress, exercise, eating (reduced in starvation), temp
pathological - hyperthyroidism/ hypothyroidism
what calories and nutrients does a typical adult male require?
0.5 - 1g/kg protein
5-10g/kg carbs
1-2g/kg fats
around 100 cal/hr = 2400calories
how can glucose be handled i.e. metabolic pathways
glycolysis - ATP and pyruvate
glucogenesis- production of glycogen
gluconeogenesis - converted to aa
describe glycogenolysis and glycogensis. plus the control.
glycogen is phosphorylated to released glucose-P (glycogen phosphorylase, debranching enzyme)
the reverse can also happen (glycogen synthase, branching enzyme)
glucose 1P to glucose 6P to glucose
enyzme pathways are regulated by a number of hormones - adrenaline, cortisol , glucagon, insulin
how long before glycogen stores are exhausted?
3-4 hours
describe the process of aerobic respiration…
glycolysis - 10 steps - glucose to pyruvate. produces net 2 ATP, 2NADH and 2 pyruvate.
pyruvate enters mitochondria
LINK reaction
- pyrvuvate to acetyl coA (pyruvate dehydrogenase)
- CO2 and NADH produced
krebs cycle
* cycle of enzyme reactions
* starting with citrate and ending with oxaloacetate
* oxaloacetate combines with acetyl coA to madke citrate.
* produces NADH, FADH ATP and CO2
oxidative phosphorylation
* inner mitochondrial membrane and inner mito space
* consists of series of electron transport carriers
* NADH is oxidised and donates electron to the chain, e is transported down the chain, releasing energy to pump H+ ions across into IMS.
* H+ builds up and flows down gradient via ATP synthase
* O2 is final e acceptor and H+ –> H20
* regenerates NAD
* produces 34 ATP
in total 38 ATP
what happens in anerobic respiration?
glycolysis produces pyruvate and 2 ATP and 2 NADH
NADH needs to be regenerated for this pathway to continue
pyruvate –> lactate (lactate dehydrogenase)
replenishes NAD (oxidised)
what substrates can undergo aerobic respiration?
glucose
aminao acids - produce pyruvate and acetyl coA and enter krebs
fats - B oxidation to produce acetyl coA
describe the process of gluconeogrenesis
describes the production of glucose from other molecules. mostly occurs in liver but also kidneys. stimulated by glucagon, inhibited by insulin
important as RBC and neurons only use glucose as substrate.
mostly via pyruvate
e.g. latate and glucogenic aa both produce pyruvate which can be converted back to glucose
also via glycerol - can undergo reverse glycolysis
allows fatty acids to produce glucose
some aa and fatty acids cant produce glucose but can produce acetyl coA and enter krebs
what immediate sources of energy in a cell do you know?
ATP
phosphocreatine
NADH
how does the body handle starvation..
starvation is defined as the failure to ingest sufficient calories to sustain normal body function
during starvation - blood glucose needs to be maintained for RBC and brain
this is via gluconeogenesis due ot fall in insulin, rise in glucagon
slowly levels of FFA and ketones rise as fats are metabolised and ketosis takes place..
first 24 hrs = glycogen stores used. glucose drops iniitially, causes increase glucagon, drop in insulin. promotes glycogenolysis
day 1 -4 = glycogen depleted, glucose levels stabilised. fat metabolism predominates. FFA and glycerol produced. FFA can be used by non-glucose dependant tissues. glycerol converted to glucose by gluconeogenesis.
day 4 plus =
FFA are converted to ketones (ketosis)
brain adapts to use ketones
what are the indications for TPN?
enteral route always prefered where possible however sometime TPN necessary
- disorders requiring complete GIT rest - pancreatitis
- post op feeding failed = more than 5 days e.g. ileus
- malnourished and unable to eat = radiotherapy
what does TPN contain?
solutions are prepared depending on requirements
water 30-40ml/kg/day
30 kcal/kg/day
1g/ kg/ day protein -
essential vitamins/minerals etc
usualy more cals and protein due to hypercatabolic state in stress/ surgery
requires central access
complications of TPN..
