MNT 2 - Exam #1 (Part 2) Flashcards Preview

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1
Q

What is Atherosclerosis?

A

-Thickening of the blood vessel walls caused by presence of plaque (AS);
-Begins as fatty, fibrous growth which may calcify over time
— Incompletely understood process;
— Involves endothelial cells, smooth muscle cells, platelets, and leukocytes;
— Begins as a response to endothelial lining injury that results in an inflammatory process;
— AS occudes lumen of blood vessels = ischemia

2
Q

What can Atherosclerosis lead to?

A

This can lead to an infarct =

  1. Myocardial Infarction (MI)/ CAD
  2. CVA
  3. Peripheral vascular disease (PVD)
  4. CHF
3
Q

What studies have greatly contributed to the epidemiological study of CVD?

A
  1. Framingham Study
  2. National Health and Nutrition Examination (NHANES) Surveys
  3. National Cholesterol Education Program (NCEP)
4
Q

What are the risk factors for Atherosclerosis?

A
  • Family history
  • Age and gender
  • Obesity
  • Dyslipidemia
  • Hypertension (can initiate AS lesion/ cause plaque to rupture)
  • Physical inactivity
  • Atherogenic diet
  • Diabetes mellitus
  • Impaired fasting glucose and metabolic syndrome
  • Cigarette smoke
  • Sleep Apnea
5
Q

What was the MRFIT study?

A

(Multiple Risk Factor Intervention Trial);

  • 366,000 men & women;
  • Compared mortality rates for “low risk” vs “high risk” individuals
6
Q

MRFIT “Low Risk”

A

(ABSENCE of risk factors)

  • serum chol. </equal to: 120/80mmHg
  • Non-cigarette smokers
7
Q

MRFIT “High Risk”

A

(WITH risk factors);

  • serum chol. >200;
  • BP> 120/80mmHG;
  • Smokers
8
Q

What was the Nurses’ Health Study?

A
  • 84,129 women;
  • Identified 5 healthy lifestyle factors
    1. No cigarettes
    2. ½ glass wine/day
    3. 30 mins. or more/day mod./vigorous P.A.
    4. BMI< 25
    5. Diet with:
    6. lower Trans fats & glycemic load,
    7. Higher cereal fiber, omega 3’s,folate, and P/S ratio
9
Q

What were the results of the Nurses Health Study?

A
  • 14 year period =
  • 3 healthy factors present: risk of CHD reduced by 57%;
  • 4 healthy factors present: risk reduced by 66%;
  • 5 healthy factors present: risk reduced by 83%
10
Q

What defines Obesity?

A
  • Major Risk Factor of so many diseases!;
  • BMI = >29.9
  • Waist Circumference (40 men, 35 women);
  • *NCEP Adult treatment panel III (ATPIII) identified waist girth alone as suitable identifier of risk
11
Q

What other Atherosclerosis risk factors are associated with Obesity?

A
  • Dyslipidemia
  • HTN
  • Physical Inactivity
  • Diabetes
12
Q

What does a LOW level of Adiponectin predict?

A
  • Hypertension
  • Myocardial infarction
  • Coronary dysfunction
  • All related to high levels of LEPTIN;
  • *Adiponectin DECREASES with decreased adipose tissue
13
Q

How is HTN a risk factor for atherosclerosis?

A

[HTN = CV condition & risk factor for other forms of CVD]

  • Mechanism =
    1. Increased pressure against endothelium can cause initial lesion;
    2. Changes in pressure can cause established plaque to rupture leading to an event such as infarct or proliferation of plaque;
  • Site = Force of BP amplified where vessels branch b/c obstructive plaque is more common in these areas
14
Q

How does BP related to Atherosclerosis?

A

Elevated Blood Pressure/Hypertension Remains One of the Most Important Multipliers for Cardiovascular Risk:

15
Q

What is a BP of >140/90mmHG associated with?

A
  • 69% of first myocardial infarctions;
  • 74% of cases of coronary heart disease;
  • 77% of first strokes;
  • 91% of cases of heart failure;
  • 277,000 deaths in 2003;
  • $63.5 billion annually (direct/indirect)
16
Q

How is Physical Inactivity related to Atherosclerosis?

A

Impact of Physical Inactivity on CVD risk similar to: impact of dyslipidemia, HTN, cigarettes

17
Q

What are the BENEFIT of ACTIVITY?

