Hepatic Flashcards

1
Q

how many lobes does the liver consist of ?

A

two

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2
Q

what are the lobes dividied by ?

A

the hepatic vein

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3
Q

where is the liver located ?

A

upper right corner of the abdomen

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4
Q

hepatic artery ?

A

supplies 25% of the total blood flow and provides most of the oxygen. This is coming from the heart.

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5
Q

portal vein ?

A

drains most of the gastrointestinal tract (GI). It supplies 75% of the blood flow and transports the most recently absorbed material from the intestines to the liver.This comes from the intestines.

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6
Q

what does the liver store ?

A

glycogen, vitamins and iron.

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7
Q

the liver contains an extensive reticuloendothelila system , why ?

A

for the synthesis and breakdown of blood cells.

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8
Q

what’s the primary function of the liver cells ?

A

metabolize, detoxify and excrete both endogenous and exogenous compounds (first pass metabolism). This will include metabolism and excretion of drugs and toxins

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9
Q

describe cholesterol ?

A

waxy , fat like substance that is a sterol , steroid alcohol. It is found in all cells of the body as it is part of the lipid bilayer.

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10
Q

how is cholesterol in the body ?

A

75% of the cholesterol is synthesised and the other 25% comes from our diet.

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11
Q

where does cholesterol synthesis mainly occur ?

A

liver , cytoplasm and the ER

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12
Q

what is the rate limiting step of cholesterol synthesis ?

A

HMG-CoA reductase reaction is the rate limiting step as it is at the start of the reaction.

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13
Q

what step does pharmacological intervention occur at and give an example ?

A

the HMG - CoA reductase stage , statins

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14
Q

what hormones are cholesterol part of ?

A

sex hormones such as testosterone , hormones released by the adrenal gland.

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15
Q

how is the bile acids and cholesterol involved?

A

cholesterol is required for production and bile acids used for neutralisation

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16
Q

describe atheroscelerosis ?

A

formation of fatty plaques in the blood vessels and they can lead to heart attacks , strokes , angina and an increased risk of coronary heart disease. This is due to a narrowing of the artery and this causes an abnormal blood flow and oxygen delivery.

17
Q

risk factors ?

A

diet , medical conditions such as diabetes and hypertension. Genetics , sex , age , smoking and inactivity and obesity.

18
Q

what are chylomicrons ?

A

small fat globules composed of protein and fat.

19
Q

if a person is suffering from high cholesterol levels what will the ratio of lipoproteins be ?

A

LDL will be high. The ratio of HDL:LDL is important in cholesterol levels.

20
Q

what are aplolipoproteins?

A

proteins that bind lipids

21
Q

how many classes are there ?

A

6

22
Q

ApoA-I ?

A

synthesised in the liver and intestines. They are structural in HDL and reverse cholesterol transport

23
Q

ApoA-V ?

A

synthesised in the liver and they modulate triglyceride incorporation into the hepatic VLDL

24
Q

ApoB-100 ?

A

synthesized in the liver and it is a structural portien of the VLDL , IDL and LDL

25
Q

ApoB-48 ?

A

synthesized in the intestine and it is a structural protein of chylomicrons

26
Q

ApoE ?

A

synthesized in the liver , brain , skin , gonads and spleen. It is a structural in HDL and they can reverse cholesterol transport

27
Q

why are statins used to treat hyperlipidemia ?

A

These work by decreasing the blood cholesterol and also lowering the risk of cardiovascular death. Statins works by increasing the ratio towards the HDL and lowering the LDL.

28
Q

mechanisms of statins ?

A

They inhibit an early and rate limiting step in cholesterol biosynthesis , the HMG-CoA reductase. This inhibits the hepatic cholesterol synthesis which results in an increased expression of the LDL receptor gene. This decreases the free cholesterol causes membrane-bound SREBPs to be cleaved and translocated to the nucleus to bind the sterol responsive element of the LDL receptor gene. This enhances transcription and increases the synthesis of LDL receptors. It also reduces the degradation of LDL receptors.

29
Q

statins on Rho and Rac

A

blocks Rho and Rac so this causes more eNOS to be produced and less of the reactive oxygen species NAP(P)H-ox

30
Q

statins on triglyceride levels ?

A

decrease them

31
Q

adverse effects of statins ?

A

Hepatotoxicity
• Elevated hepatic transaminase values
• One case of liver failure per million person-years of use
Myopathy
• One death per million prescriptions caused by rhabdomyolysis

32
Q

what are surrogate markers ?

A

not direct effects

33
Q

name some factors that lead to the fatty plaque formation ?

A
  • Platelet activation
  • Thrombotic effect as this leads to coagulation
  • Platelet stability
  • Vascular inflammation
  • SMC hypertrophy
  • Endothetlial dysfunction
  • Proliferation
  • Vasoconstriction
34
Q

JUPITER ?

A

Justification for the use of statins in primary prevention: an Intervention Trial Evaluating Rosuvastatin.

35
Q

what was it for ?

A

This was a randomised, double-blind, placebo-controlled primary prevention trial studying the patients without evidence of CVD.

36
Q

what did the treatment with Rosuvastatin do ?

A

lower LDL and risk of CVD and atherosclerosis progression.