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NUTR 441 > CHD > Flashcards

CHD Flashcards

1
Q

other names for CHD?

A

coronary artery disease, ischemic heart disease

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2
Q

heart disease resulting from lack of adequate blood flow in blood vessels serving the heart or myocardium

A

coronary heart disease

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3
Q

major underlying cause of CHD is _____

A

atherosclerosis

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4
Q

what is atherosclerosis?

A

structural and compositional changes in the innermost or intimal layer of arteries producing impaired blood flow

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5
Q

atherosclerosis in coronary arteries can result in:

A

angina, myocardial infarction

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6
Q

what is angina?

A

chest pressure/pain, can be chronic, sign of not enough O2 going into heart

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7
Q

how to treat angina?

A

use patches to administer nitroglycerin

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8
Q

what is MI?

A

ischemia in the coronary arteries resulting in necrosis ,tissue damage, sometimes sudden death

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9
Q

atherosclerosis in cerebral arteries can cause ____ and in limbs can cause ___

A

stroke; peripheral artery disease (peripheral vascular disease)

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10
Q

major nonmodifiable risk factors for CHD

A

^ age, male sex, fam history of CHD (esp premature CHD), diabetes mellitus

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11
Q

major modifiable risk factors for CHD

A

tobacco smoke, high BP, dyslipidemia, physical inactivity, overweight, prediabetes

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12
Q

how to treat hypertension?

A

early and aggressively

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13
Q

hypertension is risk factor for:

A

CHD, stroke, kidney damage

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14
Q

systolic vs diastolic?

A

heart contracts, highest pressure ; between beats, dilation of heart, lowest measure of arterial blood pressure

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15
Q

prehypertension systolic is ___ and diastolic is ___

A

130-139; 85-89

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16
Q

___% of ppl in Canada have hypertension; over ___ people 60-70yrs

A

21.8; half

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17
Q

what are the two major systems controlling BP?

A

sympathetic nervous (short term) and renal (long term)

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18
Q

how does sympathetic nervous control BP?

A

stim adrenal glands to release epinephrine/norephinephrine to stim heart beat faster and more forcefully, arterioles constrict

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19
Q

how does renal control BP?

A

^ excretion of salt and water, decrease blood volume, decrease BP (reninangiotensin system)

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20
Q

what causes BP to increase ?

A
  • heart pumping more blood more forcefully or more rapidly
  • if arterioles constrict blood is forced thru narrower space
  • if veins constrict, decrease capacity to hold blood so more blood forced into arteries
  • if fluid added to bloodstream ^ blood volume
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21
Q

what Is primary / essential hypertension?

A

85-90% of cases, it is an inherited abnormality affecting constriction of arterioles interacting with adverse enviro factors, promoting atherosclerosis which feeds into promoting more hypertension

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22
Q

what is secondary hypertension?

A

from CKD (retaining sodium and water) and primary aldosteronism

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23
Q

reversible risks for hypertension

A

obesity (pro-inflammatory), poor diet, high sodium, sedentary, high alcohol consumption, high stress, smoking

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24
Q

mean daily Na intake of Canadians is ___

A

2760mg

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25
Q

more than ___% of males age 14-30 consume excess lvls Na

A

90

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26
Q

sources of Na?

A

bakery products, mixed dishes, processed meats, cheeses, soups, sauces, condiments

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27
Q

physical activity guidelines for treatment and prevention of hypertension

A

30-60min moderate intensity 4-7 days / week

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28
Q

to reduce possibility of becoming hypertensive, reduce sodium intake towards ____mg/day

A

2000

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29
Q

is DASH to test specific nutrient or diet pattern?

A

diet pattern

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30
Q

increasing K intake monitored closely if:

A

pt taking renin-angiotensin-aldosterone inhibitors, pt on other drugs that can cause hyperkalemia, pt with CKD (GFR < 45ml/min), pt with baseline serum potassium >4.5mmol/L

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31
Q

MI warning signs that should prompt ppl to call 911

A

chest discomfort or other areas of upper body, SOB, sweating, nausea, lightheadedness

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32
Q

signs of stroke that should prompt ppl call 911

A

facial droop, arms, slurred speech, time

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33
Q

major category of lipid-lowering drugs used

A

statins

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34
Q

how does statin work?

