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CVPR > Atherosclerosis/MI/Peripheral Artery Diseases > Flashcards

Atherosclerosis/MI/Peripheral Artery Diseases Flashcards

1
Q

Fatty Streak

A 
occurs early on in the disease process before it becomes obstructive. asymptomatic
Endothelial dysfunction
Lipoprotein Entry and Modification
Leukocyte Recruitment
Foam Cell formation
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2
Q

what is endothelial dysfunction?

A

Stressors, mostly at arterial branch points impair atheroprotective function. More broadly, stressors, cause an imbalance between vasodilation and vasoconstriction.
Also associated with increased coagulability, increased adhesion synthesis, chemokine release and reactive oxygen species.

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3
Q

What happens with lipoprotein entry?

A

LDLs migrade through the endothelium and accumulate in the subendothelail space where they are modified by oxidation and glycosylation.

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4
Q

What cells are recruited to the fatty streak?

A

macrophages and T-cells

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5
Q

What T cells contribute to Atherosclerosis?

A

TH1 and Th17

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6
Q

TH1 produces what cytokines

A

IFNy

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7
Q

TH-17 produces what cytokines

A

IL17a, IL21, IL22

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8
Q

what cytokines are triggered with oLDL

A

TNFalpha, IL1, IL6, IFN

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9
Q

what T cells inhibit atherosclerosis?

A

Tregs which produce TGF beta and IL10

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10
Q

What helps in leukocyte recruitment?

A

increased expression of VCAM1 on endothelial surface and Increase in Monocyte Chemotactic Protein 1 (MCP1).
These interact with CD11c and VLA-4 on the macrophages.

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11
Q

Reversible Risk Factors for Atherosclerosis

A

Smoking, hypertension, hyperlipidemia

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12
Q

Questionable whether effective treatment to decrease risk of atherosclerosis

A

DM, obesity, obesity, increased inflammation, psychiatric disorders, sedentary lifestyle.

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13
Q

non alterable changes for atherosclerosis risk

A

Male, Males >45, Females >55, genetics

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14
Q

what are non traditional markers of atheroscelrosis?

A

ApoB, lipoprotein A, CRP, homocystein

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15
Q

Plaque Progression

A

the fibrous and occlusive plaque that leads to stable angina and claudication.
Activated macrophages
Smooth muscle cell migration and proliferation
Secretion of ECM/degradation
start of the weakening of fibrous cap to cause instability and necrosis.

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16
Q

what weakens the fibrous cap?

A

increased expression of IFNy, MMPs and TF

MMPs activate collaginase and gelatinases

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17
Q

What causes plaque to rupture?

A

increased accumulation of Foam and T cells, so much so that there is increased ECM exposure
Neovascularization

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18
Q

what makes a stable vs. an unstable plaque

A

stable is calcified with decreased amounts of lipid, inflammation, and apoptosis.
Unstable is uncalcified, with increased amounts of lipid, inflammation, apoptosis, and it is neovascularized

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19
Q

plaque rupture or thrombosis causes

A 
unstable angina (still reversible effects)
MI, stroke or CLI
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20
Q

Complications of atherosclerosis

A

infarction, hemorrhage, emobolization, aneurysm, microvessel growth/intraplaque hemorrhage

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21
Q

how is smoking a risk factor for atherosclerosis?

A

Increased Platelet activation, increased fibrinogen

hydrocarbons, increased endothelial dysfunction and decreased HDL

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22
Q

Why is hypertension a risk factor of atherosclerosis?

A

Increase shear stress to cause endothelial injury, pathological signaling and circulating hormones.

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23
Q

why is DM a risk factor for atherosclerosis?

A

Inflammation, oxidative stress, dyslipidemia

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24
Q

NO synthesis is triggered by..

A

ACh, Bradykinin, thrombin, serotonin, shear stress

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25
Q

Cofactors of NO synthesis

A

Calmodulin, NAPDH, BH4

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26
Q

what is NO synthesized from

A

Arginine

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27
Q

Cholesterol normal function

A

synthesis and repair of membranes.

