Chapter 15 and 16 Flashcards

1
Q

What is coronary heart disease (CHD)?

A

Coronary Heart Disease is the cause of premature death in developed countries

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2
Q

Modifiable Risk Factors of CHD

A

hyperlipidemia
hypertension
cigarette smoking
a low level of HDL cholesterol

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3
Q

Non modifiable Risk Factors pf CHD

A

male gender
family history of premature CHD
aging (men over 45, women over 55)

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4
Q

Steps in pathogenesis of atherosclerosis

A

1) damage to endothelium, followed by invasion of macrophages
2) Endothelial and macrophage growth factors stimulate smooth muscle cells to migrate to the tunica intima and proliferate
3) Oxidized cholesterol accumulates in and around macrophages (foam cells) and muscle cells
4) Collagen and elastic fibers form a connective
tissue matrix that results in a fibrous plaque

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5
Q

Cholesterol

A

precursor to steroid compounds that fulfill vital physiologic functions. “Sterols” make ”steroids” and vitamin D

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6
Q

Triglycerides

A

composed of fatty acids and glycerol, are oxidized to generate energy for muscle contraction and metabolic reactions

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7
Q

What can all cells do?

A

synthesize cholesterol

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8
Q

What is the central site of processing for lipoprotein metabolism?

A

liver

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9
Q

Three sources where cholesterol is derived

A

(1) biosynthesis from acetyl-CoA
(2) delivery of dietary cholesterol by chylomicron remnants
(3) endocytosis of low-density–lipoprotein (LDL) cholesterol by LDL receptors

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10
Q

Ezetimibe

A

inhibits the absorption of dietary and biliary cholesterol from the intestines

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11
Q

Statins

A

HMG-CoA reductase inhibitors that block the rate-limiting step in cholesterol biosynthesis

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12
Q

Bile acid–binding resins

A

inhibit the reabsorption of bile acids from the gut

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13
Q

Niacin

A

inhibits the secretion of very-low-density lipoproteins (VLDLs) from the liver, and fibrates such as gemfibrozil stimulate lipoprotein lipase to increase
the hydrolysis of VLDL triglycerides and the delivery of fatty acids to adipose and other tissues

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14
Q

Exercise

A

increases lipoprotein lipase activity and lowers
triglyceride levels while increasing HDL levels

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15
Q

Fish Oil

A

A prescription-strength formulation of omega-3 carboxylic acid (Epanova) is also available

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16
Q

Mechanism of Action of Fish Oil

A

The reduction of the synthesis of triglycerides in the liver may be caused because eicosapentaenoic acid and docosahexaenoic acid are poor substrates for the enzymes responsible for the synthesis of triglycerides

17
Q

Lovastatin and Simvastatin

A

inactive prodrugs that must be converted to active metabolites in the liver, whereas the other
statins are active compounds

18
Q

Rosuvastatin

A

most potent statin currently
available after atorvastatin

19
Q

Statins

A

most important drugs for treating hypercholesterolemia

20
Q

Rosuvastatin and Atorvastatin

A

greatest effect on triglyceride levels and can be useful in treating patients with mixed hyperlipidemia

21
Q

Simvastatin

A

had a lower rate of death, myocardial infarction,
stroke, and revascularization procedures

22
Q

What is the earliest stages of statin-induced myopathy and consists of muscle ache or weakness without elevated creatine kinase levels?

A

Myalgia

23
Q

Bile acid–binding resins that are
moderately effective drugs for hypercholesterolemia and have an excellent safety
record

A

Cholestyramine, colestipol, and colesevelam

24
Q

Evolocumab and alirocumab are monoclonal antibodies to a protease enzyme that
destroys LDL receptors in the liver. This enzyme is known as

A

proprotein convertase subtilisin/kexin type 9 (PCSK9)

25
Q

When a small blood vessel is injured…

A

hemorrhage is prevented by vasoconstriction followed by formation of a platelet plug and a fibrin clot

26
Q

After the vessel is repaired…

A

the clot is removed via the process of fibrinolysis

27
Q

Arterial thrombi

A

often overlaid on a disrupted atherosclerotic plaque that exposes blood to plaque material that initiates platelet aggregation and coagulation

28
Q

coronary artery atherosclerosis can promote

A

the formation of thrombi that obstruct blood flow and cause myocardial infarction (death of tissue from lack of blood supply)

29
Q

Formation of thrombi in cerebral arteries can cause an

A

ischemic stroke

30
Q

Venous thrombi

A

initiated by venous blood pooling and sluggish blood flow that promotes expression of adhesion factors on the surface of venous endothelial cells

31
Q

Pulmonary embolism (PE)

A

thrombi can dislodge from leg veins and travel to
the lungs. Pathologic Thrombus Formation

32
Q

Thrombin

A

proteolytically cleaves small peptides from fibrinogen, allowing fibrinogen to polymerize and form a fibrin clot
potent platelet activator and mitogen

33
Q

Warfarin

A

Inhibits synthesis of coagulation factors whose formation is dependent on vitamin K

34
Q

ecchymoses

A

Patients should be instructed to report any signs of bleeding, including hematuria and bleeding into the skin