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Cardiovascular Disease Flashcards

1
Q

Risk factors for CVD

A 
age 
- male >45
- female >55 
family history
smoking
hypertension (HTN)
diabetes mellitus
weight
- abdominal obesity 
ethnicity
- asian, hispanic, metabolic dysregulation
hyperlipidemia ~ high LDL, cholesterol, low HDL
sedentary lifestyle
dietary choices
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2
Q

Coronary Heart Disease

A
  • # 1 cause of mortality in men and women in Canada
  • irregular thickening inner layer of coronary artery walls, narrowing the internal channel and reducing blood supply to the heart
  • leads to MI (myocardial infarction)
  • focus on modifiable risk factors (diet)
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3
Q

Other definitions of CHD

A
  • some localized damage or angina in the heart due to artery blockage but the heart still functions (collaterol, small arteries)
  • may not be damage until time progresses
  • may be due to complete blockage from MI
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4
Q

CVD - coronary heart disease

A
  • 80% of coronary heart disease caused by atherosclerosis ~ process and composition of plaques
  • narrowing and progressive occlusion of arteries
  • major contributor of hyperlipidemia
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5
Q

atherosclerosis

A
  • increase fatty acid streaks form on arterial wall
    • small deposits of lipid
    • normal process but when they form plaque it is abnormal ~ immune reaction
  • damage to arterial wall occurs
    • hypertension
    • smoking
  • -viral attack
    • excess lipids
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6
Q

two effects from damage to the arterial walls

A
  • platelets aggregate ~ release growth factors, smooth muscle proliferation
  • exposure to LDL ~ oxidation of cholesterol, local inflammatory response ~ attracts macrophages which engulf cholesterol
    foam cells: oxidative damage to LDL in bloodstream stimulate WBC to bind and absorb damaged LDL ~ WBC fill with cholesterol
  • bulging lesions, secretions that further damage smooth muscle
  • plaque formation
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7
Q

increased risk of CHD ~ atherosclerosis

A
  • high total cholesterol
  • high LDL
  • low HDL
  • high TAGs
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8
Q

cholesterol

A
  • essential metabolite in animal cells ~ synthesized mainly in liver and intestine
  • important structure for myelin sheeth, structure, precursor for bile acids, several hormones
  • 80% endogenous via HMG-CoA reductase
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9
Q

plasma cholesterol regulation

A
  • 25-75% dietary intake is absorbed / not absorbed as well if there is fibre
  • endogenous synthesis is main componenet: HMG:CoA reductase enzyme by LDL
  • excretion ~ biliary secretion and excretion in feces
    30-60% reabsorbed
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10
Q

lipoproteins

A
  • solubilize cholesterol
  • allow transport in blood
  • complex of lipid and protein
    ~ hydrophobic core of TAG, esterified cholesterol
    ~ hydrophilic surface of PL, free cholesterol and apoproteins
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11
Q

HDL

A
  • high density lipoprotein has less fat in it

- more cholesterol and protein

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12
Q

LDL

A
  • low density lipoprotein has more fat in it
  • less protein
  • unloads TAG at the adipose tissue and LPL helps cleave the TAG and ship it into the tissue
  • it becomes higher density when it releases fat since protein is heavy
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13
Q

VLDL

A
  • highest level during fasting
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14
Q

apoproteins

A
  • stabilizes lipoprotein particles
  • activates enzymes for lipid metabolism ~ when VLDL hits surface, it actives LPL and HL
  • mediating uptake of cholesterol and TAG by tissues (recognized by membrane receptors)
  • major determinate of plasma lipid concentrations
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15
Q

apoB

ApoB48

A

apoB ~ receptor binds to LDL, not found in HDL

apoB48 ~ chylomicrons from the intestines

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16
Q

apolipprotein components and function

A
  • lipids (TAG, chol, PL, chol esters) are insoluble and so bind with apoproteins to solubilize lipids
  • apoproteins maintain structural integrity of lipoproteins
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17
Q

density of lipoprotein increases as proportion of protein _____ and lipid ______.

A
  • density increases as proportion of protein increases and lipid decreases
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18
Q

srum lipoproteins

A

Chylomicrons - to liver
VLDL - shipped from the liver an TG is high
higher density and smaller area - gets rid of fat from peripheral tissues, will get more and more dense

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19
Q

chylomicrons

A
  • composed mainly of TAG
  • synthesized in intestines
  • transport lipid to tissues
  • transports cholesterol to liver (remnants)
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20
Q

VLDL

A
  • synthesized in liver
  • transport TAG to tissue
  • good indicator of what last meal was
  • most postprandial rise is VLDL
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21
Q

IDL

A
  • remnants of CM and VLDL once depleted of TAG
  • has higher concentration of cholesterol
  • precursor to LDL
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22
Q

