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HUB3006F > Nutrition & CVS > Flashcards

Nutrition & CVS Flashcards

1
Q

What causes Ischemic heart disease?

A

(An acute myocardial infarction)

Results from an obstruction of coronary artery - most often due to build up of atherosclerotic plaque

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2
Q

What are the main physiological functions of Cholesterol?

A
  1. Main part of plasma membrane
  2. Precursor of bile acids (essential for fat digestion)
  3. Precursor of steroid hormones
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3
Q

In what form are most cholesterol molecules in the plasma?

A

Circulate in the form of cholesteryl esters

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4
Q

What are Triglycerides?

A
  • Non-polar hydrophobic mols

- Generate free fatty acids (FFA)

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5
Q

What are Phospholipids?

A
  • Polar mols, more soluble than cholesterol and triglycerides
  • Present in the cell membrane as sphingomyelin
  • Key role in transduction pathways: DAG & FFA
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6
Q

What is the structure of the Lipoprotein Transport System?

A

Phospholipid & Free cholesterol envelope with a core of cholesteryl esters & triglycerides

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7
Q

What is the functions of the apolipoprotein?

A

‘Controls the structure of the lipoprotein’

  1. Assembly & secretion of the lipoprotein (Apo B)
  2. Structural integrity of the lipoprotein
  3. Coactivator or inhibitor of enzymes (Apo A & Apo C)
  4. Binding or docking to specific receptors and proteins for cellular uptake of a lipid component
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8
Q

What are the different types of lipoprotein?

A

o HDL – high density lipoprotein (“Good”)
o LDL – low density lipoprotein (“Bad”)
o IDL – intermediate density lipoprotein
o VLDL – very low …
i. Chylomicron is largest (lowest density)

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9
Q

Where is the major site of cholesterol biosynthesis?

A

The liver

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10
Q

What is the site of origin, role, and most abundant constituents of Chylomicrons?

A

Site of Origin:
o Intestines

Role:
o Takes up dietary fat & transport to other lipoproteins

Most abundant constituents:
o Triglycerides

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11
Q

What is the site of origin, role, and most abundant constituents of VLDL?

A

Site of Origin:
o Liver

Role:
o Transports fat from liver to periphery

Most abundant constituents:
o Triglycerides

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12
Q

What is the site of origin, role, and most abundant constituents of LDL?

A

Site of Origin:
o VLDL

Role:
o Transports cholesterol from liver to periphery

Most abundant constituents:
o Cholesterol

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13
Q

What is the site of origin, role, and most abundant constituents of HDL?

A

Site of Origin:
o Liver

Role:
o Transports excess cholesterol from periphery to the liver

Most abundant constituents:
o Protein, phospholipids, cholesterol

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14
Q

How is exogenous Cholesterol acquired?

A
  • LDL (is cholesterol & apoB) binds to receptor on exterior of peripheral cell
  • LDL & LDL-R (receptor) internalized into an endosome inside cell
  • Endosome fuses with lysosomes to release free cholesterol into cell
  • ApoB degraded– receptor recycled back into plasma membrane

OR

  • Cholesterol can also be formed in cells in smooth EndoR
    o HMG-CoA reductase (enzyme) is the rate limiting step
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15
Q

What is the cellular destination of cholesterol?

A

o It can be stored in cells as cholesteryl ester stores by enzymes ACAT

o It can also exit peripheral cells in the presence of ABCA1 – joins HDL to be transported back into plasma

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16
Q

What are physiological cholesterol/lipid concentrations?

A

o Total cholesterol: <5.0 mmol/L
o LDL cholesterol: < 3.0 mmol/L
o HDL cholesterol: > 1.0 mmol/L
o Triglycerides: < 1.7 mmol/L

17
Q

What is arteriosclerosis?

A

Hardening (sclerosis) of the arteries (arterio-)

  • Atherosclerosis:
    o Build up of fats, cholesterol & other substances in the medium & large artery walls
  • Arteriolosclerosis:
    o Hardening & loss of elasticity of arterioles or small arteries and is most often associated with hypertension & diabetes mellitus
  • Monckeberg’s arteriosclerosis:
    o Deposit of Ca in small & medium arteries – makes walls stiff, but NOT narrow
18
Q

What are the major risk factors for developing atherosclerosis?

A 
Smoking: 
o	Damages endothelium
o	Increases platelet activity
o	Promotes platelet thrombosis
o	Increases plasma fibrinogen
o	Increases MDL, promotes vasoconstriction

Diet:
o High in saturated fat increases LDL cholesterol

High blood pressure:
o Leads to vascular inflammation through activation of angiotensin 2

Lack of exercise:
o To do with blood pressure and LDL cholesterol

High levels of sugar in blood

19
Q

What is in an atherosclerosis plaque?

A
  • Intracellular and extracellular cholesterol & phospholipids
  • Inflammatory cells (macrophages)
  • Smooth muscle cells
  • Connective tissue (collagen, elastic fibers)
  • Ca deposit.
20
Q

Where do atherosclerosis plaques generally build up?

A

o Regions of branching of arteries
o Areas with marked curves where geometry is irregular
o Regions where blood undergoes sudden change in velocity or direction of flow

21
Q

What is the origin of atherosclerosis plaques?

