CHD Flashcards
1
Q
other names for CHD?
A
coronary artery disease, ischemic heart disease
2
Q
heart disease resulting from lack of adequate blood flow in blood vessels serving the heart or myocardium
A
coronary heart disease
3
Q
major underlying cause of CHD is _____
A
atherosclerosis
4
Q
what is atherosclerosis?
A
structural and compositional changes in the innermost or intimal layer of arteries producing impaired blood flow
5
Q
atherosclerosis in coronary arteries can result in:
A
angina, myocardial infarction
6
Q
what is angina?
A
chest pressure/pain, can be chronic, sign of not enough O2 going into heart
7
Q
how to treat angina?
A
use patches to administer nitroglycerin
8
Q
what is MI?
A
ischemia in the coronary arteries resulting in necrosis ,tissue damage, sometimes sudden death
9
Q
atherosclerosis in cerebral arteries can cause ____ and in limbs can cause ___
A
stroke; peripheral artery disease (peripheral vascular disease)
10
Q
major nonmodifiable risk factors for CHD
A
^ age, male sex, fam history of CHD (esp premature CHD), diabetes mellitus
11
Q
major modifiable risk factors for CHD
A
tobacco smoke, high BP, dyslipidemia, physical inactivity, overweight, prediabetes
12
Q
how to treat hypertension?
A
early and aggressively
13
Q
hypertension is risk factor for:
A
CHD, stroke, kidney damage
14
Q
systolic vs diastolic?
A
heart contracts, highest pressure ; between beats, dilation of heart, lowest measure of arterial blood pressure
15
Q
prehypertension systolic is ___ and diastolic is ___
A
130-139; 85-89
16
Q
___% of ppl in Canada have hypertension; over ___ people 60-70yrs
A
21.8; half
17
Q
what are the two major systems controlling BP?
A
sympathetic nervous (short term) and renal (long term)
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
19
Q
how does renal control BP?
A
^ excretion of salt and water, decrease blood volume, decrease BP (reninangiotensin system)
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
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
22
Q
what is secondary hypertension?
A
from CKD (retaining sodium and water) and primary aldosteronism
23
Q
reversible risks for hypertension
A
obesity (pro-inflammatory), poor diet, high sodium, sedentary, high alcohol consumption, high stress, smoking
24
Q
mean daily Na intake of Canadians is ___
A
2760mg
25
more than ___% of males age 14-30 consume excess lvls Na
90
26
sources of Na?
bakery products, mixed dishes, processed meats, cheeses, soups, sauces, condiments
27
physical activity guidelines for treatment and prevention of hypertension
30-60min moderate intensity 4-7 days / week
28
to reduce possibility of becoming hypertensive, reduce sodium intake towards ____mg/day
2000
29
is DASH to test specific nutrient or diet pattern?
diet pattern
30
increasing K intake monitored closely if:
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
31
MI warning signs that should prompt ppl to call 911
chest discomfort or other areas of upper body, SOB, sweating, nausea, lightheadedness
32
signs of stroke that should prompt ppl call 911
facial droop, arms, slurred speech, time
33
major category of lipid-lowering drugs used
statins
34
how does statin work?
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
35
new class of drug recently approved consisting of monoclonal antibodies that inactivate pro protein converts subtilisin-kexin type 9
PCSK9 inhibitor
36
how does PCSK 9 inhibitor work?
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)
37
these drugs are peroxisome proliferator-activated receptor a (PPARa) ligands, major drugs for treating elevated TG
fibrates
38
why aren't bile acid resins used any more?
fat malabsorption effects (GI), plus made in a bad tasting powder that no one likes to drink
39
how do bile acid resins work?