LDL

A
  • deliver cholesterol to tissues
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23
Q

HDL

A
  • transport cholesterol from tissues to liver
  • modified type of ApoB proteins
  • has more PL and cholesterol ester
  • little TG and free cholesterol so it is less sticky
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24
Q

Cholesterol - TAG

A
  • high CHO intake stimulates pancreas to secrete insulin, converts glucose to acetyl-coa which makes FAs
  • calories ingested and not used by tissues immediately are converted to TAG
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25
Hyperlipidemia
- risk of CHD increases with -- high serum cholesterol, high LDL, low HDL and high TAG - all measures should be done while fasting
26
modifiable risks classification for hyperlippidemia
- blood pressure - smoking status - nicotine - makes oxidative stress worse and HTN; weight loss, medication,
27
non modifiable classiciation for hyperlipidemia
- age | - gender
28
Cholesterol synthesis
- mainly in liver and intestine free chol --> cholesterol ester via ACAT (acyl CoA cholesterol acyl transferase) acetate --> free cholesterol via HMG-CoA reductase
29
regulations of cholesterol synthesis
- if you eat a lot of cholesterol.. HMG coA reductase will be at basal level (producing minimal free cholesterol) - oversupply of cholesterol activates ACAT to make esters for storage
30
two mechanisms to control excessive cholesterol
- high cholesterol inhibits HMG-reductase (inhibits free cholesterol synthesis) - increased cholesterol inhibit synthesis of LDL receptors (decreases uptake)
31
Tight control of cholesterol
- LDL receptors bind most efficiently at serum LDL of 1.3 mmol/L - excess is removed from blood by scavenger pathway with monocytes, macrophages and foam cells
32
Continued increase in LDL levels ?
- no inhibition of cholesterol and LDL receptor - levels can be hard to lower - cells will eventually burst and release contents, thus increasing risk of blockage
33
high plasma LDL and advanced lesions
high LDL - LDL infiltration - oxidized LDL and macrophages, foam cells, fatty streaks --> endothelial injury - adherance of platelets - release of PDGF - cell proliferation - advanced lesion
34
Hypertension
- high blood pressure - common cause of renal failure - many have no symptoms - primary/essential hypertension = influenced by diet and lifestyle - secondary hypertension = results from another condition such as endocrine, renal or neurological disorders
35
systolic blood pressure / diastolic blood pressure
normal is 140/90 mmHg | - at least 2 elevated blood pressure readings on two or more occasions
36
stage 1 HTN
140-159/90-99 mmHg
37
stage 2 HTN
160-179-100-109 mmHg
38
stage 3 HTN
>180/>110 mmHg (be hospitalized) | - only true stages if both pressures are abnormal
39
HTn - CVD risk
- optimal with respect to CV risk <12-/80 mmHg
40
Hypertension - Purpose of Nutrition Care
- chronic may not have symptoms and so compliance becomes an issue - to prevent or control high BP, alone or in conjunction with drug therapy - reduce morbidity and mortability associated with hypertension, stroke CV
41
treatment of HTN
- is based on risk factors (age, gender, smoking, renal disease etc) - lifestyle modification - DASH diet and pharmacological treatment
42
lifestyle modification of HTN
- weight reduction - controlled alcohol intake - potassium (60 mmol/d) - calcium and magnesium - restrict Na intake if >44yoa ( 87-130 mmol/d = 2000-3000 mg/day) Ai for Na = 1500 mg ~upper limit aim - reduce saturated fat/cholesterol = sticky, rigid increases blood pressure - reduce smoking ~ cessation causes rigid blood vessels
43
Treatment - weight reduction
- doesn't completely correct the problem - abdominal girth correlates to higher BP - weight loss of 4.5 kg is effective - important for elderly
44
treatment - alcohol intake
- maybe - excess intake associated with higher BP - may causes resistance to medication
45
Health Consequences of High Sodium Intake
- rise in BP - increase stroke risk, progression of renal disease and proteinuria - obesity - renal stones and osteoperosis *kidneys try to excrete excess Na, overworked, Ca comes out too - increases asthma risk - stomach cancer
46
Potassium
- counterbalance some effects of high Na in diet - genetics - assist in controlling BP and protect against development of HTN - fresh fruits and vegetables, supplements
47
magnesium
- association between lower intakes and increased BP | - no evidence that increased intake will lower BP
48
DASH diet | Dietary Approaches to Stop Hypertension
- heavily focused on Na and K - may replace meds in pt at stage 1 - may also be due to weight loss - not a vegetarian diet - potassium, magnesium, fibre, calcium, total fat, saturated fat, cholesterol and protein - lean meats and fish consumption - emphasizes whole grains, vegetables and low fat dairy products - limits fat, cholesterol and fat