Precursor to steroid hormones

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28
Q

Triglyceride normal function

A

Fuel for muscles, forms adipose tissue

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29
Q

Lipoprotein structure

A

Hydrophobic core of TG and CE

Hydrophilic surface of phospholipids, cholesterol, and apoprotein.

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30
Q

Chylomicron

A

Packaged dietary lipids

Mostly made up for TGs

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31
Q

VLDL

A

Liver Lipid Structure

55% TG, 20% cholesterol, 15% PL, 10% Protein

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32
Q

LDL

A

Created from LDL

50% cholesterol

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33
Q

HDL

A

Extracts Cholesterol from cells to take to liver
Increases NO, inhibits adhesion, LDLoxidation and TF
40% protein, 30% Cholesterol, 30% PL. NO Triglycersides.

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34
Q

what lipid structure is mostly triglycerides

A

Chylomicron > VLDL

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35
Q

what structure is mostly cholesterol

A

LDL

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36
Q

what structure is mostly protein

A

HDL

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37
Q

what is the difference between Chylomicron and VLDL?

A

synthesis - cylomicron is dietary, VLDL is liver.
Cylomicron is virtually all Triglycerides.
VLDL: is 55% TG, 20% cholesterol, and then small amount of PL and proteins

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38
Q

what makes up total cholesterol?

A

LDL + HDL + VLDL

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39
Q

VLDL =

A

TG/5 if TG

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40
Q

LDL =

A

Total Cholesterol - HDL - (TG/5)

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41
Q

what is recommended for LDL if 1 or less risk factors?

A

160 below

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42
Q

what is recommended for LDL if 2 or more risk factors?

A

130 blow (100)

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43
Q

what is recommended for LDL if CAD, ASCVD, DM?

A

100 below (70)

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44
Q

Path for exogenous lipids

A

Dietary fat –> Chylomicron –> LPL removes TG to form Remnant (decreased size) –> binds to remnant on receptor on liver.

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45
Q

Endogenous LIpids

A

Liver produces VLDL –> LPL removes TG to form IDL –> LPL removes TG to from LDL –> LDL binds to LDL receptor on cells.

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46
Q

HDL path

A

Nascent HDL has no lipids and only protein, but trough LCAT turns into mature HDL with cholesterol and takes it to liver.

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47
Q

when are statins recommended?

A

Known ASCVD
LDL >190
if you have DM >40y/o and LDL >70
If you are >40 YO without ASCVD or DM with 10 year risk >7.5%

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48
Q

High does statins

A

Atorvastatin and Rosuvastatin

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49
Q

Low dose statin

A

Sminvastatin, Pravastatin, Lovastatin, fluvastatin, Pitavastatin

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50
Q

how much fat should be in a heart healthy diet?

A

5-6% saturated fats, no trans fat

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51
Q

Hypertriglyceridemia

A

If moderate: risk factor of atherosclerosis

If severe - risk of acute pancreatitis

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52
Q

Primordial Prevention

A

Steps before development of risk factors

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53
Q

Primary Prevention

A

Steps before development of disease

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54
Q

Secondary Prevention

A

Steps after disease to halt progression (confirmed CAD, MI, Angina, stroke, PAD)
Prevent plaque rupture

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55
Q

Tertiary Prevention

A

Steps to reduce disability and minimize suffering

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56
Q

Pharmacologic Secondary Prevention

A 
Thromboxane Synthesis Inhibitiors
P2Y12 Antagonists
GP IIb/IIIa antagonists
Beta Blockers
RAAs (ACEI, ARBs, AA)
Statins
Vasodilators, diuretics, CCBs
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57
Q

