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GI > Liver lover lol alliteration > Flashcards

Liver lover lol alliteration Flashcards

1
Q

Major aspects of structure which influence function?

A

Vascular system
Biliary 🌳-system of ducts 🚌bile out of liver➩small intestine
3D arrangement of liver cells w vascular + biliary systems

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2
Q

Blood supply to liver?

A

75% from portal vein

25% from hepatic artery

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3
Q

Where do the central veins of liver lobules drain?

A

➩ hepatic vein ➩ vena cava

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4
Q

1ᵒ cells of liver + function?

A

Hepatocytes 60%– perform metabolic functions
Kupffer cells 30%– type of tissue macrophage
Others -endothelial cells+stellate cells

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5
Q

What’s the functional unit of the liver?

A

Hepatic lobule - hexagonal plates of hepatocytes around central hepatic vein – each 6 corners is triad of branches of portal vein, hepatic artery, bile duct

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6
Q

What are sinusoids?

A

small channels lined w hepatocytes

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7
Q

What’s the biliary system?

A

hepatocytes⇶bile –> channels between cells-canalinculi –> small ducts –> large ducts–>
anastomose onto common bile duct

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8
Q

How liver’s microstructure supports its roles?

A

↑ SA for exchange of ∞
Separation of blood from bile
Pumps positioning achieves specific localisation of materials at cellular level

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9
Q

How Kupffer cells act as protective barrier?

A

Removes gut 🐛 ∴ <1% entering portal blood succeeds in passing via liver➩systemic circulation

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10
Q

What’s bile?

A

Fluid=water, electrolytes, organic∞-bile acids, cholesterol, bilirubin,phospholipids

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11
Q

How’s bile secreted?

A
  • by hepatocytes-bile salts, cholesterol, other organic constituents
  • by epithelial cells lining bile ducts-watery solution of Na+HCO3, stimulated by Secretin∵acid in duodenum
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12
Q

How much bile does a human produce daily?

A

400-800ml

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13
Q

Diff processes of bile→duodenum?

A

Bile from hepatic ducts–>common bile duct–>duodenum
OR
diverted via cystic duct–>GALL BLADDER–>conc +stored 30-50ml–>⇶ by cholecystokinin ∵ fat in duodenum

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14
Q

What’s the entry➩ doudenum is controlled by?

A

Sphincter of Odii

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15
Q

How’s gallstone produced?

A

Abnormal conditions–>cholesterol ppts in gallbladder–>

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16
Q

Types of stones?

A

cholesterol 80% + pigment 20%

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17
Q

What causes gallstones?

A
  • ↑fat diet
  • ↑synthesis of cholesterol
  • Inflammation of GB epithelium changes mucousa absorption
  • ⇑ absorption of H2O+bile salts–>cholesterol conc
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18
Q

Risk factors of gallstones?

A

♀,obesity, ⇑ oestrogen eg 🤰, HRT

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19
Q

Where do gallstones form?

A

anywhere along biliary tract

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20
Q

What are bile acids?

A

derivatives of cholesterol, made in hepatocytes

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21
Q

How are bile acids made?

A

cholesterol→cholic + chenodeoxycholic acids–>conjugated w glycine/taurine–>↑ solubility➩cannaliculi–> the intestinal 🐛converts → 2ᵒ bile acid

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22
Q

What’s the enterohepatic circulation of bile acids?

A

Bile acids from liver/gall bladder➩ small intestine for fat absorption–> re-absorbed in terminal ileum–>hepatic portal vein–>liver–>taken up in hepatocytes–>re-secreted in new bile

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23
Q

How often bile acids recirculated?

A

6-8x per day

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24
Q

How much bile acids reabsorbed?

A

95%.. 5% lost in faeces

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25
Q

Function of bile?

A
  • Emulsification for fat digestion + absorption
  • Bile+pancreatic juice neutralises gastric juice as enters small intestine
  • Aids digestive 𝔼
  • Remove waste from blood -bilirubin +cholesterol
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26
Q

How much cholesterol is eliminated daily?

A

500g cholesterol→ bile acids

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27
Q

What’s bilirubin?

A

Yellow pigment from Hb breakdown

Useless+toxic but ~6g/day .. a lot

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28
Q

How’s aged 🔴 destroyed?

A

Digested by macrophages
Fe- recycled
Globin chains-catabolized
Haem (porphyrin)-eliminated

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29
Q

Where’s 🔴 digested?

A

mostly in spleen

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30
Q

Formation + removal of bilirubin?

A

Haem→free bilirubin–>released into plasma carried bound to albumin–>absorbed by hepatocytes –>conjugated w glucoronic acid→bile–>metabolised by intestinal lumen–>faeces/urine

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31
Q

Why’s faces brown + urine yellow?

A

Stercobilin – metabolite

Yellow urobilin + urobilinogen-metabolite

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32
Q

What’s jaundice?

