Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

103: Theme 3 - 304 - Cardiovascular > Lipids > Flashcards

Lipids Flashcards

1
Q

What are the four pathways for lipid transport?

A
  • Exogenous: gut–> periphery, via chylomicrons - Endogenous: liver–> periphery, via VLDL - Reverse: periphery –> liver: via HDL - Bile production: liver –> digestive tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What lipoproteins transport fat in the exogenous pathway, and where are they taken up?

A
  • small intestine packages lipids as chylomicrons - taken up by the liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What lipoproteins transport fat in the endogenous pathway, and where are they taken up

A
  • packaged into VLDL - taken up in the periphery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What lipoproteins transport fat in the reverse cholesterol transport and where are they taken?

A
  • packed into HDL - taken up by the liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where in the periphery are most lipids stored and used?

A
  • stored in adipose tissue - and muscle tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the conditions for reverse cholesterol transport?

A
  • occurs when the lipid supplies in the liver are being diminished - this is a sign of reduced body lipid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

GIve an overview description of bile production and recycling

A
  • Bile produced from cholesterol in the liver - released into the gut and gall bladder via the cystic duct - most bile acids are absorbed in the gut and returned to the liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the main function of lipoprotein lipase?

A
  • metabolises triglycerides so they can be removed from VLDL and moved to capillary membrane of blood vessels - triglycerides –> fatty acids + glycerol - cell surface linked enzyme in the capillary walls
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are apolipoproteins and what do they do?

A
  • amphipathic lipid-carrying protein in lipoprotein particles - allows lipids to be transported as they are not soluble in plasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain why big lipoprotein particles have lower density compared to smaller lipoproteins

A
  • lipids hav e alower density than proteins - larger lipoproteins have more triglycerides than smaller ones - smaller lipoproteins tend to have more cholesterol and proteins - therefore larger lipoproteins are less dense
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is Low Density Lipoprotein the most dangerous?

A
  • LDL can store blood cholesterol that can not be stored elsewhere , largest store of cholesterol esters
  • therefore LDL is an indicator of excess lipids in the body being transported to the liver from the periphery
  • Excess LDL and its content i.e cholesterol esters can accumulate in atheromas, hence the beginnings of atherosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why is High Density Lipoprotein an indicator of cardiptection?

A
  • lipids being moved form the periphery to liver in reverse cholesterol transport - HDL is an indicator of low lipid states - occurs when cholesterol is being consumed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why does Very Low Density Lipoprotein indicate a risk of atherogenesis?

A
  • VLDL is transports triglycerides and endogenous cholesterol from the liver to adipose and muscle tissue - in the periphery triglycerides are removed from VLDL forming IDL - this is an intermediate to LDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Intermediate Density Lipoprotein?

A
  • it is the lipoprotein formed after triglycerides have been removed from VLDL - this then becomes LDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does a chylomicron do?

A
  • it transport triglycerides and fatty acids (exogenous lipids) from the gut to the periphery - elevated after eating fatty meals - not usually an indicator of CV risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give two endocrine cell types in the pancreas, and describe their primary secretion

A
  • Beta cells: secrete Insulin at high blood glucose levels - Alpha cells: secrete Glucagon at low blood glucose levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the action of Insulin and Glucagon?

A
  • Insulin stimulate adipocytes to absorb glucose - Glucagon stimulates the liver to release glucose both act in order to normalize blood glucose levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Type II diabetes and what causes it?

A
  • relative insulin deficiency, caused by insulin resistance - a reduction in adipocyte absorption of glucose - results in high levels of circulating glucose - aka adult onset diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is hypercholesterolaemia and what causes it?

A
  • high plasma cholesterol levels - environmental and genetic factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What drugs are used to treat hypercholesterolemia and how do they work?

A
  • Statins - block endogenous cholesterol synthesis by blocking HMG-CoA Reductase: this is the beginning step to cholesterol synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is metabolic syndrome?

A
  • a cluster of related CVD risk factors - including, high BP, high fasting glucose, high LDL cholesterol, low HDL cholesterol, high triglycerides - associated with insulin resistance and central obesity (apple vs pear)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

alongside the other 2 steps

What is Beta oxidation?

A
  • the pathway from fatty acids to Acetyl-CoA - takes place in the mitochondrion, and peroxisomes - releases free energy, successive removal of 2-carbon fragments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Lipogenesis?

A
  • the pathway from Acetyl-CoA to fatty acids
  • process depends on fatty acid synthase
  • the Acetyl CoA needs to be made into citrate first
  • occurs in the cytosol - Acetyl-CoA + ATP + e –> fatty acid +CO2 + CoA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is Acetyl-CoA and give its uses?