Class 1 post ACS or PCI

A

P2Y12 inhibitor + aspirin for 1 year

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58
Q

Class 1 Post Bypass

A

Aspirin 1 year

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59
Q

Class 1 Post Stroke

A

Aspiring +/- Clopidogrel chronically

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60
Q

Class 1 PAD symptomatic

A

Aspirin or Clopidogrel

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61
Q

Class 1 beta blockers

A

with LVEF less than 40% with heart failure symptoms or MI or ACS in last three years

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62
Q

Class 2a Beta Blockers

A

-LVEF Less than 40% wihthout HF symtpoms OR no change in LVEF but with history of MI or ACS

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63
Q

Class 1 for ACEI

A

LVEF Less than 40% with DM, HTN, Chronic Kidney Disease

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64
Q

Class 1 for ARBs

A

LVEF Less than 40% with prior MI or HF symptoms or ACE I intolerant

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65
Q

Class I for AA

A

Post MI with LVEF Less than 40% with BB + ACEI/ARB + HF or DM

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66
Q

Recommendations for BP

A

Under 60 less than 140/90; over 60 less than 150/90

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67
Q

are non statin cholesterol lowering effective?

A

not really because they don’t have vasodilation effects

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68
Q

Class I DM management to lower CV risk

A

Lifestyle changes with PCP

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69
Q

Class IIa and IIb DM management to lower CV risk

A

IIA: metforming
IIB: HbA1C

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70
Q

Depression and Class IIa

A

assessment of depression

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71
Q

Class IIb depression

A

Treat depression, but does not lower CV risk.

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72
Q

Lifestyle modifications CLass I

A

BMI 18.5-24.9 Men less than 40 inches; women less than 35 inches

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73
Q

Primary Prevention

A

for 20-79 yo asses Risk Factors every 4-6 years. for thoes 40-99 calcuate 10 year risk factor.

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74
Q

If 10 year risk factor is greater than 7.5%

A

Cholesterol lower, obesity, lifestyle changes

75
Q

If 10 year risk factor is less than 7.5%

A

Assess 30 Year or lifetime risk

76
Q

Primary Prevention for Adults 50-59; >10% 10 year risk

A

LD aspirin

77
Q

Primary Prevention for Adults 60-69; >10% 10 year risk

A

Individual decision about apirin

78
Q

Primary Prevention for adults 70

A

No recommendation

79
Q

Depression and CV disease

A

depression predicts mortality after CV, adverse outcomes among HF, decline in heath status.
Dose response relationship
increased cost of care for those Post MI and CHF

80
Q

How is depression related to CV disease

A

depression triggers defective serotonin –> dysfunctional amygdala–> leads to both autonomic dysfunction and hypercorticolemia –> increased cholecatamines, inflammation, endothelial dysfunction, platelet activation.

81
Q

Depression treatment and CV disease

A

Treatment lowers Platelet activation markers, HR variability, inflammation, normalizes brain serotonin.
Treatment improves depression, quality of life, physiology
No known effect on adherence, cost, CV events.

82
Q

Percentage of CV patients with undiagnosed depression

A

75.5%

83
Q

What contributes to Oxygen supply

A

Oxygen content (hemoglobin and systemic O2) and coronary blood flow

84
Q

What determines perfusion pressure

A

is approximately aortic diastolic pressure

85
Q

what determines coronary blood flow

A

perfusion pressure, perfusion time, vascular resistance

86
Q

Myocyte Oxygen Delivery =

A

CBF * O2 content (intrinsic control)

87
Q

Autoregulation

A

protection of small changes in perfusion pressure at small arterioles. Dilation of vessels downstream of stenosis to decrease resistance to accomodate for drop in pressure. This makes sure that flow is maintained.

88
Q

If diastolic perfusion pressure is low, what can you do?

A

prevent hypotension

89
Q

If diastolic time is low, what can you do?

A

rate slowing drugs

90
Q

is coronary resistance is high, what can you do?

A

vasodilators or angioplasty

91
Q

if oxygen content is low, what can you do?