A
  • Decreases BP;
  • Decreases TAG;
  • Increases HDL cholesterol → HAS NOT show to reduce LDL cholesterol or total cholesterol → ONLY raises good, doesn’t lower the bad;
  • Improves endothelial function;
  • Decreases platelet aggregation;
  • Helps with weight reduction
18
Q

Risk for Death related to Fit vs. Unfit MEN:

A
  • Normal Weight – Unfit 3.1X greater risk;
  • Overweight – Unfit 4.5X greater risk (fit 1.5X);
  • Obese – Unfit 5X greater risk (fit 1.6X)
19
Q

What were the results of the Nurse’s health study and Fit vs. Unfit Women?

A
1. Normal Weight 
 — Less than 1hr PA = 2.9X
— 1-3.5hr/wk PA = 1.6X
 — More than 3.5hr/wk PA = 1X
2. Overweight
— Less than 1hr PA = 4.3X
— 1-3.5hr/wk PA = 2.1X
— More than 3.5hr/wk PA = 1.5X 
3. Obese 
— Less than 1hr PA = 4.7X
— 1-3.5hr/wk PA = 2.5X
— More than 3.5hr/wk PA = 1.9X
20
Q

How do glucose abnormalities related to Atherosclerosis?

A

— Impaired fasting glucose associated with increased risk of CVD mortality; IFG = plasma glu of 110-125mg/dL;
— CVD Mortality risk with Diabetes:
-CAD = most common cause of death for patients with DM
-Individuals with type 1 and 2 DM have 2-4 times greater CVD mortality risk than non diabetics

21
Q

What are the Metabolic Risk Factors?

A
  1. Abdominal obesity – waist cir. >40in. Men/ 35in. women;
  2. Insulin resistance – FBG>/=100mg/dL or previously diagnosed T2DM;
  3. Dyslipidemia – any abnormalities in a lipid panel;
  4. TAG >/= 150mg/dL;
  5. HDL cholesterol < 40mg/dL men; < 50mg/dL women;
  6. HTN – BP >/= 130/85 mmHg or previously dx’s HTN;
  7. Prothrombotic state = abnormality in blood coagulated
22
Q

What is the NCEP Definition of Metabolic Syndrome?

A

(National Cholesterol Education Program);

-Individual has 3 metabolic risk factors

23
Q

What else is seen elevated with Metabolic Syndrome?

A

-Higher CRP seen w/ Metabolic syndrome);
→ CRP (C-reactive protein) is an acute phase reactant, a protein made by the liver and released into the bloodstream within a few hours after tissue injury, the start of an infection, or other cause of inflammation

24
Q

What is the mechanisms for vascular injury in DM?

A

(Metabolic syndrome);
-Dyslipidemia = low HDL; high Triglycerides;
-Hypertension;
-Obesity;
-Hyperglycemia
= Increased Free Fatty Acids cause endothelial dysfunction and are PRO-inflammatory
= Oxidative Stress is increased by multiple cardiovascular risk factors

25
Q

How are LESIONS in the arteries formed?

A
  • Damage to endothelial layer = inflammatory process = attracts platelets;
  • Platelets attach to endothelium and form small Clot (mural thrombus);
  • Platelets adhere to subendothelial surface & secrete Adenosine diphoshate (ADP) and platelet derived growth factor (PDGF).
26
Q

What are the effects of ADP and PDGF?

A
  • ADP and PDGF respectively promote platelet aggregation and attract monocytes, smooth muscle cells, and other cells.;
  • Net result: increase in collagen and other fibrous growth;
  • Plaque increases in size causing artery to EXPAND outward
27
Q

Stage 1 of Plaque Progression

A

-Monocytes (phagocytic WBCs) circulate in bloodstream and respond to injury in artery wall

28
Q

Stage 2 of Plaque Progression

A
  • Monocytes slip under blood vessel cell and engulf LDL cholesterol making FOAM CELLS;
  • Thin layer of foam cells develops = FATTY STREAK
29
Q

Stage 3 of Plaque Progression

A
  • Fatty streak thickens and forms plaque that accumulates more lipids, smooth muscle cells, collagen, and debris;
  • If artery expands to accomodate thickening plaque, and contains a large lipid core with a fibrous coating, it is vulnerable to rupture and thrombosis
30
Q

What are the classes of Lipoprotiens?

A
  1. Chylomicrons, VLDL, and their catabolic remnants;
  2. LDL;
  3. HDL
31
Q

What are Chylomicrons, VLDL, and their catabolic remnants?