A
  • it is a mediating molecule in the krebs cycle - used as an energy mediator - can be used to form ketone bodies in the mitochondrion - can be used to form cholesterol
25
Q

What is fat mobilization?

A
  • when fatty acids are released from adipose tissue in times of stress in order to release energy - fatty acids are shortened by 2 carbons at a time to produce ATP + Acetyl-CoA
26
Q

What are the uses of cholesterol?

A

Acts as a precursor to - bile acids - steroid hormones - Vitamin D Provides structure and stability to cell membrane

27
Q

General Cholesterol facts

A
  • obtained from the diet or the liver
  • it is heavily recycled due to high metabolic cost to produce it seen in bile salts and the endogenous pathway sometimes partially soluble due to the OH group
  • it is amphipathic
  • stored in most tissues as cholesterol esters, makeing it very insoluble
28
Q

What are cholesterol esters?

A
  • cholesterol molecules that have bonded with a fatty acid
  • formation is catlaysed by ACAT (acetyl-CoA transferaase)
  • hydrolysed by lipases to reform its reactants 75% of plasma cholesterol
  • 43% cholesterol linoleate
  • 23% cholesterol oleate
29
Q

Give examples of steroids

A
  • Cholesterol - Vitamin D (sort of) - Cortisol: by the adrenal cortex - Testosterone
30
Q

What are ketone bodies?

A
  • water soluble molecules containing the ketone group that are produce in the liver from Acetyl-CoA breakdown during fasting - they last 5 hours, if they aren’t used they will be lost - act as a major energy source for the brain and heart
31
Q

Give two examples of ketone bodies and a brief life cycle

A

Acetoacetic Acid & beta-hydroxybutyric acid - these two spontaneously breakdown if they are not used - through decarboxylation acetone is formed - this is then eliminated by the kidney as waste

32
Q

What is ketogenesis?

A

this occurs when acetyl-CoA cannot enter the citric acid cycle during starvation - usually when more acetyl-coA is produced than can be processed by the citric cycle

33
Q

What is the importance of unsaturated fatty acids

A
  • increases the fluidity of cell membranes most naturally occuring FA are cis - they form a kink in the carbon backbone - interferes with the phospholipid bilayer - less likely to form a solid matrix
34
Q

What are the 3 steps and products in Beta Oxidation?

A

1) activated by Coenzyme A in the cytosol forms Acyl-CoA, synthesised by acyl-coA dehydrogenase, FAD into redFAD
2) allows the fatty acid to be transported across the mitochondrial membrane
3) progressive oxidation of fatty acids along the carbon chain
- produces 1 FADH2 , 1 NADH molecule

35
Q

How are short-chain fatty acids transported?

A
  • in albunin molecueles
36
Q

How does CoA get out of mitochondria?

What occurs in the citrate malate cycle?

A
  • Acetyl-CoA converted to citrate for transport out of the mitochondria then back to acetyl CoA in the cytosol for use in the fatty acid synthesis
  • the Oxaloacetate produced is then converted back to pyruvate for transport back into the mitochondria for use in ATP synthesis
37
Q

Where does fatty acid synthesis take place?

A
  • liver and adipocytes
  • occurs in the cytosol
  • derived from acetyl-CoA from the mitochondria
38
Q

What are the steps for cholesterol biosynthesis?

A
  • Acetyl CoA →HMG-CoA –HMG-CoA reductase →Mevalonate → squalene → cholesterol
39
Q

What enzyme hydrolyses TG on digestion after emulsification?

A
  • Pancreatic Triacylglycerol Lipase
40
Q

Go through the lipid transport system

A
  • Chylomicrons: deliver dietary TGs to muscle and adipose tissue + dietary cholesterol to the liver
  • VLDL: transport endogenous TGs and cholesterol
  • LDL: transport cholesterol from liver to tissues
  • HDL: transport cholesterol from tissues to liver i.e. remove cholesterol from tissues
41
Q

How are lipids taken up by cells?

A
  • Chylmicrons and VLDL particles give up TG to tissues by the action of tissue-bound lipases
  • liver recognises remnants of these particles by their ApoE content and takes them up for re-cycling
  • LDL particles contain ApoB-100 which is recognized by cell surface LDL receptors (LDLRs)
42
Q

Explain the regulation of LDL receptors

A
  • down-regulated by PCSK9: proprotein convertase subtilisin/Kexin type 9
  • up-regulated by SREBPs: sterol regulatory element-binding protein
43
Q

What are the major CVD risk factors found in the Framingham Heart Study?

A
  • High blood pressure
  • High blood cholesterol
  • Smoking
  • Diabetes
  • Sedentary behaviour/ inactivity
  • Obesity
44
Q

Who would be given primary lipid modification prevention, and what does this treatment entail?