A

o Exact cause unknown
o Slow and complex disease that may start in childhood
a. Thought that buildup sometimes starts in teenagers and can take 30 years to be detected
o Chronic inflammatory response in wall arteries
o Accumulation of macrophages
o Promoted by low density lipoproteins (LDL) – carry cholesterol and triglycerides
o Inadequate removal of fat and cholesterol (by HDL) (high density lipoproteins)

22
Q

What are the steps in the formation of an atherosclerotic plaque?

A
  1. Endothelial damage occurs resulting in:
    o Excess LDL
    o Oxidative stress
  2. Damage summons immune system and inflammatory cells to assess damage
    o Monocytes infiltrate intima of damaged vessel wall from blood
    o Become activated Macrophages
  3. Excess LDL can enter the vessel wall because of the endothelial damage
  4. Oxidative stress -> LDL in intima will be oxidized
    o Leads to a buildup of oxLDL cholesterol inside the wall in the presence of activated macrophages
  5. Activated macrophages will try to mop up the excess oxLDL – incorporation of the lipid into themselves -> Foam Cells
  6. oxLDL inactivates nitric oxide (NO) causing vasoconstriction:
    o Increase in platelet addition
    o Increase in Plasminogen Activator Inhibitor (PAi)
    o Decrease of Tissue Plasminogen Activator (t-PA)
    o Increase of Tissue Factor
    o Decrease in Thrombomodulin
    o Activation of Heparan Sulfates
    o Consequence of decrease in endothelial NO:
    i. Increase in procoagulant milieu (favours enhanced platelet thrombus formation)
    ii. Decrease anticoagulant mechanisms
  7. oxLDL activates different inflammatory responses - triggers recruitment of more monocytes -> more activated macrophages within the wall
  8. Fat streak formed from accumulation of foam cells and migrated smooth muscle cells from media
  9. Smooth muscle cells are responsible for deposition of elastin & collagen forming the Fibrous Cap
  10. Eventually get a rupture of fibrous cap which exposed all the thrombogenic content of core of plaque to the circulating blood.
  11. Results in formation of thrombus in the vessel and complete obstruction of vessel
23
Q

What are the therapeutic approaches to Angina?

A
  • Nitrates:
    o Provides exogenous source of vasodilator Nitrous Oxide
  • B-blockers
    o Reduce O2 demand of heart – relax heart and blood vessels, can help reduce blood pressure
  • Ca blockers
    o Act mainly by vasodilation
    o Reduces peripheral resistance
  • ACE inhibitors (angiotensin converting enzyme)
    o Block vasoconstrictor Angiotensin 2
  • Aspirin
    o Has anti platelet aggregation property
    o Anti-inflammatory effect
  • Lipid lowering agents
24
Q

What are 6 Lipid Lowering Agents?

A
  1. Statins
  2. Resins
  3. Fibres
  4. Nicotinic acid
  5. Ezetimibe
  6. PCSK9 inhibitors: New drug
25
Q

What effect does Statin have on Angina?

A
  • Decreases hepatic cholesterol by inhibiting HMGCoA reductase
  • Improves endothelial function
  • Metabolizes platelets & reduces fibrinogen
  • Reduce inflammatory effect
26
Q

What effect does Resins have on Angina?

A
  • Bind to bile acids to promote secretion into intestine
  • Increased loss of hepatic cholesterol to the bile acid
  • Hepatic cellular cholesterol decreases leading to increase in hepatic LDL receptor repopulation -> blood LDL more rapidly removed & total cholesterol can fall
  • Side effect: may increase triglyceride & HMGCoA reductase activity – so combination therapy has been suggested
27
Q

What effect does Fibrates have on Angina?

A
  • Reduces cholesterol less than Statin & Nicotinic acid
  • Prime action = decreases triglyceride
  • Promotes fatty acid oxidation -> reduces synthesis of VLDL by reducing [triglycerides]
28
Q

What effect does Nicotinic Acid have on Angina?

A
  • First drug shown to reduce overall mortality
  • Cheapest drug
  • Decreases mobilization of FFA from adipose tissue -> less substrate for hepatic synthesis of lipoprotein lipids
  • Results in less secretion of LDL and VLDL
29
Q

What effect does Ezetimibe have on Angina?

A
  • Selectively inhibits absorption of cholesterol in intestine -> decrease in delivery of intestinal cholesterol in liver
  • Results in decrease of hepatic cholesterol & increase in clearance of cholesterol from the blood
30
Q

What effect does PCDK9 inhibitor have on Angina?

A
  • Target an increase in LDL-R (receptor)
  • PCSK9 binds to LDL-R on surface of hepatocyte -> internalisation & degradation of LDL-R in lysosome
  • This reduces number of LDL-R on surface because they can’t be recycled (degraded in lysosome)
  • Inhibition of PCSK9 therefore increases number of LDL-R on surface -> increases uptake of LDL in liver, and reduces LDL cholesterol levels in the blood
31
Q

What is a coronary angiogram?

A

Dye injected into coronary arteries - xRay shows where obstruction occurs

32
Q

What is an interventional Approach to Angina?

A
  • Coronary Angiogram

- Percutaneous Transluminal Coronary Angioplasty

33
Q

What is Percutaneous Transluminal Coronary Angioplasty?

A

o Catheter with uninflated balloon inserted through coronary artery
o Balloon inflated at the plaque site which breaks the plaque and reopens the artery
o Stent then inserted to ensure artery stays open
• Stent is a mesh that will stay in coronary artery to make sure that the vessel will stay open after the inflation of the balloon.

HUB3006F (8 decks)

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