A

block HMG-CoA reductase which is rate limiting step in de novo cholesterols synthesis–>also weakly affect HDL-C and TG in addition to affect on LDL-C

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35
Q

new class of drug recently approved consisting of monoclonal antibodies that inactivate pro protein converts subtilisin-kexin type 9

A

PCSK9 inhibitor

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36
Q

how does PCSK 9 inhibitor work?

A

causes decreased LDL-receptor degradation, increased recirculation of the receptor to surface of hepatocytes, this lowering LDL cholesterols in bloodstream (even greater effect than statins but is injected and expensive)

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37
Q

these drugs are peroxisome proliferator-activated receptor a (PPARa) ligands, major drugs for treating elevated TG

A

fibrates

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38
Q

why aren’t bile acid resins used any more?

A

fat malabsorption effects (GI), plus made in a bad tasting powder that no one likes to drink

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39
Q

how do bile acid resins work?

A

bind bile acid which are excreted in GIT, increases demand by liver for cholesterol (make more bile acids)–>up regulation to increase transcription of LDL receptor gene to bring in more chlolesterol–>plasma LDL-C decreases

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40
Q

these are better tolerated than cholestyramine and on its own has weak effects on serum LDL-C (mostly used in combo with statins)

A

cholesterol absorption inhibitors

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41
Q

would be the most effective agent for increasing HDL but little used cuz severe effect of flushing, also lack of ability to reduce CHD events

A

nicotinic acid

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42
Q

drug classes of antihypertensives:

A

thiazide diuretics, beta-adrenergic blockers, ACE inhibitors, angiotensin 2 receptor blockers, Ca channel blockers

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43
Q

main type of diuretic used to treat hypertension that increases kidney excretion of Na and water–>decrease BV–>BV dilate

A

thiazides (potential for hypokalemia)

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44
Q

how do beta-adrenergic blockers work?

A

block beta-receptors in heart (sympathetic nervous system) to decrease heart rate and cardiac output, also inhibit renin release, note potential for hyperkalemia

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45
Q

how does ACE inhibitor work?

A

lower BP by ^ dilation of arterioles by blocking angiotensin-converting enzyme, decreasing production of angiotensin 2 (note potential for hyperkalemia)

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46
Q

how does angiotensin 2 receptor blocker work?

A

lower BP by interfering with renin-angiotensin system, similar target as ACE inhibitors so shouldn’t be used with them (potential for hyperkalemia)

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47
Q

how do Ca channel blockers work?

A

cause arterioles to dilate by altering mvmt of Ca (note grapefuit drug interaction )

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48
Q

subclass of Ca channel blockers that primarily reduce heart rate and strength of contraction

A

verapamil and diltiazem

49
Q

this drug increases strength of heart contractions, slows resting heart rate and may be used in chronic management of arrhythmias

A

digitalis

50
Q

examples of anti platelet agents used in small amounts as preventative measures?

A

ASA, clopidogrel, ticagrelor, prasurgrel

51
Q

how does warfarin work?

A

reduce ability of blood to clot by antagonizing vit K-dependent production of clotting factors, used to reduce risk of stroke and MI

52
Q

advantages of newer anticoag meds?

A

lack need for regular blood monitoring, no need to monitor vit K

53
Q

vit K AI for M is __ and F is ___

A

120mg ; 90 mg

54
Q

warfarin has narrow therapeutic window that is assessed by measuring ____ expressed as ____

A

prothrombin time ; internationalized ratio

55
Q

term for too much clotting (ie. not enough warfarin action)

A

sub therapeutic INR

56
Q

what is %TTR?

A

% time in the therapeutic range

57
Q

major food sources of vit K

A

green leafy veg, vit k supplement, canola/cottonseed/soybean/olive oil

58
Q

why hard to follow recommendations for Vit K?

A

hard to get accurate sense how much is being eaten, want to have leafy greens cuz healthy, oils used in day to day (baking, cooking, dressings, mayo)

59
Q

best strategy for confirming suspected diet vit K interaction with warfarin?

