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CV Week 2 > Cardiac Metabolism and Dysfunction > Flashcards

Cardiac Metabolism and Dysfunction Flashcards

0
Q

What are the conditions necessary for the energy metabolism of the cardiac mm?

A
  • ATP (continuous supply)
  • O2 (continuous supply)
  • high respiratory metabolism
  • mitochondria (half of the cytosol)
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1
Q

Discuss the presence or lack of mitochondria, oxygen and what fuel molecules are used in the erythrocytes, cardiac mm, and SK mm.

A

Mitochondria Oxygen Fuel Molecule Used
Erythrocytes - + Glucose
Cardiac mm + + Glucose, FA, Ketone Bodies
Skeletal mm + +/- Glucose, FA, Ketone Bodies

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2
Q

What are the energy reserves for the cardiac mm?

A
  • Glycogen

- Phosphocreatine (high energy phosphate bond)

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3
Q

What is the function of creatine kinase (CK)?

A

creatine +ATP -> creatine-phosphate (phosphocreatine) +ADP

CK catalyzes this reaction.

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4
Q

How does the energy sources change under normal and starvation conditions?

A

Normal conditions: glucose, FA (favored)

Starvation: FA, Ketone Bodies (not favored)

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5
Q

Draw a figure showing the fates of glucose.

A

pp. 10

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6
Q

What causes lactic acidosis?

A

Glycolysis under anaerobic conditions produces lactate. Lactic acid lowers pH.

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7
Q

What causes pain (angina pectoris)?

A

The narrowing of the coronary arteries due to atheroscleorosis and/or spasm (less common) result in an imbalance demand and supply of blood flow to the cardiac mm. The lack of O2 results in anaerobic glycolysis producing lactate.The lactate, and hydrogen ion symport removes both ions from the cell. However,
if blood-flow is inadequate-> H ion can’t escape fast enough from the cell tissue->PAIN (stimulation of pain nerve cells-nociceptors)

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8
Q

Define angina pectoris

A

“strangling pain in the chest” radiating to both shoulder and arm or occasionally to the jaw or neck.

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9
Q

What is the difference b/n angina pectoris and myocardial infarction?

A

MI is not reversible, ischemia persists long enough to cause necrosis to the cardiac mm, pain lasts longer and is more severe.

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10
Q

What is the consequence of a blood clot at the site of blood vessel narrowing?

A
  • causes occlusion in the artery
  • MI in the areas that are affected by this blockage (If area 2 was supplied by the artery that was blocked, then area 2 will die).
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11
Q

What are the 6 major risk factors for coronary heart disease (CHD)?

A

1) Diabetes
2) Smoking
3) Hypertension
4) Family history of premature CHD
5) High serum triglyceride (TG) levels
6) High serum cholesterol levels

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12
Q

What were the results of the Multiple Risk Factor Intervention Trial (MRFIT)?

A
  • Followed 362,662 men over 6 years

- Showed that CHD mortality increased over 4-fold with total cholesterol level climbing from 150mg/dl to 300mg/dl

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13
Q

Where are plasma lipoproteins synthesized?

A
  • Intestine

- Liver

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14
Q

What is the composition and function of lipoproteins?

A

Lipids and proteins (apoproteins)

-solubilize fat for transportation in blood and carry fats to and from the tissues

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15
Q

How can lipoproteins carry non-polar molecules in the blood?

A

They will form balls, where the exposed portion is the polar head of phospholipids with unesterifed cholesterol interspersed in the phospholipids. The inner core is triglycerides and cholesteryl esters.

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16
Q

What are the 4 types of lipoproteins and identify their size, density, source and associated apoprotein?

A

Size Density Source Apoprotein
Chylomicron Large 0.98 Intestine B-48,C-II, E
VLDL Smaller 1.006 Liver B-100,C-II, E
LDL Small 1.1 Catabolism of VLDL B-100
HDL Smallest 1.2 Liver, intestine A-1, C, E

17
Q

What do the chylomicrons transport?

A

triglycerides,
cholesterol, and
fat-soluble vitamins

18
Q

What is the main tissue that takes FA?

A

Adipose tissue

19
Q

Show how the chylomicron is processed in the body (starting from synthesis).

A

Intestine->chylomicron->periphery->chylomicron remnant (deliver cholesterol)->Liver

20
Q

T/F Chylomicron remnants may play a role in atherogenesis.

A

T. Atherogenesis is the formation of plaques in the inner lining (Intima) of arteries.

21
Q

How are LDLs formed?

A

VLDL are converted to LDL.

22
Q

What is known as bad cholesterol?

A

LDL-it imposes direct risk for atherogenesis.

23
Q

Draw a timeline showing the synthesis and final destination of VLDL.

A

Liver->VLDL->periphery->VLDL remnant->LDL->both VLDL and LDL can deliver cholesterol to the Liver

24
Q

What is known as good cholesterol?

A

HDL-play a role in fighting artherogenesis by picking up cholesterol from the periphery and delivering it to liver.

25
Q

Show the how HDL is processed in the body.

A

Liver and Intestine-> HDL->periphery->cholesterol-rich HDL->Liver

26
Q

What is the role of HDL?

A
  • Remove cholesterol from periphery and deliver it to the liver
  • Reverse cholesterol trafficking (taking cholesterol from LDL)
  • Inhibit LDL binding to arterial wall
  • Inhibit the oxidation of LDL
27
Q

Draw a comprehensive flow chart that shows how chylomicrons, HDL, LDL, and VLDL are processed in the body.

