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4 - Med > Gastroenterology Physiology > Flashcards

Gastroenterology Physiology Flashcards

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
Q

what is lipolysis ? describe it
what is it stimulated by ? (2)

A

when energy needed form fat stores in adipose tissue, TG are hydrolysed into FAs (stimulated by adrenaline + glucagon)

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26
Q

once TGs are broken down to FAs, where do they go ? what happens ?

A

these enter circulation bound to albumin => transport to liver => hepatocytes break down partially and then beta oxidation

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27
Q

where does beta oxidation occur ?

A

in mitochondria of any cell

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28
Q

what is end product of beta-oxidation ?

A

acetyl Co-A

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29
Q

which clotting factors are produced by the liver ?

A

II, VII, IX, X
(1972)

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30
Q

where does protein breakdown occur ? where is especially important ?

A

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)

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31
Q

how many Amino acids are there ? how many can be synthesised and how many from diet ?

A

20 are needed
- 10 can be synthesised
- 10 needed from diet (essential AAs)

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32
Q

what is protein synthesis stimulated by ?

A

insulin and growth hormones

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33
Q

name some plasma proteins ? what pressure do they exert ?

A

albumin, globulin, fibrinogen, CRP
- also produce oncotoic pressure

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34
Q

describe the glycogen store distribution in the body ?

A

100g in liver
300g in skeletal muscle

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35
Q

which vitamins are stored in the liver ?

A

lipid soluble vitamins (ADEK) plus B12 all stored in liver

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36
Q

what minerals are stored in the liver ?

A

Fe2+
Cu2+

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37
Q

what 3 glands is saliva produced by ?

A

3 paired ducted exocrine glands
- parotid
- submandibular
- sublingual

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38
Q

what would stimulate increased saliva secretion ? what CNs ?

A

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
Q

what would cause decreased saliva production ?

A

autonomic control
SNS => NAd release => decreased saliva production form acing cells

40
Q

what drugs would help with excess alive production ?

A

anticholinergics helps with excess salvia production (or is SE of anti-cholinesterase)

41
Q

what is the function of saliva ?

A
  • lubrication
  • digestion
  • keeping mucosa moist
  • maintain alkaline emoliant
42
Q

describe the constituents of saliva ? (6)

A
  • water
  • electrolytes
  • bicarb
  • bacteriostats
  • mucus
  • enzymes
43
Q

what are the 3 different phases to swallowing ?

A
  • voluntary phase (mastication)
  • pharyngeal
  • oesophageal
44
Q

describe the pharyngeal phase of swallowing ? what happens when bolus moves to pharynx ? (4)

A

bolus moves to pharynx =>
- inhibit respiration
- raises larynx
- closes glottis
- opens upper oesophageal sphincter

45
Q

describe the muscle in the oesophagus ?

A

superior 1/3 is voluntary muscle and lower 2/3 smooth muscle propelled by peristalsis waves

46
Q

what is the function of the stomach ? (2)

A
  • preliminary digestion
  • destroying micro organisms
47
Q

what is the pH of the stomach ?

A

pH 1.5 - 3.5

48
Q

where is HCl produced ? how

A

parietal cells actively transport H+ and Cl- into stomach lumen

49
Q

what 2 stimulates would increase gastric acid secretion ?

A

cephalic phase (seeing or chewing food) or gastric phase (stomach distension) => stimulate ACh production by X nerve

50
Q

what does X nerve stimulation cause in relation to the stomach ?

A

gastrin (hormone) secretion form G cells

51
Q

from what is gastrin produced by and what does it act on and what does this cause ?

A

gastrin secreted by G cells => acts on parietal cells on CCK receptors => increase ATPases in parietal cells membranes => increase acid production

52
Q

what decreased gastric acid production ? (3)

A
  • somatostain
  • CCK
  • secretin
53
Q

what do parietal cells produce ? (2)

A
  • HCl
  • intrinsic factor
54
Q

what do chief cells produce ? (1)

A
  • pepsinogens
55
Q

what do enterochromaffin like cells produce ?

A

histamines

56
Q

what hormonal signals are involved in appetite control ? when stomach empty ?

A

stomach empty => gremlin production from pancreas + secretion into stomach => appetite stimulation

57
Q

what hormone is involved in appetite suppression ? released from where ?

A

leptin release from adipocytes => suppression of appetite

58
Q

how does NSAID use affect gastric mucus production ?

A

NSAID use => block prostaglandin synthesis => reduce gastric mucus secretion + reduce mucosal blood flow => mucus less effective at protecting stomach epithelium => peptic ulcers

59
Q

how does X nerve affect gastric mucus production ?