A

diet diary to track usual pattern is over time

60
Q

high diet vit K associated with:

A

more stable anticoagulant therapy (higher %TTR, fewer INR tests)

61
Q

why aren’t vit K supplements recommended to increase Vit K intake?

A

often supposed to have certain amount but don’t meet range

62
Q

why recommendation to alter kcal intake and exercise to achieve/maintain healthy BMI?

A

ease dyslipidemia (higher circumstances LDL), lose wt will lower LDL, TG, BP, inflammation, IR

63
Q

why keep total fat in range?

A

keep TG down, indirectly to help maintain healthy wt/lose wt

64
Q

why sat fat < or = 5-6% energy?

A

reduce dyslipidemia (LDL)

65
Q

why trans < 1 % of energy?

A

reduce dyslipidemia)

66
Q

why is <300mg cholesterol controversial?

A

cutting it out won’t lower blood cholesterol since it is largely genetic. if we reduce diet intake, de novo synth goes up. No good evidence for this

67
Q

why recommendation of low GI foods and < sugar beverages?

A

2ndary mechanism: increased energy–>dyslipidemia (raise TG with high CHO and GI, insulin resistance) Extra CHO first stored as glycogen, then into TG fatty acids. Eating high GI foods –> chronic high BG

68
Q

why choose fibre?

A

soluble fibre binds bile and lowers LDL so less dyslipidemia and inflammation. Fibre ferments into SCFA, less insulin resistance

69
Q

why reduce sodium?

A

lower BP

70
Q

why limit alcohol < or = 2 drinks a day for men and < or = 1 drink a day for women?

A

large amounts influence TG and hypertension

71
Q

why fish > or = 2x a week?

A

effects to reduce blood TG and platelet aggregation, inflammation

72
Q

why recommend diet rich in fruits/veg?

A

reduce inflammation by antioxidant comps, reduce BP, fibre reduce LDL; indirect effects of maintaining healthy wt, better micronutrient status

73
Q

veg and low fat diets ^ formation of :

A

VLDL particles

74
Q

TG in very high range place pt at risk for:

A

pancreatitis

75
Q

familial combined hyperlipidemia defect is:

A

hepatic overproduction of apoB100 or defect in gene that produces hepatic lipase (triglyceride removal from bloodstream)

76
Q

rare disease where catabolism of VLDL and chylomicron remnants is delayed cuz apoE2 replaces E3 and E4

A

familial dysbetalipoproteinemia

77
Q

seven major risk factors identified by Framingham study are:

A

age, sex, BP, total and HDL , smoking, glucose intolerance, left ventricular hypertrophy

78
Q

adult optimal total cholesterol level:

A

<170mg/dL, HDL at least 50mg/dL

79
Q

an inflammatory marker specific to vascular inflammation recently made available:

A

Lp-PLA2

80
Q

factors associated with ^ fibrinogen:

A

smoking, diabetes, hypertension, obesity, sedentary lifestyle, ^ TG, genes

81
Q

CRP levels are inversely correlated with ____

A

veg based diet

82
Q

what is trimethylamine-N-oxide (TMAO)?

A

gut biota-dependent metabolite that contributes to heart disease (produced by liver after intestinal bacteria have digested animal protein)

83
Q

what is Mediterranean diet pattern?

A

> servings fruit/veg, emphasize root and greens, whole grains, fatty fish, < red meat, >lean meat and low fat dairy products, nuts, legumes, olive/canola/nut oil; moderate total fat, low sat fat, high PUFA, high fibre

84
Q

What is DASH diet pattern?

A

^ fruits and veg, low fat dairy, whole grains, fish, nuts, low animal protein/sugar

85
Q

OmniHeart trial replaced 10% total daily energy from CHO with protein and other replaced same amt CHO with unsaturated fat. Which one better at lowering CVD risk?

A

replacing with protein

86
Q

ongoing research to suggest that only this type of very restricted diet can actually reverse CVD

A

vegan diet

87
Q

how does physical activity lower risk?

A

retard atherogenesis, ^ vascularity of. myocardium,^ fibrinolysis, ^ HDL, ^ glucose tolerance and insulin sensitivity, help wt management, v BP

88
Q

stress hormone ____ released after stim of symptoms nervous system and accelerates the formation of plaque

A

angiotensin 2

89
Q

this metric captures cumulative damage of obesity over years

A

obese-years

90
Q

increased risk in men > ___yrs and women > ____ years

A

45; 55

91
Q

how does omega 3 fat from fish lower TG lvls

A

by inhibiting VLDL and apoB100 synth, decreasing postprandial lipemia

92
Q

how are omega-3s from vegetables cardioprotective?

A

stim production of nitric oxide, a substance that stim relaxation of blood vessel wall

93
Q

med procedures common with CHD:

A

PCI, stents, CABG

94
Q

how to calculate blood pressure?

A

peripheral resistance x cardiac output

95
Q

what does angiotensin 2 do to ^ BP? (visceral adiposity)

A

promotes development of large dysfunctional adipocytes which produce ^ amounts of leptin and reduce adiponectin which activate the SNS; also inflammation in BV wall through release of cytokines, pro inflammatory transcription factors, adhesion molecules

96
Q

why visceral fat bad?

A

synthesizes increased amounts of angiotensinogen which activates RAS

97
Q

why dairy intake improve blood pressure?

A

potentiate ^ intracellular calcium concentration–> ^ 1,25-vitamin D3 and PTH levels–>calcium influx into smooth muscle cells and greater vascular resistance; peptides from milk proteins function as ACEs that lower BP

98
Q

why vitamin D good for BP?

A

^ endothelial function, reduce RAS activity, lower PTH levels

99
Q

magnesium role in BP?

A

inhibitor of smooth muscle contraction, can be vasodilator

100
Q

supplemental doses of potassium more effective in these ppl:

A

blacks, higher initial BP, higher sodium intake

101
Q

potential mechanism by how K lowers BP?

A

decreased vascular smooth muscle contraction by altering membrane potential or restoring endothelium-dependent vasodilation

102
Q

3 objectives for evaluating pt with hypertension:

A

1) identify possible causes 2) assess presence or absence of target organ disease and clinical CVD 3) identify other CVD risk factors that help guide treatment

103
Q

compensatory mechanisms that are activated to restore homeostasis in HF development:

A

SNS, RAS, cytokine–>sodium retention, vasoconstriction

104
Q

a substance that is secreted by ventricles in response to pressure, and is predictive of severity of HF and mortality:

A

B-natriuretic peptide (BNP)

105
Q

heart’s compensation techniques;

A

1) increase force of contraction 2) increase in size 3) pump more often 4) stim the kidneys to conserve Na and water

106
Q

earliest symptom of HF?

A

SOB

107
Q

loss of O2 to brain causing brief loss of consciousness

A

syncope

108
Q

first symptom of HF in older adults

A

dry cough with generalized weakness and anorexia

109
Q

involuntary wt loss of at least 6% nonedematous body wt during 6month period, mostly LBM

A

cardiac cachexia

110
Q

lack of blood flow to gut leads to :

A

loss of bowel integrity–>bacteria and other endotoxins enter the bloodstream–>cytokine activation

111
Q

heart failure in middle age is caused by ___ and in older adults caused by ___

A

CAD; hypertension

112
Q

^ TNF-alpha and adinopectin is associated with:

A

lower BMI, smaller skin fold, decreased plasma total protein lvls

113
Q

risk factors for HF:

A

hypertension, diabetes, CHD, left ventricular hypertrophy

114
Q

secondary prevention strategies to prevent further cardiac probs include:

A

ACE inhibitors (first line), angiotensin receptor blockers, aldosterone blockers, beta blockers, digoxin

115
Q

why ACE inhibitors first line defence?

A

inhibit RAS and improve symptoms, quality of life, exercise tolerance, and survival

116
Q

this is converted to nitric oxide which is an endothelium derived relaxing factor

A

L-arginine

117
Q

meal strategies for HF?

A

small, frequent meals and potential caloric supplements

118
Q

thiamin deficiency caused by ____

A

loop diuretics

119
Q

nutrition goals of acute post transplant pt:

A

1) provide adequate protein and kcal to treat catabolism and promote healing 2) monitor and correct electrolyte abnormalities 3) achieve optimal blood glucose control

NUTR 441 (14 decks)

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