A
  • > 30mn (largest)

- Potentially PRO-inflammatory

32
Q

What are LDLs?

A
  • 20-22nm;

- Potentially PRO-inflammatory

33
Q

What are HDLs?

A

→ GOOD cholesterol;

  • 9-15nm;
  • Potentially ANTI-inflammatory
34
Q

How do LDLs cause inflammation in the arteries?

A
  • LDL enter artery wall and can be modified;
    1. LDL leaves lumen and enters the intima of the artery;
    2. Oxidation of Lipids and ApoB;
    3. Hydrolysis of Phosphatifylcholin to Lysophospahatidylcholine;
    4. Aggregation;
    5. Other modifications =
  • MODIFIED LDLs — modified LDLs are PROinflammatory
35
Q

What is the Intima?

A
  • The tunica intima (“inner coat”), or intima for short, is the innermost tunica (layer) of an artery or vein.;
  • It is made up of one layer of endothelial cells and is supported by an internal elastic lamina;
  • The endothelial cells are in direct contact with the blood flow.
36
Q

How do Monocytes differentiate into Macrophages?

A
  1. Monocytes enter the intima;
  2. MCP-2 attaches to monocyte ;
  3. Modified LDLs promote the differentiation of monocytes into macrophages
37
Q

What is the effect of Modified LDLs on the newly formed macrophages?

A
  • Modified LDL Induces Macrophages to Release Cytokines That Stimulate Adhesion Molecule Expression in Endothelial Cells;
  • LDL enhances monocytes being taking into the intima, promotes the differentiation of monocytes to macrophages and the development of cytokines → Ultimate formation of foam cells which are the first step of atherosclerosis;
  • **If LDLs do NOT become modified, then they do NOT contribute to the oxidation and formation of the foam cells
38
Q

What is the protective effect of HDLs?

A

HDL Prevents Formation of Foam Cells =

The HDL inhibits the oxidation of LDL, so there is no enhancement of monocytes turning into macrophages

39
Q

What are the are the clinical manifestation of Atherosclerosis?

A
  • Asymptomatic = little or no symptoms;

- May progress to ischemic heart disease

40
Q

What are the procedures that are utilized to treat atherosclerosis?

A
  1. PCI (percutaneous coronary intervention) = Balloon tipped catheter inserted in groin and Often involves a stent;
  2. CABG;
  3. Medications
41
Q

What are the drug therapies used for primary prevention of atherosclerosis?

A
  1. MHG-CoA reductase inhibitors (statins);
  2. Bile acid sequestrants;
  3. Nicotinic acid;
  4. Fibric acids
42
Q

What are the side effects or interactions of Statins?

A
  • Side effects = myopathy and increased liver enzymes;

- Food-drug interactions = nausea, dyspepsia, abd pain, constipation, diarrhea, flatulence

43
Q

What are the side effects or interactions of Bile Acids Sequestrants?

A

Side effects = gesture distress, constipation, decreased drug absorption;
-Food-drug interactions = decreased absorption of minerals and fat-soluble vitamins;

44
Q

What are the side effects or interactions of Nicotinic acid (niacin)?

A
  • Side effects = flushing, hyperglycemia, hyperuriecmia (gout), hepatotocxicity;
  • Food-drug interactions = dry mouth, N/V, peptic ulcer, dyspepsia, cramps, diarrhea, flatulence
45
Q

What are the side effects or interactions of Fibric acids?

A
  • Side effects = Gallstones, myopathy;

- Food-drug interactions = N/V constipation, flatulence

46
Q

What are the clinical effects of atherosclerotic drugs?

A

These drugs can lower cholesterol MUCH more than medications!! Statin drug may truly be necessary to controlling cholesterol levels depending on the individual. → Sometimes diet will be enough, but should still be followed to not exacerbate

47
Q

What are the ATP III Guidelines?

A

(Adult Treatment Panel);

  • Developed by National Cholesterol Education Program (NCEP);
  • Treat patients with CHD;
  • Focus on prevention of CHD in those with multiple risk factors;
  • LDL cholesterol- primary target of therapy
48
Q

What are the Step of the ATP III?

A
  1. Obtain Lipid Profile;
  2. Identify clinical atheroslerotic dx = high risk for CHD events (CHD risk equivalents);
  3. Identify Other Major Risk Factors that modify LDL Goals;
  4. LDL Goals based on Risk Assessment;
  5. Determine Risk Category;
  6. Initiate TLC if LDL above goal
49
Q

What are the levels of LDL cholesterol?

