Flashcards in MNT 2 - Exam #1 (Part 2) Deck (77)
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
What can Atherosclerosis lead to?
This can lead to an infarct =
1. Myocardial Infarction (MI)/ CAD
3. Peripheral vascular disease (PVD)
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)
What are the risk factors for Atherosclerosis?
-Age and gender
-Hypertension (can initiate AS lesion/ cause plaque to rupture)
-Impaired fasting glucose and metabolic syndrome
What was the MRFIT study?
(Multiple Risk Factor Intervention Trial);
-366,000 men & women;
-Compared mortality rates for “low risk” vs “high risk” individuals
MRFIT “Low Risk"
(ABSENCE of risk factors)
-serum chol. -Non-cigarette smokers
MRFIT “High Risk"
(WITH risk factors);
-serum chol. >200;
What was the Nurses’ Health Study?
-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
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%
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
What other Atherosclerosis risk factors are associated with Obesity?
What does a LOW level of Adiponectin predict?
*All related to high levels of LEPTIN;
**Adiponectin DECREASES with decreased adipose tissue
How is HTN a risk factor for atherosclerosis?
[HTN = CV condition & risk factor for other forms of CVD]
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
How does BP related to Atherosclerosis?
Elevated Blood Pressure/Hypertension Remains One of the Most Important Multipliers for Cardiovascular Risk:
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)
How is Physical Inactivity related to Atherosclerosis?
Impact of Physical Inactivity on CVD risk similar to: impact of dyslipidemia, HTN, cigarettes
What are the BENEFIT of ACTIVITY?
-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
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)
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
— Less than 1hr PA = 4.3X
— 1-3.5hr/wk PA = 2.1X
— More than 3.5hr/wk PA = 1.5X
— Less than 1hr PA = 4.7X
— 1-3.5hr/wk PA = 2.5X
— More than 3.5hr/wk PA = 1.9X
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
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
What is the NCEP Definition of Metabolic Syndrome?
(National Cholesterol Education Program);
-Individual has 3 metabolic risk factors
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
What is the mechanisms for vascular injury in DM?
-Dyslipidemia = low HDL; high Triglycerides;
= Increased Free Fatty Acids cause endothelial dysfunction and are PRO-inflammatory
= Oxidative Stress is increased by multiple cardiovascular risk factors
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).
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
Stage 1 of Plaque Progression
-Monocytes (phagocytic WBCs) circulate in bloodstream and respond to injury in artery wall
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
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