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

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1

What is Atherosclerosis?

-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

What can Atherosclerosis lead to?

This can lead to an infarct =
1. Myocardial Infarction (MI)/ CAD
2. CVA
3. Peripheral vascular disease (PVD)
4. CHF

3

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

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

4

What are the risk factors for Atherosclerosis?

-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

What was the MRFIT study?

(Multiple Risk Factor Intervention Trial);
-366,000 men & women;
-Compared mortality rates for “low risk” vs “high risk” individuals

6

MRFIT “Low Risk"

(ABSENCE of risk factors)
-serum chol. -Non-cigarette smokers

7

MRFIT “High Risk"

(WITH risk factors);
-serum chol. >200;
-BP> 120/80mmHG;
-Smokers

8

What was the Nurses’ Health Study?

-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

What were the results of the Nurses Health Study?

*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

What defines Obesity?

*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

What other Atherosclerosis risk factors are associated with Obesity?

-Dyslipidemia
-HTN
-Physical Inactivity
-Diabetes

12

What does a LOW level of Adiponectin predict?

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

13

How is HTN a risk factor for atherosclerosis?

[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

How does BP related to Atherosclerosis?

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

15

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

-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

How is Physical Inactivity related to Atherosclerosis?

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

17

What are the BENEFIT of ACTIVITY?

-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

Risk for Death related to Fit vs. Unfit MEN:

-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

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

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

How do glucose abnormalities related to Atherosclerosis?

— 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

What are the Metabolic Risk Factors?

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

What is the NCEP Definition of Metabolic Syndrome?

(National Cholesterol Education Program);
-Individual has 3 metabolic risk factors

23

What else is seen elevated with Metabolic Syndrome?

-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

What is the mechanisms for vascular injury in DM?

(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

How are LESIONS in the arteries formed?

-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

What are the effects of ADP and PDGF?

-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

Stage 1 of Plaque Progression

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

28

Stage 2 of Plaque Progression

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

29

Stage 3 of Plaque Progression

-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

What are the classes of Lipoprotiens?

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