A

⇑ of free or conjugated bilirubin accumulate in ECF
∴
Yellow discoloration of the skin, sclera,mucous membranes is observed
Normal plasma [bilirubin] = 0.5mg/dl
discolouration >1.5mg/dl

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33
Q

What’s ‘green jaundice’?

A

mutation of biliverdin reductase gene ∴biliverdin NOT→ bilirubin∴ built up in plasma

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34
Q

Types of jaundice?

A

Pre-hepatic (haemolytic)
Hepatic
Post-hepatic (obstructive)

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35
Q

What’s pre-hapatic jaundice?

A
  • ⇑🔴breakdown eg neonatal jaundice

- ⇑unconjugated bilirubin

36
Q

What’s hepatic jaundice?

A
  • Hepatocyte damage (>80%) eg cirrhosis,💊, hepatitis A,B,C,E, Gilberts Syndrome
  • ⇑conjugated +/or unconjugated bilirubi
37
Q

What’s post-hepatic jaundice?

A
  • ⇑conjugated bilirubin
  • Obstruction ➩duodenum
  • Enters circulation➩ dark urine eg gallstones, carcinoma of pancreas/bile ducts
38
Q

What’s Gilbert’s syndrome?

A

congenital disorder where ↓𝔼 that conjugates bilirubin w glucoronic acid–>↑unconjugated bilirubin

39
Q

Why does neonatal jaundice occur?

A

Fetal Hb →adult Hb so ⇑🔴breakdown results –> normal physiological jaundice but liver’s immature- delay in processing

40
Q

Treatment for neonatal jaundice?

A

Sunlight includes blue light- filters out (UVA, UVB, UVC, IR etc) ↓ risk of over-heating or sunburn

41
Q

What’s the Glucose Buffer Function?

A

Humans (pre-prandial) 4-5.9mmol/L

42
Q

What’s glycogenesis?

A

glucose → glycogen (stimulated by insulin). Liver stores glycogen 80g

43
Q

What’s glycogenolysis

A

glycogen→glucose stimulated by glucagon + A

44
Q

What’s gluconeogenesis?

A

lactate, AA & glycerol (from TGC)→glucose

45
Q

What’s glycolysis?

A

glucose → pyruvate releasing E to form ATP + NADH

46
Q

How’s fat metabolised in liver?

A

TCG oxidized in hepatocytes
Lipoproteins synthesised in liver
⇑Carb+🐟 → FA + TCGs – stored in adipose
Synthesis of cholesterol + phospholipids- some→lipoproteins

47
Q

What’s citric cycle?

A

FA enter it to release E + → ketone bodies

48
Q

Sources of FA for metabolism?

A

Dietary source of TCGs
TCGs stored in adipocytes
TCGs synthesised in the liver

49
Q

How’s 🐟 metabolised in liver?

A

Deamination + transamination of AA-non-nitrogenous of AA → glucose +lipids
Synthesis of non-essential AA
Synthesis of nearly all plasma proteins (90%) 15-50g/day
Synthesis of urea-removes NH3

50
Q

Why remove NH3?

A

Depress cerebral blood flow + cerebral O2 consumption.

Toxic especially to 🧠–>hepatic encephalopathy

51
Q

Where does NH3 come from?

A

deamination + gut 🐛

52
Q

What toxic substances does the liver excrete?

A

Bilirubin. NH3. Hormones eg all steroid (androgens, oestrogens, cortisol, aldosterone, thyroxine),💊+ exogenous toxins (asprin, paracetamol, ethanol)

53
Q

What are steroid hormones excreted as?

A

glucuronide/sulphate conjugates

54
Q

If ⇑steroid hormones what happens?

A

gonadal dysfunction ♂

spider angioma in ♀

55
Q

How does liver metabolise drugs + hormones?

A 
Phase 1 (primarily oxidation/reduction)
Phase 2 (conjugation)
phase 3 ATPase pumps to eliminate➩blood or bile
56
Q

What happens in phase 1?

A

In SER, catalysed by cytochrome P450- substrate → polar compound

57
Q

What happens in phase 2?

A

↑solubility by conjugating w Glucuronyl

58
Q

Features of paracetamol?

A

Acetaminophen
Has narrow therapeutic index–>overdose
Max dose 4g/day or 1g/dose
❌after 🥤

59
Q

How’s paracetamol metabolised?

A
  • Glucoronidation (45-55%)
  • Sulfation (20-30%)
  • N-hydroxylation+dehydration → NAPQI (toxic)–>detoxified by glutathione (GSH) conjugation (<15%) in phase 2
60
Q

How paracetamol overdose occurs?

A

Incomplete metabolism∵

𝔼 saturated + glutathione stores depleted–> liver necrosis + kidney damage by toxic metabolites

61
Q

Treatment for paracetamol overdose?

A

N-acetylcysteine : the precursor to glutathione ∴ increases it’s levels

62
Q

Why does paracetamol have 2 phase effect?

A

feel fine after od∴dont seek help until late

63
Q

What happens after drinking🥤?

