Gastroenterology Physiology Flashcards
name some functions of the liver ?
- bile role ?
- excretion of ?
- metabolism of ?
- activation of ?
- storage of ?
- synthesis of ?
- detoxification of ?
- Bile production + excretion
- excretion (of bilirubin + cholesterol + drugs)
- metabolism (of fats + proteins + carbs)
- enzyme activation
- storage (glycogen + vitamins + minerals)
- synthesis (of plasma proteins (albumin) + clotting factors)
- blood detoxification
what is the blood supply to the liver ?
dual blood supply
- hepatic artery
- portal vein
describe hepatic histology - what is the portal triad
liver arranged into hepatic lobules with portal triad (hepatic artery + portal vein + bile duct) at edge and central hepatic vein
what are the different zones within hepatocytes ?
histological
- hepatocytes within lobule arranged into zones 1-3 which receive progressively less oxygen
- zone 3 (closest to central vein - anything toxic most likely to impact here)
what does acute liver injury result in ? generally
damage to + loss of hepatocytes (by necrosis or apoptosis)
what does chronic liver damage lead to ?
fibrosis => cirrhosis => HCC
what are the different forms of bilirubin ? soluble or insoluble ?
- unconjugated (lipid soluble, insoluble in water so can only travel in blood stream bound to albumin, cannot be directly excreted)
- conjugated (water soluble, so can travel in bloodstream without transport protein (albumin)
where is haemoglobin broken down ? and what is it broken down into ?
reticuloendothelial cells (macrophage) take up RBC and metabolic haemoglobin into haem + globin)
what is globin broken down into ? what happen to this ?
glib further broken down to AA and recycled)
what is haem broken down into ? what enzyme does this
haem converted to iron and biliverdin catalysed by haem oxygenase
- biliverdin then further converted to UC bilirubin
after conversion in reticuloendothelial cells, what happens to the UC ?
UC travels to liver (bound to albumin)
what happens when UC gets to liver ?
glucoronic acid is added (catalysed by glucouryltransferase) => CB (water soluble)
what happens to the CB in the liver ?
no water soluble so it is excreted into duodenum in the bile
what happens to the bilirubin in the colon ? what is the end product called ?
in colon, bacteria remove glucoronic acid => UCB (urobilinogen)
what happens to urobilinogen in the colon ?
- 90% further oxidised to sterocobilin (excreted through faeces)
- 10% (reabsorbed into blood via portal vein - some transported to kidneys and excreted at urobilin and some enters enterohepatic circulation and transported back to liver)
what are the 3 different types of jaundice ? state whether each is conjugated or unconjugated
- pre hepatic (UC)
- hepatic (C)
- post-hepatic (C)
what causes pre-hepatic jaundice ? generally
excessive RBC breakdown (overwhelms livers ability to conjugate bilirubin)
what causes hepatic jaundice ? generally ?
dysfunction of hepatic cells
what causes post-hepatic jaundice ? generally
obstruction of biliary drainage
pre hepatic jaundice, describe the:
- urine
- stools
- itching
- liver tests
- urine: normal
- stools: normal
- itching: no
- liver tests: normal
cholestatic (hepatic/post-hepatic jaundice), describe the:
- urine
- stools
- itching
- liver tests
- urine: dark
- stools: may be pale
- itching: maybe
- liver tests: abnormal
what is jaundice ?
yellowing of skin, sclerae + mucosa from increased plasma bilirubin
causes of jaundice in a previously stable patient with cirrhosis ? (4)
- sepsis
- malignancy
- GI bleeding
- alcohol
name some common lipid forms in the body ? (3)
- triglycerides
- phospholipids (both comprise FA)
- cholesterol
what is lipolysis ? describe it
what is it stimulated by ? (2)
when energy needed form fat stores in adipose tissue, TG are hydrolysed into FAs (stimulated by adrenaline + glucagon)
once TGs are broken down to FAs, where do they go ? what happens ?
these enter circulation bound to albumin => transport to liver => hepatocytes break down partially and then beta oxidation
where does beta oxidation occur ?
in mitochondria of any cell
what is end product of beta-oxidation ?
acetyl Co-A
which clotting factors are produced by the liver ?