A

-Optimal - 190

50
Q

What are the levels of Total Cholesterol?

A

-Desirable = 240

51
Q

What are the levels of HDL cholesterol?

A

-Low = /= 60 (NEGATIVE risk factor = removes one risk factor from the total count)

52
Q

What are the identified atherosclerotic diagnosis?

A
  • High risk for CHD events (CHD risk equivalents) =
    1. Clinical CHD → Check the chart, would be diagnosed by an MD;
    2. Symptomatic carotid artery disease;
    3. Peripheral artery disease;
    4. Abdominal aortic aneurysm – An abdominal aortic aneurysm is an enlarged area in the lower part of the aorta, the major blood vessel that supplies blood to the body; The aorta, about the thickness of a garden hose, runs from your heart through the center of your chest and abdomen.
53
Q

What are the other major risk factors that modify LDL goal for ATP 3/TLC?

A
  1. Cigarette Smoking;
  2. HTN (BP > 140/90 or on antihypertensive medication);
  3. Low HDL cholesterol (< 40 mg/dL);
  4. **An HDL greater than 60 REMOVES one risk factor → Protective factor ;
  5. Family history of premature CHD = Male: 1st degree relative < 55 years; Female: 1st degree relative < 65 years;
  6. Age: men > 45 years, women > 55 years
54
Q

What are the LDL goals based on Risk Assessment for ATP 3/TLC?

A
  1. CHD and CHD risk equivalents (highest risk) → LDL goal: < 100 mg/dL = DM would be a risk equivalent;
  2. Multiple risk factors (+ 2) (those that modify LDL level) → LDL goal: < 130 mg/dL;
  3. Zero to one risk factor → LDL goal: < 160 mg/dL;
    - **very high risk: optional goal: LDL < 70mg/dl (conflicting evidence) → HIGHER the RISK, LOWER the GOAL!!;
    - Risk equivalents: other forms of CAD, Diabetes
55
Q

What determines the Risk Category for ATP 3/TLC?

A
  1. Establish LDL goal of therapy ;
  2. Determine need for TLC (Therapeutic Lifestyle Change diet);
  3. Determine level for drug consideration
56
Q

What is the TCL diet?

A
  • Therapeutic Lifestyle Changes (TLC) =
    1. Multifaceted lifestyle approach;
    2. ↓ in saturated fat and cholesterol;
    3. Using plant stanol/sterols and increased intake of soluble fiber ;
    4. Weight management;
    5. Increased physical activity (at least moderate) → Should expend at least 200 kcal/day from exercise
57
Q

What are are the main recommendations?

A
  1. Fat = 25-35% of total calories;
  2. Sat. Fat = < 7% kcal;
  3. CHO = 50-60% kcal;
  4. Fiber = 30grams;
  5. Pro = 15% kcals;
  6. Chol = 200mg/day
    * *Fat is more liberal with TLC; Much lower with the DASH (25% total and 6% saturated)
58
Q

Other TLC Recommendations

A
  1. Sodium: < 1% total energy; Add omega 3 Fatty acids: 1g EPA & DHA/d (current lack of conclusive data) ;
    * *emphasis on SOLUBLE fiber – insoluble fiber does not effect serum lipids = Oats, flax seed, apples;
    * *(Don’t forget weight reduction, physical activity/cardiac rehab.)
59
Q

How do Plant Sterol esters and stand esters help cholesterol and LDL?

A

-Plant sterol esters and stanol esters assist in lowering Total Cholesterol and LDL by:
— Inhibiting absorption of dietary cholesterol
—*caution re: use with normocholesterolemic individuals, children and pregnant women: can affect absorption of beta carotene, alpha tocopherol

60
Q

How does soluble fiber help lower cholesterol?

A
  • Decreases absorption of lipids;

- Binds bile acidsà increased bile acid excretion

61
Q

Sources of soluble fiber & plant sterol/stanol esters; Tips for consumers; Dietary modifications

A
  • Soluble fiber: fruit, vegetables, oats, soy. (beans required in larger quantity to have similar effect);
  • Plant sterol/stanol esters: Benecol or Promise active → NOT recommended for people who do not have cholesterol problems;
  • Dietary modifications to decrease SFA/ increase PUFA
62
Q

How do Triglycerides relate to CHD?

