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4 - Med > Gastroenterology Physiology > Flashcards

Gastroenterology Physiology Flashcards

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1
Q

name some functions of the liver ?
- bile role ?
- excretion of ?
- metabolism of ?
- activation of ?
- storage of ?
- synthesis of ?
- detoxification of ?

A
  • 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
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2
Q

what is the blood supply to the liver ?

A

dual blood supply
- hepatic artery
- portal vein

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3
Q

describe hepatic histology - what is the portal triad

A

liver arranged into hepatic lobules with portal triad (hepatic artery + portal vein + bile duct) at edge and central hepatic vein

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4
Q

what are the different zones within hepatocytes ?

A

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)

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5
Q

what does acute liver injury result in ? generally

A

damage to + loss of hepatocytes (by necrosis or apoptosis)

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6
Q

what does chronic liver damage lead to ?

A

fibrosis => cirrhosis => HCC

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7
Q

what are the different forms of bilirubin ? soluble or insoluble ?

A
  • 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)
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8
Q

where is haemoglobin broken down ? and what is it broken down into ?

A

reticuloendothelial cells (macrophage) take up RBC and metabolic haemoglobin into haem + globin)

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9
Q

what is globin broken down into ? what happen to this ?

A

glib further broken down to AA and recycled)

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10
Q

what is haem broken down into ? what enzyme does this

A

haem converted to iron and biliverdin catalysed by haem oxygenase
- biliverdin then further converted to UC bilirubin

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11
Q

after conversion in reticuloendothelial cells, what happens to the UC ?

A

UC travels to liver (bound to albumin)

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12
Q

what happens when UC gets to liver ?

A

glucoronic acid is added (catalysed by glucouryltransferase) => CB (water soluble)

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13
Q

what happens to the CB in the liver ?

A

no water soluble so it is excreted into duodenum in the bile

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14
Q

what happens to the bilirubin in the colon ? what is the end product called ?

A

in colon, bacteria remove glucoronic acid => UCB (urobilinogen)

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15
Q

what happens to urobilinogen in the colon ?

A
  • 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)
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16
Q

what are the 3 different types of jaundice ? state whether each is conjugated or unconjugated

A
  • pre hepatic (UC)
  • hepatic (C)
  • post-hepatic (C)
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17
Q

what causes pre-hepatic jaundice ? generally

A

excessive RBC breakdown (overwhelms livers ability to conjugate bilirubin)

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18
Q

what causes hepatic jaundice ? generally ?

A

dysfunction of hepatic cells

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19
Q

what causes post-hepatic jaundice ? generally

A

obstruction of biliary drainage

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20
Q

pre hepatic jaundice, describe the:
- urine
- stools
- itching
- liver tests

A
  • urine: normal
  • stools: normal
  • itching: no
  • liver tests: normal
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21
Q

cholestatic (hepatic/post-hepatic jaundice), describe the:
- urine
- stools
- itching
- liver tests

A
  • urine: dark
  • stools: may be pale
  • itching: maybe
  • liver tests: abnormal
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22
Q

what is jaundice ?

A

yellowing of skin, sclerae + mucosa from increased plasma bilirubin

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23
Q

causes of jaundice in a previously stable patient with cirrhosis ? (4)

A
  • sepsis
  • malignancy
  • GI bleeding
  • alcohol
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24
Q

name some common lipid forms in the body ? (3)