A

tx anemia and hypoxemia

92
Q

what contributes to O2 demand

A

HR, wall tension, inotropic state

93
Q

when does troponin I rise?

A

3-4 hours, peaks at 18-36 hours

94
Q

when does CK-MB rise?

A

3-8 hours, peaks 24 hours

95
Q

Functional Flow measurement in CV

A

upstream and downstream catheter to measure pressure difference.
At rest, pressure might be similar.
Administer vasodilator to mimic exercise and increase flow. Is distal coronary/aortic

96
Q

what populations is BNP naturally higher?

A

Women, elderly, renal insufficiency

97
Q

A type B type C type BNP

A

A is from atrium, B is from ventricles, C is endothelium

98
Q

Stroke is due to…

A

Atheroembolism (Cartoid bifrication ) goes to ophthalmic artery
Thromboembolism from Left Atrial appendage

99
Q

MI is due to..

A

Rupture plaque, in situ thromobsis

Stable obstructive plaque

100
Q

Claudication is due to..

A

obstructive stable plaque

101
Q

Acute Limb Ischemia is due to..

A

Atheroembolization or thromboembolization (rarely in situ thrombosis)

102
Q

Venous vs Arterial Thrombosis

A

Thrombosis: rich in fibrin and RBC due to stasis, there is usually a genetic and environmental predisposition.
Arterial: Platelet rich due to plaque rupture that occurs in areas of high flow, due to atherosclerosis, trama.

103
Q

Arterial vs venous thrombosis treatment

A

Arterial: antiplatelet
Venous: anticoagulation

104
Q

stress testing with left main a. or 3 vessel CAD

A

75-95% sensitive

105
Q

Sensitivity of stress testing with 1 Vessel CAD

A

only 25-70%, LAD>RCA>circumflex

106
Q

expected results of a stress tests

A 
HR above 85%
increase in BP systolic >20 mmHg
Duration of exercise
ECG
symptoms
107
Q

pharmacologic vasodilators for stress tests

A

dipyradimole, adenosine, regadenoson, dobuatmine (HR dependent)

108
Q

Imaging of stress test

A

due to abnormal baseline ECG, to do with increased sensitivity, localization of damage, pre-op cardiac risk assessment, myocardial variability.
Done with radionucleotide perfusion

109
Q

Thallium 201

A

Older contract method of Stress imaging - K analog that must be imaged rapidly

110
Q

Tecnetium 99m

A

new contrast, monovalent liophilic cation that does not need to be imaged rapidly

111
Q

what happens with exercise to the wall thickness and motion

A

increase in rate and thickens with exercise and chamber size decreases.

112
Q

Tx of stable angina - basic regimen

A

Antianginal - nitrates, beta blocker
antihypertensives
lipid lowering
anti-platelet

113
Q

Tx of unstable angina - basic regimen

A 
Hosptialization
IV nitroglycerin
Beta blockers
Antiplatelet
anticoagulation
Catheterization
114
Q

Tx of Acute MI - basic regimen

A

ASAP repurfusion with angioplastly or thrombolytic of no cath lab.

115
Q

Problems with baloon angioplasty

A

recurrent symptoms within 6 months (keloid not atheroscelrosis scar)
solution: stents

116
Q

PAD

A

flow limiting lesion that limits blood flow to the limbs due to atherosclerosis.

117
Q

Epidemiology of pAD

A

10-12% of adults have it

20% are over 70 yo or younger with smoking and diabetes

118
Q

risk factors of PAD

A

DM (4x), Smoking (2-3X), Lipids (2x), HBP (2X)

119
Q

How many factors does PAD increase CV death

A

6X

120
Q

what arteries are affected with PAD?

A

aortoiliac, superficial femoral, tibial a.