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
40
these are better tolerated than cholestyramine and on its own has weak effects on serum LDL-C (mostly used in combo with statins)
cholesterol absorption inhibitors
41
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
nicotinic acid
42
drug classes of antihypertensives:
thiazide diuretics, beta-adrenergic blockers, ACE inhibitors, angiotensin 2 receptor blockers, Ca channel blockers
43
main type of diuretic used to treat hypertension that increases kidney excretion of Na and water-->decrease BV-->BV dilate
thiazides (potential for hypokalemia)
44
how do beta-adrenergic blockers work?
block beta-receptors in heart (sympathetic nervous system) to decrease heart rate and cardiac output, also inhibit renin release, note potential for hyperkalemia
45
how does ACE inhibitor work?
lower BP by ^ dilation of arterioles by blocking angiotensin-converting enzyme, decreasing production of angiotensin 2 (note potential for hyperkalemia)
46
how does angiotensin 2 receptor blocker work?
lower BP by interfering with renin-angiotensin system, similar target as ACE inhibitors so shouldn't be used with them (potential for hyperkalemia)
47
how do Ca channel blockers work?
cause arterioles to dilate by altering mvmt of Ca (note grapefuit drug interaction )
48
subclass of Ca channel blockers that primarily reduce heart rate and strength of contraction
verapamil and diltiazem
49
this drug increases strength of heart contractions, slows resting heart rate and may be used in chronic management of arrhythmias
digitalis
50
examples of anti platelet agents used in small amounts as preventative measures?
ASA, clopidogrel, ticagrelor, prasurgrel
51
how does warfarin work?
reduce ability of blood to clot by antagonizing vit K-dependent production of clotting factors, used to reduce risk of stroke and MI
52
advantages of newer anticoag meds?
lack need for regular blood monitoring, no need to monitor vit K
53
vit K AI for M is __ and F is ___
120mg ; 90 mg
54
warfarin has narrow therapeutic window that is assessed by measuring ____ expressed as ____
prothrombin time ; internationalized ratio
55
term for too much clotting (ie. not enough warfarin action)
sub therapeutic INR
56
what is %TTR?
% time in the therapeutic range
57
major food sources of vit K
green leafy veg, vit k supplement, canola/cottonseed/soybean/olive oil
58
why hard to follow recommendations for Vit K?
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
best strategy for confirming suspected diet vit K interaction with warfarin?
diet diary to track usual pattern is over time
60
high diet vit K associated with:
more stable anticoagulant therapy (higher %TTR, fewer INR tests)
61
why aren't vit K supplements recommended to increase Vit K intake?
often supposed to have certain amount but don't meet range
62
why recommendation to alter kcal intake and exercise to achieve/maintain healthy BMI?
ease dyslipidemia (higher circumstances LDL), lose wt will lower LDL, TG, BP, inflammation, IR
63
why keep total fat in range?
keep TG down, indirectly to help maintain healthy wt/lose wt
64
why sat fat < or = 5-6% energy?
reduce dyslipidemia (LDL)
65
why trans < 1 % of energy?
reduce dyslipidemia)
66
why is <300mg cholesterol controversial?
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
why recommendation of low GI foods and < sugar beverages?
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
why choose fibre?
soluble fibre binds bile and lowers LDL so less dyslipidemia and inflammation. Fibre ferments into SCFA, less insulin resistance
69
why reduce sodium?
lower BP
70
why limit alcohol < or = 2 drinks a day for men and < or = 1 drink a day for women?
large amounts influence TG and hypertension
71
why fish > or = 2x a week?
effects to reduce blood TG and platelet aggregation, inflammation
72
why recommend diet rich in fruits/veg?
reduce inflammation by antioxidant comps, reduce BP, fibre reduce LDL; indirect effects of maintaining healthy wt, better micronutrient status
73
veg and low fat diets ^ formation of :
VLDL particles
74
TG in very high range place pt at risk for:
pancreatitis
75
familial combined hyperlipidemia defect is:
hepatic overproduction of apoB100 or defect in gene that produces hepatic lipase (triglyceride removal from bloodstream)
76
rare disease where catabolism of VLDL and chylomicron remnants is delayed cuz apoE2 replaces E3 and E4
familial dysbetalipoproteinemia
77
seven major risk factors identified by Framingham study are:
age, sex, BP, total and HDL , smoking, glucose intolerance, left ventricular hypertrophy
78
adult optimal total cholesterol level:
<170mg/dL, HDL at least 50mg/dL
79
an inflammatory marker specific to vascular inflammation recently made available:
Lp-PLA2
80
factors associated with ^ fibrinogen:
smoking, diabetes, hypertension, obesity, sedentary lifestyle, ^ TG, genes
81
CRP levels are inversely correlated with ____
veg based diet
82
what is trimethylamine-N-oxide (TMAO)?
gut biota-dependent metabolite that contributes to heart disease (produced by liver after intestinal bacteria have digested animal protein)
83
what is Mediterranean diet pattern?