A
  • triglycerides
  • phospholipids (both comprise FA)
  • cholesterol
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25
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)
26
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
27
where does beta oxidation occur ?
in mitochondria of any cell
28
what is end product of beta-oxidation ?
acetyl Co-A
29
which clotting factors are produced by the liver ?
II, VII, IX, X (1972)
30
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)
31
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)
32
what is protein synthesis stimulated by ?
insulin and growth hormones
33
name some plasma proteins ? what pressure do they exert ?
albumin, globulin, fibrinogen, CRP - also produce oncotoic pressure
34
describe the glycogen store distribution in the body ?
100g in liver 300g in skeletal muscle
35
which vitamins are stored in the liver ?
lipid soluble vitamins (ADEK) plus B12 all stored in liver
36
what minerals are stored in the liver ?
Fe2+ Cu2+
37
what 3 glands is saliva produced by ?
3 paired ducted exocrine glands - parotid - submandibular - sublingual
38
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
39
what would cause decreased saliva production ?
autonomic control SNS => NAd release => decreased saliva production form acing cells
40
what drugs would help with excess alive production ?
anticholinergics helps with excess salvia production (or is SE of anti-cholinesterase)
41
what is the function of saliva ?
- lubrication - digestion - keeping mucosa moist - maintain alkaline emoliant
42
describe the constituents of saliva ? (6)
- water - electrolytes - bicarb - bacteriostats - mucus - enzymes
43
what are the 3 different phases to swallowing ?
- voluntary phase (mastication) - pharyngeal - oesophageal
44
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
45
describe the muscle in the oesophagus ?
superior 1/3 is voluntary muscle and lower 2/3 smooth muscle propelled by peristalsis waves
46
what is the function of the stomach ? (2)
- preliminary digestion - destroying micro organisms
47
what is the pH of the stomach ?
pH 1.5 - 3.5
48
where is HCl produced ? how
parietal cells actively transport H+ and Cl- into stomach lumen
49
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
50
what does X nerve stimulation cause in relation to the stomach ?
gastrin (hormone) secretion form G cells
51
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
52
what decreased gastric acid production ? (3)
- somatostain - CCK - secretin
53
what do parietal cells produce ? (2)
- HCl - intrinsic factor
54
what do chief cells produce ? (1)
- pepsinogens
55
what do enterochromaffin like cells produce ?
histamines
56
what hormonal signals are involved in appetite control ? when stomach empty ?
stomach empty => gremlin production from pancreas + secretion into stomach => appetite stimulation
57
what hormone is involved in appetite suppression ? released from where ?
leptin release from adipocytes => suppression of appetite
58
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
59
how does X nerve affect gastric mucus production ?
X nerve innervation => prostaglandin release => increase gastric mucus production
60
what are the 3 parts to the small intestine ?
- duodenum - jejunum - ileum
61
what are the 4 main layers to the small intestine ? innermost to outermost
innermost - mucosa - submucosa - muscular externa - adventitia
62
what is contained within the submucosa of the small intestine ?
contains blood vessels, lymph + sub mucosal plexus
63
describe the structure of the muscular external of the small intestine ?
2 smooth muscle layers with myenteric plexus between
64
what does presence of fat in small intestine stimulate ?
CCK release from I cells => gall bladder contraction (bile => cystic duct)
65
what is the function of bile ? (2)
- emulsification + absorption of fat - prevention of gall stone formation
66
what are the sontituents of bile ?
- bile acids - cholesterol - phospholipids - bile pigment (bilirubin) - electrolyes - water
67
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
68
what are the 2 primary bile acids ?
- cholic acids - chemodeoxycholic acid
69
where is bile made ? and stored ?
bile assess out of liver through the bile ducts + concentrated and stored in gallbladder
70
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)
71
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
72
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
73
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
74
what are the BMI ranges for - underweight - target - overweight - obese
- underweight: <18.5 - target: 18.5 - 25 - overweight: 25 - 30 - obese: 30 - 35
75
what is cholestasis ?
blockage of flow of bile
76
what is cholelithiasis ?
gallstones
77
what is choledocholethiasis ?
gall stones in the bile duct
78
what is binary colic ?
intermittent RUQ pain that's caused by gallstones irritating bile duct
79
what is cholecystitis ?
inflammation of gallbladder
80
what is cholangitis ?
inflammation of bile ducts
81
what is gall bladder empyema ?
pus in the the gall bladder
82
what is cholecystectomy ?
surgical removal of GB
83
what are aminotransferases ? and when are they released ?
(AST, ALT) - released in bloodstream after hepatocellular injury
84
what can cause raised alkaline phosphatase ?
can be raised due to liver, bone or placental issues
85
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)
86
what tests are useful to monitor hepatic function ?
- serum albumin - serum bilirubin - PTT (INR)
87
how would LFT be affected in ALD ?
AST:ALT > 2:1 normal ALP increased GGT macroctyosis
88
describe the LFT results in a cholestasis predominant liver injury ?
ALP + GGT v high AST/ALT mildy raised
89
name some causes of severe ulcers ?
- Crohns - coeliac disease - behcets - trauma - infection (herpes, syphillus)
90
candidiasis RF ? (4)
- extremes of age - DM - ABx use - immunosuppression
91
candidiasis Mx ?
- nystatin suspension - fluconazole for oropharyngeal thrush
92
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
93
what is virchows node ? where ? indicates what ?
virvowhs node (L supraclavicular node): suggests intra-ado malignancy

4 - Med (21 decks)

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