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Clinical Nutrition > Cardiovascular Disease > Flashcards

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
Q

Hyperlipidemia

A
  • risk of CHD increases with – high serum cholesterol, high LDL, low HDL and high TAG
  • all measures should be done while fasting
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26
Q

modifiable risks classification for hyperlippidemia

A
  • blood pressure
  • smoking status
  • nicotine
  • makes oxidative stress worse and HTN; weight loss, medication,
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27
Q

non modifiable classiciation for hyperlipidemia

A
  • age

- gender

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28
Q

Cholesterol synthesis

A
  • mainly in liver and intestine
    free chol –> cholesterol ester via ACAT (acyl CoA cholesterol acyl transferase)

acetate –> free cholesterol via HMG-CoA reductase

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29
Q

regulations of cholesterol synthesis

A
  • 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
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30
Q

two mechanisms to control excessive cholesterol

A
  • high cholesterol inhibits HMG-reductase (inhibits free cholesterol synthesis)
  • increased cholesterol inhibit synthesis of LDL receptors (decreases uptake)
31
Q

Tight control of cholesterol

A
  • 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
Q

Continued increase in LDL levels ?

A
  • 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
Q

high plasma LDL and advanced lesions

A

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
Q

Hypertension

A
  • 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
Q

systolic blood pressure / diastolic blood pressure

A

normal is 140/90 mmHg

- at least 2 elevated blood pressure readings on two or more occasions

36
Q

stage 1 HTN

A

140-159/90-99 mmHg

37
Q

stage 2 HTN

A

160-179-100-109 mmHg

38
Q

stage 3 HTN

A

> 180/>110 mmHg (be hospitalized)

- only true stages if both pressures are abnormal

39
Q

HTn - CVD risk

A
  • optimal with respect to CV risk <12-/80 mmHg
40
Q

Hypertension - Purpose of Nutrition Care

A
  • 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
Q

treatment of HTN

A
  • is based on risk factors (age, gender, smoking, renal disease etc)
  • lifestyle modification - DASH diet and pharmacological treatment
42
Q

lifestyle modification of HTN

A
  • 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
Q

Treatment - weight reduction

A
  • doesn’t completely correct the problem
  • abdominal girth correlates to higher BP
  • weight loss of 4.5 kg is effective
  • important for elderly
44
Q

treatment - alcohol intake

A
  • maybe
  • excess intake associated with higher BP
  • may causes resistance to medication
45
Q

Health Consequences of High Sodium Intake

A
  • 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
Q

Potassium

A
  • 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
Q

magnesium

A
  • association between lower intakes and increased BP

- no evidence that increased intake will lower BP

48
Q

DASH diet

Dietary Approaches to Stop Hypertension

A
  • 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
Q

benefits of DASH

A
  • more palatable
  • less restrictive
  • builds on general recommendations
  • low GI suppresses appetite
50
Q

Association between inflammation and CVD

A
  • 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
Q

Cardiac Surgery

A
  • 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
Q

purpose of nutrition care - cardiac surgery

A
  • 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
Q

Diet therapy - Cardiac Surgery

A
  • nutrition assessment: comorbidities, baseline lab values and lipid profile, anthropometrics
54
Q

Diet thereapy - Cardiac surgery

Energy

A
  • 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
Q

Diet therapy following Cardiac Surgery

A
  • may have Na restriction ~ fluid retention increases cardiac effort
  • normal diet restrictions for cormobidities
  • maybe supplements
  • can use nutrition support
56
Q

long term nutrition care post surgery

A
  • 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
Q

Drug Nutrient Interactions ~ Surgery

- digitalis (eg. Digoxin)

A
  • hypokalemia: nausea, vomiting, anorexia, abdominal pain, mental changes and arrhythmias
  • hypomagnesium and hypercalcemia
58
Q

Drug Nutrient Interactions ~ Surgery

Diuretics (eg Lasix) **

A
  • know foods with potassium in them
  • hypokalemia (severe)
  • low zinc levels: low gut motility and taste
  • contribute to hypercholesteremia
  • may cause hyperglycemia - rare
59
Q

Drug Nutrient Interactions ~ Surgery

aminodarone (anti-arrhythmic and vasodilator)

A
  • nausea, increase or decrease appetite, constipation, metal taste
60
Q

Drug Nutrient Interactions ~ Surgery

anticoagulants * (eg heparin, coumadin) **

A
  • require consistent intake of Vit K

- consistent amount of green leafy vegetables, cabbage, brussel sprouts

61
Q

Drug Nutrient Interactions ~ Surgery

A
  • nausea, vommiting, diarrhea, abdominal pain
62
Q

homocysteine

A
  • 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
Q

homocysteinuria

A
  • increase concentrations of circulating homocysteine and urinary homocysteine
64
Q

Hyperhomocysteinemia (Hhcy)

A
  • high occurance in pt with CAD
  • Cystathionine B-synthesis deficiency (B6)
  • methylenetetrahydrofolate reductase deficiency (B12)
65
Q

2 Pathways

A
  • 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
Q

Cystathionine B synthase

A
  • trans-sulphuration
  • converts homocysteine to cysteine and then is excreted
  • vitamin B6 **
67
Q

Methionine Synthase

A
  • remethylation of homocysteine to methionine

- vitamin B12/folate

68
Q

determinants of Plasma Homocysteine

A
  • unmodifiable = age (30+years), gender (males) genetics
  • modifiable = diatary (folate, B6,B12) 100x RDA
    • PA, smoking, coffee, alcohol contribute to oxidative stress (indirect)
69
Q

other factors causing hyperhomocysteinemia

A
  • 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
Q

cause and effect

A

smoking, hypertension, low folate and B vitamins = stroke, MI, venous thrombosis, atherosclerosis

71
Q

potential CVD mechanisms

A
  • endothelial cell toxicity ~ increased free radical formation
  • proliferation of smooth muscle cells ~ increased tissue factor activity
  • thrombus formation ~ increase platelet adherence
72
Q
  • Classification of Homocysteinemia
A

moderate - 15 to 30 umol/l

intermediate - >30 to 100 umol/l

severe - >100 umol/l

73
Q

Supplementation

A
  • 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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