A
  • those with no previous history of CVD and
  • a QRISK2 > 10%
  • Statin: Atorvastatin 20 mg
45
Q

Who would be given secondary lipid modification prevention, and what does this treatment entail?

A
  • those with a history of CVD
  • Statin: Atorvastatin 80 mg
46
Q

What is Ezetimibe and what is its effect?

A
  • a potent and selective inhibitor of absorption of cholesterol in the SI
  • reduces the contribution of dietary and biliary cholesterol
  • therefore reduces the flux of cholesteryl esters into VLDL particles
  • 10mg/day induces a 20% reduction in LDLC and 8% reduction in TG
47
Q

What are BIle Acid Sequestrants (Resins) and what is their effect?

  • side effects?
A
  • they bind bile acids in the intestine, interrupting the enterohepatic circulation of bile
  • causes increased conversion of cholesterol into bile acids in the liver
  • treatment limited by constipation and flatulence, older resins cause oesophageal irritation
48
Q

What are Fibrates and what is their effect?

A
  • they lower blood cholesterol, triglyceride reduces by 25-50% and increase HDL-C by 15-25% they:
  • increase peripheral lipolysis by activating lipoprotein lipase
  • decrease hepatic triglyceride production
  • modulation of LDLR/ligand interaction
  • they stimulate reverse cholesterol transport
49
Q

What is Omega 3 and what is their effect?

A
  • fish oils
  • they inhibit lipogenesis and stimulate beta-oxidation (conversion of triglycerides to acetyl-CoA which can enter the TCA cycle)
  • reduces the rate of secretion of VLDL triglyceride
  • shown to significantly reduce the risk for sudden death caused by cardiac arrhythmias and all-cause mortality in patients with known coronary heart disease
50
Q

What is PCSK9 and what is their effect?

A
  • they are binding proteins, primarily expressed in hepatocytes,
  • they bind to LDL-Receptors and promote the receptor degradation after they have been endocytosed alongside the LDL particles
  • this reduces the number of LDLR on the cell surface membrane
  • therefore reduces the number of LDL particles that can be removed from circulation
51
Q

What is the action of PCSK9 inhibitors?

A
  • inhibit the action of PCSK9 binding proteins on LDL-receptors
  • this reduces the amount of LDLR degradation
  • this increase the number of LDLR on cell surface membranes and increase the number of LDL particles that can be removed from circulation
52
Q

What is the lipoprotein pattern of abnormality seen in Hypercholesterolaemia?

A
  • raised total cholesterol and LDL
  • usually seen in familial hypercholesterolemia where total cholesterol levels range between 7-20mmol/L in heterozygotes or higher in rare homozygous between 15-30mmol/L
53
Q

What is the lipoprotein pattern of abnormality seen in Mixed hyperlipidemia (dyslipidemia)

A
  • raised total cholesterol and LDL with raised TG and often low HDL
  • seen in patients with glucose intolerance and diabetes
  • arises from increased production and reduced breakdown of triglyceride-rich lipoproteins
54
Q

What is the lipoprotein pattern of abnormality seen in Hypertryglyceridaemia?

A
  • this is less common and ay be familial
  • tends to cause harm through acute pancreatitis
55
Q

What causes Familial Hypercholesterolaemia (FH)?

A
  • Mutations in the LDLR gene that encodes the LDLR protein which reduces its function
  • In a few cases (~ 3%) with the same clinical phenotype; it is either a mutation in ApoB which is the part of LDL that binds with the receptor, or
  • a gain of function mutation in LDL receptor degradation (PCSK9).
56
Q

What are the clinical presentations of Familial Hypercholesterolaemia (FH)?

A
  • Tendon Xanthoma (knuckles and Achilles tendon)
  • Corneal arcus
  • (in homozygous cases bumps of cholesterol deposits can be seen all over the skin)
57
Q

What would the following symptoms be diagnostic of if seen on an ultrasound scan of the carotid arteries?

  • intimal thickening in both carotid arteries
  • with intimal calcification and soft plaques in the left internal carotid artery,
  • diffuse narrowing of the left vertebral artery with
  • reduction in the flow velocity
A
  • Extensive atherosclerosis
58
Q

What would the treatment be for FH?

A
  • Low Saturated Fat Diet and exercise
  • Statins
  • Possible addition of cholesterol absorption inhibitor (ezetimibe)
  • Rarely resins/surgery/LDL apheresis
  • Anti–PCSK9
  • Involve patient self-help group, offer DNA testing and get the family tested.

103: Theme 3 - 304 - Cardiovascular (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions