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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
Function of bile?
- Emulsification for fat digestion + absorption - Bile+pancreatic juice neutralises gastric juice as enters small intestine - Aids digestive 𝔼 - Remove waste from blood -bilirubin +cholesterol
26
How much cholesterol is eliminated daily?
500g cholesterol→ bile acids
27
What's bilirubin?
Yellow pigment from Hb breakdown | Useless+toxic but ~6g/day .. a lot
28
How's aged 🔴 destroyed?
Digested by macrophages Fe- recycled Globin chains-catabolized Haem (porphyrin)-eliminated
29
Where's 🔴 digested?
mostly in spleen
30
Formation + removal of bilirubin?
Haem→free bilirubin-->released into plasma carried bound to albumin-->absorbed by hepatocytes -->conjugated w glucoronic acid→bile-->metabolised by intestinal lumen-->faeces/urine
31
Why's faces brown + urine yellow?
Stercobilin – metabolite | Yellow urobilin + urobilinogen-metabolite
32
What's jaundice?
⇑ 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
33
What's 'green jaundice'?
mutation of biliverdin reductase gene ∴biliverdin NOT→ bilirubin∴ built up in plasma
34
Types of jaundice?
Pre-hepatic (haemolytic) Hepatic Post-hepatic (obstructive)
35
What's pre-hapatic jaundice?
- ⇑🔴breakdown eg neonatal jaundice | - ⇑unconjugated bilirubin
36
What's hepatic jaundice?
- Hepatocyte damage (>80%) eg cirrhosis,💊, hepatitis A,B,C,E, Gilberts Syndrome - ⇑conjugated +/or unconjugated bilirubi
37
What's post-hepatic jaundice?
- ⇑conjugated bilirubin - Obstruction ➩duodenum - Enters circulation➩ dark urine eg gallstones, carcinoma of pancreas/bile ducts
38
What's Gilbert’s syndrome?
congenital disorder where ↓𝔼 that conjugates bilirubin w glucoronic acid-->↑unconjugated bilirubin
39
Why does neonatal jaundice occur?
Fetal Hb →adult Hb so ⇑🔴breakdown results --> normal physiological jaundice but liver's immature- delay in processing
40
Treatment for neonatal jaundice?
Sunlight includes blue light- filters out (UVA, UVB, UVC, IR etc) ↓ risk of over-heating or sunburn
41
What's the Glucose Buffer Function?
Humans (pre-prandial) 4-5.9mmol/L
42
What's glycogenesis?
glucose → glycogen (stimulated by insulin). Liver stores glycogen 80g
43
What's glycogenolysis
glycogen→glucose stimulated by glucagon + A
44
What's gluconeogenesis?
lactate, AA & glycerol (from TGC)→glucose
45
What's glycolysis?
glucose → pyruvate releasing E to form ATP + NADH
46
How's fat metabolised in liver?
TCG oxidized in hepatocytes Lipoproteins synthesised in liver ⇑Carb+🐟 → FA + TCGs – stored in adipose Synthesis of cholesterol + phospholipids- some→lipoproteins
47
What's citric cycle?
FA enter it to release E + → ketone bodies
48
Sources of FA for metabolism?
Dietary source of TCGs TCGs stored in adipocytes TCGs synthesised in the liver
49
How's 🐟 metabolised in liver?
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
Why remove NH3?
Depress cerebral blood flow + cerebral O2 consumption. | Toxic especially to 🧠-->hepatic encephalopathy
51
Where does NH3 come from?
deamination + gut 🐛
52
What toxic substances does the liver excrete?
Bilirubin. NH3. Hormones eg all steroid (androgens, oestrogens, cortisol, aldosterone, thyroxine),💊+ exogenous toxins (asprin, paracetamol, ethanol)
53
What are steroid hormones excreted as?
glucuronide/sulphate conjugates
54
If ⇑steroid hormones what happens?
gonadal dysfunction ♂ | spider angioma in ♀
55
How does liver metabolise drugs + hormones?
``` Phase 1 (primarily oxidation/reduction) Phase 2 (conjugation) phase 3 ATPase pumps to eliminate➩blood or bile ```
56
What happens in phase 1?
In SER, catalysed by cytochrome P450- substrate → polar compound
57
What happens in phase 2?
↑solubility by conjugating w Glucuronyl
58
Features of paracetamol?
Acetaminophen Has narrow therapeutic index-->overdose Max dose 4g/day or 1g/dose ❌after 🥤
59
How's paracetamol metabolised?
- Glucoronidation (45-55%) - Sulfation (20-30%) - N-hydroxylation+dehydration → NAPQI (toxic)-->detoxified by glutathione (GSH) conjugation (<15%) in phase 2
60
How paracetamol overdose occurs?
Incomplete metabolism∵ | 𝔼 saturated + glutathione stores depleted--> liver necrosis + kidney damage by toxic metabolites
61
Treatment for paracetamol overdose?
N-acetylcysteine : the precursor to glutathione ∴ increases it’s levels
62
Why does paracetamol have 2 phase effect?
feel fine after od∴dont seek help until late
63
What happens after drinking🥤?
readily absorbed from GI but not stored ∴ oxidized in liver
64
How's 🥤oxidised?
ethanol→acetaldehyde by alcohol dehydrogenase containing the coenzyme NAD+ --> ⇑ NADH
65
How's ⇑ NADH removed?
- Used in conversion of pyruvic acid→lactic acid - Reducing agent to synthesise glycerol + FA - Used in ETC to synthesise ATP
66
What happens when NADH ❌ gluconeogenesis?
hypoglycaemia ∵ lack of glucose synthesis from pyruvic acid
67
What happens when NADH used in ETC ∴ ❌fat oxidation?
``` FA accumulation (alleviated by releasing lipids into the blood stream)--> ❤ attack Acetyl coA accumulation -->ketosis--> hepatatis, cirrosis ```
68
What's 🥤 flush?
Accumulation of acetaldehyde ∵ ALDH2 missense polymorphism mutation 50% of Asians have 1 mutant that encodes inactive mitochondrial isoenzyme
69
What are 🥤liver probs?
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
Why's alcoholic cirrhosis a degenerative disease?
liver cells damaged + replaced by scar
71
What can cause Gynecomastia?
alcoholic cirrhosis
72
What part of cell cycle are adult hepatocytes in?
G0 | NO CELL ÷
73
When do hepatocytes enter cell cycle?
After partial hepatectomy (70% liver removed by by ligation of the blood supply+resection) Toxic injury
74
When does proliferation of hepatocytes stop?
when mass of liver established
75
Pathways of liver regeneration?
- 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
Process of liver regeneration?
- 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
What coagulation factors are produced in the liver?
Fibrinogen Prothrombin Nearly all the other factors eg V, VI, IX, X, XII
78
Function of Vit K?
formation of pro-thrombin + factors II,VII, IX & X
79
What do stellate cells store?
fat-soluble vit D, K, E, A
80
What vit does liver store?
vitamin B12- last for 2 - 3 yrs | deficiency--> pernicious anemia
81
What's folate?
stored in liver vital in early 🤰
82
What's Fe stored as in liver?
ferritin
83
How does liver act as Fe buffer system?
Hepatic cells contain apoferritin -combines reversibly w Fe= ferritin Ferritin releases Fe when low
84
What's LFT?
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
Common sections of LFT?
- 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)

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