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PATHO > HLD Pharmacology > Flashcards

HLD Pharmacology Flashcards

1
Q

Atorvastatin, Simuvastatin, Rosuvastatin classification

A

HMG-CoA reductase inhibitors

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2
Q

HMG-CoA reductive inhibitors suffix

A

–statins

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3
Q

Atorvastatin, Simvastatin, Rosuvastatin MOA

A

Inhibits HMG-CoA reductase which causes less cholesterol to be made by the liver; LDL and TG decrease and HDL increases

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4
Q

Atorvastatin, Simnuvastatin, Rosuvastatin adverse effects

A

Myopathy, rhabdomyolysis (can lead to acute kidney failure), mild cramping, some hepatotoxicity

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5
Q

Atorvastatin, Simuvastatin, Rosuvastatin nursing considerations

A

Can take a couple weeks to get effects, make take with food if GI discomfort, best to take at night (simvastatin, rosuvastin), avoid alcohol

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6
Q

ezetimibe (Zetia) classification

A

Cholesterol reabsorption inhibitor

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7
Q

ezetimibe (Zetia) MOA

A

Blocks absorption of cholesterol in jejunum (dietary)

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8
Q

ezetimibe (Zetia) adverse effects

A

Muscle pain, liver damage

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9
Q

ezetimibe (Zetia) nursing considerations

A

Usually a second line therapy, the effect is greater when taken with a statin so two meds may be better, watch liver pt

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10
Q

cholesterol

A

highly insoluble; builds estrogen and testosteron, vitamin D, cortisol, bile acids, skin barrier; essential part of bilayer in all cell membranes

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11
Q

Cholesterol source

A

25% exogenous (diet); 75% endogenous (HMG-CoA reductase is the prcoess the liver uses to make cholesterol using saturated fat)

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12
Q

Liver’s negative feedback loop

A

When the liver senses high LDL with LDL receptors, there is decreased HMG-CoA production to decrease cholesterol; when more cholesterol is needed, body makes more receptors to pull more cholesterol out of the blood

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13
Q

kinds of lipoproteins

A

HDL–the good kind, higher protein content; LDL–the bad kind, leads to plaque, lower protein; VLDL–low protein and contributes to heart disease with LDL

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14
Q

hypercholesterolemia

A

hyperlipidemia/dyslipidemia; excess cholesterol in the blood

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15
Q

How to diagnose high cholesterol

A

Few symptoms, screen starting at age 20 every 5 years or in kids at high risk; look at overall cholesterol fasting numbers

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16
Q

Healthy cholesterol levels

A

Total cholesterol <200mg
HDL >50 or 60
LDL <100
Triglycerides <150

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17
Q

Familial hypercholesterolemia

A

caused by a defect in LDL receptors in liver cells; liver can’t make LDL receptors well, causing elevated LDL in blood; causes heart problems in kids; diet can’t change the amounts

18
Q

Risk factors for hyperlipidemia

A

age, family history, smoking, sedentary, obesity, poor diet, DM

19
Q

Elevated LDL and cholesterol causes

A

increased risk of atherosclerosis (decreased ability of BVs to dilate)

20
Q

arteriosclerosis

A

thickened/hardened arterial wall that decreases the arteries ability to carry oxygenated blood

21
Q

How does atherosclerosis form

A

Injury to epithelial layer on the inner BVs that causes plaque formation–chemicals from smoking, chronic hemodynamic wall stress, hyperglycemia; oxidation of epithelial tissue

22
Q

C-reactive protein (CRP) and results from it

A

Marker of systemic inflammation; can be a sign of atherosclerosis; binds to phospholipids on bacterial cell membranes and indicates increased risk of disease state

23
Q

Erythrocyte sedimentation rate (SED)

A

Inflammatory marker

24
Q

How does increased arterial permeability lead to atherosclerosis

A

Injuries make arteries more susceptible so LDL can bury in; macrophages try to eat lipids, making foam cells that appear as fatty streaks in the walls and make plaques that can expand and impede blood flow

25
Q

Inflammatory mediators

A

Released in response to arterial injury; causes accumulation of debris and lipid core which is prone to rupture and form a clot

26
Q

Biggest danger of plaques

A

They can rupture and cause platelet aggregation which can lead to thrombus formation

27
Q

s/s of blockages

A

fatigue, new inability to do things

28
Q

coronary heart disease aka coronary artery disease

A

plaque formation; most is atherosclerosis

29
Q

Ischemic heart disease

A

insufficient delivery of oxygen to heart

30
Q

Atherosclerotic CVD (ASCVD)

A

plaque build up

31
Q

How to improve atherosclerosis

A

improve LDL:HDL ratio, diet, meds, exercise, STOP SMOKING, weight loss, low fat heart healthy diet

32
Q

What do statins help with?

A

preventing heart attack and stroke, dec risk of disability, dec risk of total mortality with past history of ASCVD event

33
Q

Clinical ASCVD conditions

A

MI, acute coronary syndrome, angina, stroke or TIA, PAD, Coronary revascularization

34
Q

Are statins permanent?

A

No, must take drug for rest of life to keep endogenous cholesterol low

35
Q

Changes in cholesterol levels with statins

A

Dec LDL and triglycerides, inc HDL

36
Q

myopathy

A

muscle weakness

37
Q

Rhabdomyolosis

A

breakdown muscle fibers which can lead to acute kidney failure

38
Q

What to do before giving cholesterol meds

A

Check fasting lipid panel, ACT (liver), Creatinine (kidney fxn) bc of rhabdo, consider a secondary cause

39
Q

Additional meds for cholesterol

A

bile acid sequestrants like cholestyramine, niacin, fibric acid derivates (fibrates), fish oil

40
Q

Secondary causes of HLD (LDL)

A

Diet (sat and trans fat), weight gain, anorexia, drugs like diuretics, glucocorticoids, amiodarone, diseases like biliary obstruction, nephrotic syndrome, disorders like hypothyroidism, obesity, and pregnancy

41
Q

Secondary cause of HLD (elevated triglycerides)

A

wt gain, very low fat diet, oral estrogens, glucocorticoids, bile acid sequestrants, beta blockers, nephrotic syndrome, chronic renal failure, lipodystrophies, poorly controlled DM, hypothyroidism, obesity, pregnancy

42
Q

What drugs are best to take at night?

A

Simvustatin and Ruvostatin

PATHO (32 decks)

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