A

pp. 21

28
Q

How are type of apoproteins related to the risk of CHD?

A

Apo A levels are associated with decreased risk (HDL)

Apo E and especially Apo B levels are associated with increased risk (LDL, VLDL, VLDL and Chylomicron remnants)

29
Q

T/F Complete lipoproteins impose more risk than breakdown units of lipoproteins.

A

F. VLDLm chylomicron remnants increase risk compared to complete VLDL or chlylomicron particles.

30
Q

What are the percentages of LDL, HDL, and VLDL out of the total cholesterol?

A

65% LDL Cholesterol
25% HDL Cholesterol
10% VLDL Cholesterol

31
Q

What does a lipid profile include?

A

Directly assesses serum Normal values
Total Cholesterol 120-200 mg/dl
HDL-Cholesterol >40 mg/dl
Triglycerides 70-150 mg/dl
From which LDL-cholesterol is calculated <100 mg/dl

32
Q

What is the Friedewald formula?

A

VLDL=Triglycerides/5,
Total cholesterol=VLDL-C+HDL-C+LDL-C
We can use the above 2 equations to derive the Friedewald formula:
LDL-C=(TC)-TG/5-(HDL-C)
NOTE: serum LDL (LDL particle #) has a stronger correlation with clinical outcomes than the amount of cholesterol within the LDL particles.

33
Q

What are the 3 characters that describe atherosclerosis?

A

Disorder of arterial wall characterized by:

1) accumulation of cholesteryl ester in cells (derived from the monocyte-macrophage lineage)
2) smooth mm cell proliferation
3) fibrosis

34
Q

Label the muscular artery:

A

pp. 27

35
Q

What are the cascade of events causing the formation of atherosclerotic plaque?

A

High level of circulating lipid in the blood causes:

1) Endothelial cell receptors bind to LDL (VLDL and chylomicron remnants)
2) LDL enters Intima-if LDL is oxidized more easily enters the intima and is entrapped there
3) Endothelial injury by oxidized LDL
4) Injured endothelial cells initiate monocyte migration and macrophage formation
5) PDGF+other GF simulate migration of smooth mm cells to intima
6) Macrophage and smooth mm cells accumulate LDLs->foam cells
7) Thickened intima (collagen deposition) with roughened surface of the vessel lumen=plaque

36
Q

After formation of a plaque what are the events that lead to MI?

A

1) Distortion of sub-endothelium leads to platelet aggregation on the endothelial surface
2) Platelet release PDGF->stimulate smooth mm growth->fibrosis
3) Plaque->narrow blood vessel->Ischemia
4) Plaque bursts, blood clotting->complete blockage->cell death->MI

37
Q

T/F Formation of atheroma starts in the first decade of life.

A

F. In the first decade is the presence of foam cells, fatty streaks, third decade is intermediate lesions and atheroma, fourth decade is complicated lesion/rupture and fibrous plaque. In the first decade to third decade: growth mainly by accumulation of lipid while in the fourth decade thrombosis, hematoma is present and later smooth mm and collagen start forming.

38
Q

What are the effects to the ff. risk factors: Increased LDL, Decreased HDL, Hypertension, Cigarette smoking, Diabetes mellitus?

A

1) Increased LDL -increased lipoprotein entry into the arterial wall
(VLDL & chylomicron remnant)
2) Decreased HDL-decreased cholesterol leaving from arterial wall
3) Hypertension-arterial endothelial injury, increased lipoprotein entry
4) Smoking-arterial endothelial injury, arterial wall hypoxia &thrombosis
5) Diabetes mellitus-multiple effects (LDL modification)

39
Q

What are the dietary considerations to fight MI?

A

Decrease/avoid:

1) High cholesterol diet and saturated FA-increase LDL, VLDL remnants absorption by periphery since their uptake by the liver is decreased
2) Trans Fat-raise LDL-cholesterol and lower HDL-cholesterol
3) Obesity-mobilize free FA from periphery to liver->increase VLDL->more peripheral absorption

GOOD:

1) Monounsaturated FA-decrease TG, LDL-C, doesn’t affect HDL-C, enhance clearance of VLDL remnant and LDL
2) Omega-6-polyunsaturate FA-lower LDL-C, high concentration may lower HDL-C (limit intake), enhance clearance of VLDL remnant & LDL
3) Omega-3 polyunsaturated FA-decrease TG, inhibit VLDL & TG synthesis

40
Q

Discuss treatment options to lower blood cholesterol.

A

Dietary restrictions: 1) reduce cholesterol intake toincrease hepatic bile salt synthesis & LDL uptake
Ezetimibe: lower cholesterol absorption
Fibrate: lower cholesterol & TG absorption
Statins: inhibit cholesterol synthesis & stimulate hepatic LDL uptake

41
Q

List 4 ways of treating angina (FYI only)

A

1) Nitroglycerine and other nitrates->nitric oxide: vasodilation of coronary arteries->improve O2 delivery->wash out lactic acid
2) Ca channel blockers: coronary vasodilators
3) B-adrenergic blockers: decrease sympathetic stimulation
4) Coronary artery bypass surgery: remove veins from legs->interpose b/n aorta and coronary arteries=bypass affected area & provide affected tissue with blood supply

CV Week 2 (6 decks)

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