> 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
What is DASH diet pattern?
^ fruits and veg, low fat dairy, whole grains, fish, nuts, low animal protein/sugar
85
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?
replacing with protein
86
ongoing research to suggest that only this type of very restricted diet can actually reverse CVD
vegan diet
87
how does physical activity lower risk?
retard atherogenesis, ^ vascularity of. myocardium,^ fibrinolysis, ^ HDL, ^ glucose tolerance and insulin sensitivity, help wt management, v BP
88
stress hormone ____ released after stim of symptoms nervous system and accelerates the formation of plaque
angiotensin 2
89
this metric captures cumulative damage of obesity over years
obese-years
90
increased risk in men > ___yrs and women > ____ years
45; 55
91
how does omega 3 fat from fish lower TG lvls
by inhibiting VLDL and apoB100 synth, decreasing postprandial lipemia
92
how are omega-3s from vegetables cardioprotective?
stim production of nitric oxide, a substance that stim relaxation of blood vessel wall
93
med procedures common with CHD:
PCI, stents, CABG
94
how to calculate blood pressure?
peripheral resistance x cardiac output
95
what does angiotensin 2 do to ^ BP? (visceral adiposity)
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
why visceral fat bad?
synthesizes increased amounts of angiotensinogen which activates RAS
97
why dairy intake improve blood pressure?
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
why vitamin D good for BP?
^ endothelial function, reduce RAS activity, lower PTH levels
99
magnesium role in BP?
inhibitor of smooth muscle contraction, can be vasodilator
100
supplemental doses of potassium more effective in these ppl:
blacks, higher initial BP, higher sodium intake
101
potential mechanism by how K lowers BP?
decreased vascular smooth muscle contraction by altering membrane potential or restoring endothelium-dependent vasodilation
102
3 objectives for evaluating pt with hypertension:
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
compensatory mechanisms that are activated to restore homeostasis in HF development:
SNS, RAS, cytokine-->sodium retention, vasoconstriction
104
a substance that is secreted by ventricles in response to pressure, and is predictive of severity of HF and mortality:
B-natriuretic peptide (BNP)
105
heart's compensation techniques;
1) increase force of contraction 2) increase in size 3) pump more often 4) stim the kidneys to conserve Na and water
106
earliest symptom of HF?
SOB
107
loss of O2 to brain causing brief loss of consciousness
syncope
108
first symptom of HF in older adults
dry cough with generalized weakness and anorexia
109
involuntary wt loss of at least 6% nonedematous body wt during 6month period, mostly LBM
cardiac cachexia
110
lack of blood flow to gut leads to :
loss of bowel integrity-->bacteria and other endotoxins enter the bloodstream-->cytokine activation
111
heart failure in middle age is caused by ___ and in older adults caused by ___
CAD; hypertension
112
^ TNF-alpha and adinopectin is associated with:
lower BMI, smaller skin fold, decreased plasma total protein lvls
113
risk factors for HF:
hypertension, diabetes, CHD, left ventricular hypertrophy
114
secondary prevention strategies to prevent further cardiac probs include:
ACE inhibitors (first line), angiotensin receptor blockers, aldosterone blockers, beta blockers, digoxin
115
why ACE inhibitors first line defence?
inhibit RAS and improve symptoms, quality of life, exercise tolerance, and survival
116
this is converted to nitric oxide which is an endothelium derived relaxing factor
L-arginine
117
meal strategies for HF?
small, frequent meals and potential caloric supplements
118
thiamin deficiency caused by ____
loop diuretics
119
nutrition goals of acute post transplant pt:
1) provide adequate protein and kcal to treat catabolism and promote healing 2) monitor and correct electrolyte abnormalities 3) achieve optimal blood glucose control