A

readily absorbed from GI but not stored ∴ oxidized in liver

64
Q

How’s 🥤oxidised?

A

ethanol→acetaldehyde by alcohol dehydrogenase containing the coenzyme NAD+ –> ⇑ NADH

65
Q

How’s ⇑ NADH removed?

A
  • Used in conversion of pyruvic acid→lactic acid
  • Reducing agent to synthesise glycerol + FA
  • Used in ETC to synthesise ATP
66
Q

What happens when NADH ❌ gluconeogenesis?

A

hypoglycaemia ∵ lack of glucose synthesis from pyruvic acid

67
Q

What happens when NADH used in ETC ∴ ❌fat oxidation?

A 
FA accumulation (alleviated by releasing lipids into the blood stream)--> ❤ attack
Acetyl coA accumulation -->ketosis--> hepatatis, cirrosis
68
Q

What’s 🥤 flush?

A

Accumulation of acetaldehyde ∵ ALDH2 missense polymorphism mutation
50% of Asians have 1 mutant that encodes inactive mitochondrial isoenzyme

69
Q

What are 🥤liver probs?

A

Fatty liver : deposits of fat –>liver enlargement; strict abstinence leads to full recovery
Liver fibrosis : scar tissue; recovery possible but scar remains
Liver cirrhosis : connective tissue growth destroys liver cells; irreversible
Alcoholic hepatitis : acute + chronic hepatitis-inflammation
Alcoholic cirrhosis : injury∵⇑🥤, chronic hepatitis B/C infection,⇑Fe/Cu,💊, obstruction of the bile duct

70
Q

Why’s alcoholic cirrhosis a degenerative disease?

A

liver cells damaged + replaced by scar

71
Q

What can cause Gynecomastia?

A

alcoholic cirrhosis

72
Q

What part of cell cycle are adult hepatocytes in?

A

G0

NO CELL ÷

73
Q

When do hepatocytes enter cell cycle?

A

After partial hepatectomy (70% liver removed by by ligation of the blood supply+resection)
Toxic injury

74
Q

When does proliferation of hepatocytes stop?

A

when mass of liver established

75
Q

Pathways of liver regeneration?

A
  • growth-factor mediated pathway →HGF (hepatocyte growth factor) + TGFα(transforming growth factor alpha)
  • cytokine signalling pathway using IL-6 via TNFα binding to its receptor on Kuppfer cells
76
Q

Process of liver regeneration?

A
  • signals initiated simultaneously in the liver
  • gut-derived factors- lipopolysaccharide (LPS) unregulated+reach the liver via portal blood supply
  • activates hepatic non-parenchymal cells-Kupffer + stellate cells–>↑ tumour necrosis factor (TNF) + interleukin (IL)-6
  • insulin, epidermal growth factor (EGF), NA, triodothronine(T3),hepatocyte growth factor (HGF)
  • cooperative signals from factors allow hepatocytes to move via cell cycle–> DNA synthesis + proliferation
  • transforming growth factor (TGF) signalling❌DNA synthesis during proliferation but restored after regeneration by helping hepatocytes return to quiescent state
77
Q

What coagulation factors are produced in the liver?

A

Fibrinogen
Prothrombin
Nearly all the other factors eg V, VI, IX, X, XII

78
Q

Function of Vit K?

A

formation of pro-thrombin + factors II,VII, IX & X

79
Q

What do stellate cells store?

A

fat-soluble vit D, K, E, A

80
Q

What vit does liver store?

A

vitamin B12- last for 2 - 3 yrs

deficiency–> pernicious anemia

81
Q

What’s folate?

A

stored in liver vital in early 🤰

82
Q

What’s Fe stored as in liver?

A

ferritin

83
Q

How does liver act as Fe buffer system?

A

Hepatic cells contain apoferritin -combines reversibly w Fe= ferritin
Ferritin releases Fe when low

84
Q

What’s LFT?

A

check liver 𝔼+🐟 in your blood
Screens for hepatitis
Monitor the progression of alcoholic hepatitis,shows if treatment working
Measure the severity-scarring of the liver (cirrhosis)
Monitor side effects of 💊

85
Q

Common sections of LFT?

A
  • alanine aminotransferase (ALT) - 𝔼 in hepatocytes-in blood when hepatocytes are damaged, high levels in hepatitis and alcohol induced damage
  • aspartate aminotransferase (AST) - 𝔼 in hepatocytes, in blood when hepatocytes are damaged, high levels in hepatitis and alcohol induced damage
  • alkaline phosphatase (ALP) - 𝔼 in bile duct, indicates obstruction in bile flow
  • gamma glutamyl transferase (GGT) – indicates obstruction
  • bilirubin - jaundice
  • albumin - ↓ in chronic liver disease/malnutrition
  • clotting studies, i.e. prothrombin time (PT)-if ↓ then ↓ clotting factors or international normalised ratio (INR)

GI (15 decks)

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