II, VII, IX, X
(1972)
where does protein breakdown occur ? where is especially important ?
occurs in all cells of the body
(liver is important as it stores more protein, can rapidly synthesise or degrade proteins and AA - unlike most other tissues)
how many Amino acids are there ? how many can be synthesised and how many from diet ?
20 are needed
- 10 can be synthesised
- 10 needed from diet (essential AAs)
what is protein synthesis stimulated by ?
insulin and growth hormones
name some plasma proteins ? what pressure do they exert ?
albumin, globulin, fibrinogen, CRP
- also produce oncotoic pressure
describe the glycogen store distribution in the body ?
100g in liver
300g in skeletal muscle
which vitamins are stored in the liver ?
lipid soluble vitamins (ADEK) plus B12 all stored in liver
what minerals are stored in the liver ?
Fe2+
Cu2+
what 3 glands is saliva produced by ?
3 paired ducted exocrine glands
- parotid
- submandibular
- sublingual
what would stimulate increased saliva secretion ? what CNs ?
under autonomic control (PSNS - rest and digest)
- PSNS via CN VII + IX => Ash release => acini cells increase saliva secretion + duct cells increase HCO3- secretion
what would cause decreased saliva production ?
autonomic control
SNS => NAd release => decreased saliva production form acing cells
what drugs would help with excess alive production ?
anticholinergics helps with excess salvia production (or is SE of anti-cholinesterase)
what is the function of saliva ?
- lubrication
- digestion
- keeping mucosa moist
- maintain alkaline emoliant
describe the constituents of saliva ? (6)
- water
- electrolytes
- bicarb
- bacteriostats
- mucus
- enzymes
what are the 3 different phases to swallowing ?
- voluntary phase (mastication)
- pharyngeal
- oesophageal
describe the pharyngeal phase of swallowing ? what happens when bolus moves to pharynx ? (4)
bolus moves to pharynx =>
- inhibit respiration
- raises larynx
- closes glottis
- opens upper oesophageal sphincter
describe the muscle in the oesophagus ?
superior 1/3 is voluntary muscle and lower 2/3 smooth muscle propelled by peristalsis waves
what is the function of the stomach ? (2)
- preliminary digestion
- destroying micro organisms
what is the pH of the stomach ?
pH 1.5 - 3.5
where is HCl produced ? how
parietal cells actively transport H+ and Cl- into stomach lumen
what 2 stimulates would increase gastric acid secretion ?
cephalic phase (seeing or chewing food) or gastric phase (stomach distension) => stimulate ACh production by X nerve
what does X nerve stimulation cause in relation to the stomach ?
gastrin (hormone) secretion form G cells
from what is gastrin produced by and what does it act on and what does this cause ?
gastrin secreted by G cells => acts on parietal cells on CCK receptors => increase ATPases in parietal cells membranes => increase acid production
what decreased gastric acid production ? (3)
- somatostain
- CCK
- secretin
what do parietal cells produce ? (2)
- HCl
- intrinsic factor
what do chief cells produce ? (1)
- pepsinogens
what do enterochromaffin like cells produce ?
histamines
what hormonal signals are involved in appetite control ? when stomach empty ?
stomach empty => gremlin production from pancreas + secretion into stomach => appetite stimulation
what hormone is involved in appetite suppression ? released from where ?
leptin release from adipocytes => suppression of appetite
how does NSAID use affect gastric mucus production ?
NSAID use => block prostaglandin synthesis => reduce gastric mucus secretion + reduce mucosal blood flow => mucus less effective at protecting stomach epithelium => peptic ulcers
how does X nerve affect gastric mucus production ?