A
  • Elevated TG are also an independent risk factor for CHD;
  • Elevated TG most often seen in metabolic syndrome;
  • Elevated TG is a secondary goal in ATP III
63
Q

What factors that increase triglyceride levels?

A
  • Obesity and overweight;
  • Physical inactivity;
  • Smoking;
  • Alcohol intake → Major effect on TG;
  • High CHO diets (> 60%) → Major effect on TG;
  • Disease states ( ex: type 2 DM) = Elevated blood glucose is often seen along with elevated TGs→ Many times lowering glucose also brings down TGs
64
Q

What are the ATP 3 classifications of Triglycerides?

A
  • Normal: < 150 mg/dL;
  • Borderline-high: 150-199;
  • High: 200-499;
  • Very High: > 500
65
Q

What are the ATP 3 treatment guidelines for all TG levels?

A

-Primary goal for all with elevated TG = achieve the target goal for LDL

66
Q

What are the ATP 3 treatment guidelines for borderline high TG levels?

A

-Borderline High TG (150-199 mg/dL) = Emphasize weight reduction and ↑ exercise

67
Q

What are the ATP 3 treatment guidelines for high TG levels?

A

-High TG: (200-499 mg/dL) =
— Emphasize wt reduction and exercise;
— Drug therapy may be indicated

68
Q

What are the ATP 3 treatment guidelines for very high TG levels?

A

-Very high TG (> 500 mg/dL) =
— Very low fat diets (< 15% of calorie intake);
— Eliminate all alcohol;
— Weight reduction and increased exercise
• Drug therapy

69
Q

What are the AND Nutr. Care Manual/EAL other guides of elevated TGs?

A
  1. Avoid extremes in carbohydrate and fat intake ;
  2. Limit added sugar as much as possible ;
  3. Recommend elminitation of concentrated sweets;
  4. Limit alcohol as much as possible;
  5. Include at least 30 minutes of moderate physical activity on most days (EAL, 200);
  6. In addition, supplemental fish oil (2 g to 4 g of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) may be used under medical supervision (*Rx from MD. OTC not well regulated)
70
Q

What are the ATP 3 assessment tools for elevated TGs?

A
  1. MEDFICTS assessment tool
  2. Dietary CAGE questions (Table 13.10);
  3. REAP (Table 13.11)
71
Q

Dietary CAGE

A
C= cheese (full-fat and 2% dairy);
A= Animal fats;
G = Got it away from home;
E = eat high-fat commercial products (candy, pastries, pie, doughnuts, cookies)
72
Q

What is the REAP assessment tool?

A

Rapid Eating Assessment for Patients (REAP);

-Standardized questions about certain food consumer per week

73
Q

What are the main medication recommended by ATP 3 for treating cholesterol/CHD?

A

HMG CoA Reductase inhibitors = STATINS:

  1. Atorvastatin (Lipitor)
  2. Fluvastatin (Lescol)
  3. Lovastatin (Mevacor)
  4. Pravastatin (Pravachol)
  5. Simvastatin (Zocor)
  6. Rosuvastatin (Crestor)
74
Q

How do statins work?

A
  • block the production of cholesterol in the liver;
  • lower LDL cholesterol (18-55%) and triglycerides (7-30%);
  • Some increase in HDL cholesterol (5-15%);

Possible Side effects:

  • intestinal distress
  • Increased liver enzymes
  • muscle tenderness
75
Q

Nicotinic Acid Medications

A

Thought to:

  • Inhibit lipolysis of adipose tissue
  • Inhibit hepatic synthesis of TAG
  • lowers LDL cholesterol (5-25%)
  • raises HDL cholesterol 15-35%)
  • lowers TAG (20-50%)

Side effects = flushing, itching, hyperglycemia

76
Q

Bile Acid Sequestrants

A

Where/ How they work/ how they’re taken:

  • work inside the intestine,
  • bind to bile from the liver and prevent it from being reabsorbed into the circulatory system

Side effects/ food drug interactions:

  • constipation, gas and upset stomach
  • May decrease absorption of minerals and fat-sol. vitamins
77
Q

Fibric Acid/Fibrates

A

How they work:

  • reduce the production of triglycerides (decrease TAG 20-50%)
  • can increase HDL cholesterol (10-20%)

Side effects/ food drug interactions:

  • Gallstones, myopathy
  • N/V, constipation, flatulence