49
benefits of DASH
- more palatable - less restrictive - builds on general recommendations - low GI suppresses appetite
50
Association between inflammation and CVD
- chronic inflammation can cause morbidity and mortality - CRP monitor changes ~ an acute phase protein "inflammatory response" - predict new coronary events in pt with unstable angina and acute MI - env pathogens can contribute to chronic inflammation, producing byproducts
51
Cardiac Surgery
- coronary artery bypass graft (CABG) - percutaneous coronary angioplasty (PTCA) - ballon dilation bc plaques are blocking blood vessels, lipids lining blood vessels are sticky - atherectomy - laser catheter or rotating shaver to remove plaque
52
purpose of nutrition care - cardiac surgery
- prevent weight and fluid loss, maintain protein , support anabolism and healing post-op - promote cardiac wellness, prevent further hyperlipidemia - some pt are skinny, some are overweight - focus on maintaining weight / no loss
53
Diet therapy - Cardiac Surgery
- nutrition assessment: comorbidities, baseline lab values and lipid profile, anthropometrics
54
Diet thereapy - Cardiac surgery | Energy
- stress factor is 1.2 - 1.5 - severe heart failure may require 20-30% increase in calories (increased cardiac/pulmonary effort) - protein: 0.8-1.0 g/kg (may need to adjust for renal failure)
55
Diet therapy following Cardiac Surgery
- may have Na restriction ~ fluid retention increases cardiac effort - normal diet restrictions for cormobidities - maybe supplements - can use nutrition support
56
long term nutrition care post surgery
- TLC diet - cardiac rehab programs ~ nutrition and activity education - long term follow up of blood lipids - long term Na restriction (DASH) - maybe weight loss
57
Drug Nutrient Interactions ~ Surgery | - digitalis (eg. Digoxin)
- hypokalemia: nausea, vomiting, anorexia, abdominal pain, mental changes and arrhythmias - hypomagnesium and hypercalcemia
58
Drug Nutrient Interactions ~ Surgery | Diuretics (eg Lasix) **
- know foods with potassium in them - hypokalemia (severe) - low zinc levels: low gut motility and taste - contribute to hypercholesteremia - may cause hyperglycemia - rare
59
Drug Nutrient Interactions ~ Surgery | aminodarone (anti-arrhythmic and vasodilator)
- nausea, increase or decrease appetite, constipation, metal taste
60
Drug Nutrient Interactions ~ Surgery | anticoagulants * (eg heparin, coumadin) **
- require consistent intake of Vit K | - consistent amount of green leafy vegetables, cabbage, brussel sprouts
61
Drug Nutrient Interactions ~ Surgery
- nausea, vommiting, diarrhea, abdominal pain
62
homocysteine
- reason for other risk factors of CVD and atherosclerosis - sulfur containing aa ~ only a marker for CVD - derived from essential aa methionine - B6 and B12 and folate involved
63
homocysteinuria
- increase concentrations of circulating homocysteine and urinary homocysteine
64
Hyperhomocysteinemia (Hhcy)
- high occurance in pt with CAD - Cystathionine B-synthesis deficiency (B6) - methylenetetrahydrofolate reductase deficiency (B12)
65
2 Pathways
- varying amounts of expression - genes associated with synthesis of these pathways is affected - proteins are not made due to defects in synthesis ~ amount and activity is disrupted - provide lots of cofactors
66
Cystathionine B synthase
- trans-sulphuration - converts homocysteine to cysteine and then is excreted - vitamin B6 **
67
Methionine Synthase
- remethylation of homocysteine to methionine | - vitamin B12/folate
68
determinants of Plasma Homocysteine
- unmodifiable = age (30+years), gender (males) genetics - modifiable = diatary (folate, B6,B12) 100x RDA - - PA, smoking, coffee, alcohol contribute to oxidative stress (indirect)
69
other factors causing hyperhomocysteinemia
- renal failure (kidneys can reabsorb back and even more will filter out) - diabetes - hypothyroidism - medications (lipid lowering drugs, metformin, methotrexate, levodopa, thiazide diuretics, anticonvulsants)
70
cause and effect
smoking, hypertension, low folate and B vitamins = stroke, MI, venous thrombosis, atherosclerosis
71
potential CVD mechanisms
- endothelial cell toxicity ~ increased free radical formation - proliferation of smooth muscle cells ~ increased tissue factor activity - thrombus formation ~ increase platelet adherence
72
* Classification of Homocysteinemia
moderate - 15 to 30 umol/l intermediate - >30 to 100 umol/l severe - >100 umol/l
73
Supplementation
- pt on dialysis benefits from folate, B6, B12 and people with genetic disposition - folate supplementation independently decreases plasma homocysteine (0.5-5 mg)

Clinical Nutrition (14 decks)

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