X nerve innervation => prostaglandin release => increase gastric mucus production
what are the 3 parts to the small intestine ?
- duodenum
- jejunum
- ileum
what are the 4 main layers to the small intestine ? innermost to outermost
innermost
- mucosa
- submucosa
- muscular externa
- adventitia
what is contained within the submucosa of the small intestine ?
contains blood vessels, lymph + sub mucosal plexus
describe the structure of the muscular external of the small intestine ?
2 smooth muscle layers with myenteric plexus between
what does presence of fat in small intestine stimulate ?
CCK release from I cells => gall bladder contraction (bile => cystic duct)
what is the function of bile ? (2)
- emulsification + absorption of fat
- prevention of gall stone formation
what are the sontituents of bile ?
- bile acids
- cholesterol
- phospholipids
- bile pigment (bilirubin)
- electrolyes
- water
what happens to the gall bladder after eating ?
after eating => prescience of fat in duodenum => CCK release => gallbladder contraction + relaxes sphincter of Oddi => bile flow to duodenum
what are the 2 primary bile acids ?
- cholic acids
- chemodeoxycholic acid
where is bile made ? and stored ?
bile assess out of liver through the bile ducts + concentrated and stored in gallbladder
where are most bile acids reabsorbed ? transported back where ?
most bile acids are reabsorbed in terminal ileum + returned to liver vi HPV (liver then extracts the bile salts)
what is the spleen ? what are the 2 different parts to it ?
non-vital organ in LUQ with 2 types of tissues with different functions
- white pulp
- red pulp
what is the function of the white pulp in the spleen ?
white pulp
- lymph related nodules (malpiglian corpuscles)
- importan in normal immune response to infection
what is the function of red pulp in spleen ?
(80% red pulp)
- removal of old/damged RBC
- phagocytosis of opsonised bacteria by macrophages
- storage of RBC in case of hypovolaemia
what are the BMI ranges for
- underweight
- target
- overweight
- obese
- underweight: <18.5
- target: 18.5 - 25
- overweight: 25 - 30
- obese: 30 - 35
what is cholestasis ?
blockage of flow of bile
what is cholelithiasis ?
gallstones
what is choledocholethiasis ?
gall stones in the bile duct
what is binary colic ?
intermittent RUQ pain that’s caused by gallstones irritating bile duct
what is cholecystitis ?
inflammation of gallbladder
what is cholangitis ?
inflammation of bile ducts
what is gall bladder empyema ?
pus in the the gall bladder
what is cholecystectomy ?
surgical removal of GB
what are aminotransferases ? and when are they released ?
(AST, ALT)
- released in bloodstream after hepatocellular injury
what can cause raised alkaline phosphatase ?
can be raised due to liver, bone or placental issues
where is GGT present ?
present in liver, pancreas, renal tubules
(but not in bone so helps distinguish if Alp is raised from bone or liver)
what tests are useful to monitor hepatic function ?
- serum albumin
- serum bilirubin
- PTT (INR)
how would LFT be affected in ALD ?
AST:ALT > 2:1
normal ALP
increased GGT
macroctyosis
describe the LFT results in a cholestasis predominant liver injury ?
ALP + GGT v high
AST/ALT mildy raised
name some causes of severe ulcers ?
- Crohns
- coeliac disease
- behcets
- trauma
- infection (herpes, syphillus)
candidiasis RF ? (4)
- extremes of age
- DM
- ABx use
- immunosuppression
candidiasis Mx ?
- nystatin suspension
- fluconazole for oropharyngeal thrush
what are some causes of dysphagia ? (5)
- malignant structure (need to exclude this)
- extrinsic pressure (lung cx, LA enlargement)
- pharyngeal pouch
- neurological bulbar palsy
- achalasia
what is virchows node ? where ? indicates what ?
virvowhs node (L supraclavicular node): suggests intra-ado malignancy