related to access = infection, thrombosis, bleeding
related to TPN =
volume overload
electrolyte disturbances
hyperglycaemia
can cause derranged LFTs
what is refeeding syndrome?
severe metabolic and electrolyte disturbance following introduction of food too quickly after a prolonged period of starvation.
during starvation, metabolic pathways alter.
these require K+ and PO4 - these are driven out of cells and stores depleted
once refeeding has begun, K+ and PO4 are driven into cells (low levels intracellularly) for glycogen and fat production (insulin driven)
this reduces extracellular levels
can result in hypokalaemia, hypophosphataemia and hypomagnesaemia
arrhyhtmias, muscle weakness, confusion, seizures.
need to feed slow and monitor electrolytes
what is meant by cellular respiration?
catabolic process releasing the energy from glucose into smaller usable forms of energy ATP.
consists of glycolysis, link, krebs, oxidative phosphorylation
however also can be anaerobic (only glycolysis)
how are amino acids used as energy?
proteins hydrolysed to aa
aa deaminated
ammonia –> urea (urea cycle)
the remainder of the aa can be converted to acetyl coA –> krebs cycle.
or glucogenic aa can be converted back to glucose
what inhibits glucagon release
insulin, adrenaline, somatostatin
is autoregulation seen in the portal vein?
no, not enough smooth muscle
blood flow is directly related to portal pressure.
how does the respiratory cycle affect hepatic venous blood flow?
inspiration - negative thoracic pressure , increases CO and heptaic blood flow
expiration - the opposite
in PPV - positive pressure will reduce blood flow. PEEP reduces it further.
different types of cells seen in liver…
hepatocytes
kuppfer
sinusoidal
biliary epithelium
what is centrolobular necrosis?
occurs when there is poor o2 supply to zone 3
results in hypoxic injury to hepatocytes, poor drug detoxification so toxicity can develop
caused by hypoperfusion - hypotension, haemorrhage, sepsis
drug toxicity - halothane and paracetamol and alcohol
what intraop factors affect hepatic blood flow
perfusion pressrue = MAP - hepatic pressure
MAP = CO x SVR
low SVR due to drugs, hypovolvaemia, haemorrhage
low CO - PEEP/ IPPV, drugs
hepatic pressure - surgical pressure
what is cirrhosis?
chronic liver inflammation can result in scarring - cirrhosis.
small fibrotic liver with poor function
caused by viral hepatitis, alcohol, wilsons, autoimmune hepatitis
results in
* poor synthetic function (low albumin, clotting),
* poor metabolic function (poor fat absorption, risk of hypoglycaemia),
* poor drug detox
* increased resistance to blood flow and portal hypertension
what defines portal HTN, what are the signs?
more than 12mmHg
ascites - high venous hydrostatic pressure
splenomegaly
varices
what are the stimulus for gastrin release and its roles..
stimulus - Ach from vagus nerve, presence of peptides
roles = acid secretion, motility, stimulates pepsinogen release
what is the alkaline tide?
as HCL secreted to lumen,
HCO3 is reabsorbed into blood
how long does gastric emptying take?
starts at 20min
complete 3 to 4 hours
depends on what is eaten and external factors
what are the clinical fasting guidelines?
2 hour clear fluids
6 hours food / non clear
paeds
1 hour clear fluids
6 hours food
4 hours breast milk
what is gastric dumping syndrome?
syndrome associated with gastric surgery
loss of stomach
means suddenly food dumped into intestine
pain, bloating, hyperglycaemia
what is the role of perioperative gastric USS?
can be used to USS stomach to estimate contents to estimate risk of aspiration. stomach USS when patient in right lateral position
can be useful if limiting starvation period is necessary paediatrics, emergency theatre
or gastric emptying is slowed - trauma, diabetic neuropathy, opioid us
less than 1.5ml/kg in stomach is associated with low risk of aspiration
how can risk of aspiration perioperatively be reduced?
following fasting guidelines
RSI
other
prokinetics
antacids
reduce opioid use
gastric USS
what concerns are there is a patient with hepatitis needing surgery?
drug metabolism slowed
potential coagulopathy
risk of worsening hepatitis psot op - hepatic encephalopathy
avoid hepatotoxic drugs and those that use minimal liver metabolism