A

X nerve innervation => prostaglandin release => increase gastric mucus production

60
Q

what are the 3 parts to the small intestine ?

A
  • duodenum
  • jejunum
  • ileum
61
Q

what are the 4 main layers to the small intestine ? innermost to outermost

A

innermost
- mucosa
- submucosa
- muscular externa
- adventitia

62
Q

what is contained within the submucosa of the small intestine ?

A

contains blood vessels, lymph + sub mucosal plexus

63
Q

describe the structure of the muscular external of the small intestine ?

A

2 smooth muscle layers with myenteric plexus between

64
Q

what does presence of fat in small intestine stimulate ?

A

CCK release from I cells => gall bladder contraction (bile => cystic duct)

65
Q

what is the function of bile ? (2)

A
  • emulsification + absorption of fat
  • prevention of gall stone formation
66
Q

what are the sontituents of bile ?

A
  • bile acids
  • cholesterol
  • phospholipids
  • bile pigment (bilirubin)
  • electrolyes
  • water
67
Q

what happens to the gall bladder after eating ?

A

after eating => prescience of fat in duodenum => CCK release => gallbladder contraction + relaxes sphincter of Oddi => bile flow to duodenum

68
Q

what are the 2 primary bile acids ?

A
  • cholic acids
  • chemodeoxycholic acid
69
Q

where is bile made ? and stored ?

A

bile assess out of liver through the bile ducts + concentrated and stored in gallbladder

70
Q

where are most bile acids reabsorbed ? transported back where ?

A

most bile acids are reabsorbed in terminal ileum + returned to liver vi HPV (liver then extracts the bile salts)

71
Q

what is the spleen ? what are the 2 different parts to it ?

A

non-vital organ in LUQ with 2 types of tissues with different functions
- white pulp
- red pulp

72
Q

what is the function of the white pulp in the spleen ?

A

white pulp
- lymph related nodules (malpiglian corpuscles)
- importan in normal immune response to infection

73
Q

what is the function of red pulp in spleen ?

A

(80% red pulp)
- removal of old/damged RBC
- phagocytosis of opsonised bacteria by macrophages
- storage of RBC in case of hypovolaemia

74
Q

what are the BMI ranges for
- underweight
- target
- overweight
- obese

A
  • underweight: <18.5
  • target: 18.5 - 25
  • overweight: 25 - 30
  • obese: 30 - 35
75
Q

what is cholestasis ?

A

blockage of flow of bile

76
Q

what is cholelithiasis ?

A

gallstones

77
Q

what is choledocholethiasis ?

A

gall stones in the bile duct

78
Q

what is binary colic ?

A

intermittent RUQ pain that’s caused by gallstones irritating bile duct

79
Q

what is cholecystitis ?

A

inflammation of gallbladder

80
Q

what is cholangitis ?

A

inflammation of bile ducts

81
Q

what is gall bladder empyema ?

A

pus in the the gall bladder

82
Q

what is cholecystectomy ?

A

surgical removal of GB

83
Q

what are aminotransferases ? and when are they released ?

A

(AST, ALT)
- released in bloodstream after hepatocellular injury

84
Q

what can cause raised alkaline phosphatase ?

A

can be raised due to liver, bone or placental issues

85
Q

where is GGT present ?

A

present in liver, pancreas, renal tubules
(but not in bone so helps distinguish if Alp is raised from bone or liver)

86
Q

what tests are useful to monitor hepatic function ?

A
  • serum albumin
  • serum bilirubin
  • PTT (INR)
87
Q

how would LFT be affected in ALD ?

A

AST:ALT > 2:1
normal ALP
increased GGT
macroctyosis

88
Q

describe the LFT results in a cholestasis predominant liver injury ?

A

ALP + GGT v high
AST/ALT mildy raised

89
Q

name some causes of severe ulcers ?

A
  • Crohns
  • coeliac disease
  • behcets
  • trauma
  • infection (herpes, syphillus)
90
Q

candidiasis RF ? (4)

A
  • extremes of age
  • DM
  • ABx use
  • immunosuppression
91
Q

candidiasis Mx ?

A
  • nystatin suspension
  • fluconazole for oropharyngeal thrush
92
Q

what are some causes of dysphagia ? (5)

A
  • malignant structure (need to exclude this)
  • extrinsic pressure (lung cx, LA enlargement)
  • pharyngeal pouch
  • neurological bulbar palsy
  • achalasia
93
Q

what is virchows node ? where ? indicates what ?

A

virvowhs node (L supraclavicular node): suggests intra-ado malignancy

4 - Med (12 decks)

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