121
Q

Intermittent claudication vs. critical Leg ischemia

A

IC: cramp, calf fatigue with exercise that is resolved with rest.
CLI: decreaesd blood flow at rest that leads to ischemic ulcers, gangrene, skin necrosis

122
Q

Symptoms of CLI

A

critical leg ischemia
Ulcers, gangrene, skin necrosis
Pain in distal foot/heel, ulcers on toes and heels
worsened by elevation

123
Q

Signs of PAD

A

decreased of absent pulses
Bruits in abdominal, femoral due to turbulance.
muscle atrophy
pallor with elevation

124
Q

ABI

A

ankle brachial index: ratio of systolic ankle BP with doppler to systolic Arm BP. if BP

125
Q

Tx of PAD

A

surgery or angioplasty
Exercise training to increase muscle metabolism
Drugs - platelet inhibitors, cilostzole (vasodilators and platelet inhibitors)
Risk modification

126
Q

what does PAD cause pallor when elevated

A

stenosis cant work against gravity.

127
Q

why is foot red when hung over the bed in PAD?

A

gravity increases circulation and remains at max dilation as you dangle your foot.

128
Q

arterial aneurysm

A

extansion of all three layers of the vessel.

129
Q

Normal aortic side

A

Root is 3 cm
Distal thoracic 2.5 cm
Infrarenal aoritc 2 cm

130
Q

Definition of AAA

A

> 3cm or increase in 50%

131
Q

Fusiform vs. Saccular Aneurysm

A

Fusiform in all around, saccular is only one side.

132
Q

Pseudoaneurysism

A

accumulation of blood due to a rupture vessel wall with blood leading through a hole in the intima and media.

133
Q

Epidemiology of AAA

A

16,000 deaths/year
13 cause f death
Rupture most common with >5 cm

134
Q

Pathophysiology of AAA

A

weakened aortic wall due to decreased elastin and decreased collagen due to inflammation, proteolysis, and biochemical stress.

135
Q

Inflammation in AAA

A

B and T lymphocytes
Macrophages
Cytokines
autoantigens

136
Q

Proteolysis in AAA

A

increase in MMP 2 and 9
increase in tPA
decreases in TIMPs (regulation

137
Q

Biochemical Stress in AAA

A

Elastin distrubance, Turbulance, mural thrombus

138
Q

clinical Presentation of AAA

A

70% asymptomatic with sudden death
30% abdominal discomfort and back pain with death.
Not often found on exam, found with imaging for another problem

139
Q

Diagnosis of AAA

A

X-ray, US, CT, MRI, renal function and contrast. Arteriography - misses them becuase they are viewing lumen and not wall.

140
Q

Tx of AAA

A

surgical repair

Endovascular aortic repair (EVAR) - device to bypass aneurysm.

141
Q

Aortic Dissection

A

blood passes through tar in intima through medial layer and spreads out.
Could also be due to vaso vasorum with hemorrhage into media.

142
Q

Aortic dissection epidemiology

A

30 cases per million/year
3-5% sudden eath
1% risk of death if untreated in 24 hours, 75% in 2 weeks. 90% if untreated at 3 months.

143
Q

Risk factors of aortic dissection

A

hypertension, cocaine, CT disorders (marfans, Ehlers Hanios), bicuspid AV

144
Q

A type Aortic dissection

A

involves the asscending aorta

145
Q

B type aortic dissection

A

does NOT involve ascending aorta

146
Q

Symptoms of Aortic Dissecion

A

Severe tearing pain, stroke (carotid), syncope (vertebral), MI (coronary), intestinal ischemia, renal failure

147
Q

Symptom differences in Aortic dissection vs Aortic aneurysm

A

AA: often asymptomatic, if symptomatic has abdominal discomfort
AD: severe tearing pain

148
Q

Diagnosis of Aortic Dissection

A

CT, trans esophageal ECHO, angiography

149
Q

Tx of Aortic Dissection

A

Decreased BP meds, Nitrates, ACEI, CCB, Pain relief

Surg: repair, stent, synthetic graft

150
Q

Venous Thromboembolic Disease

A

prone to development of thrombus in superficial and deep veins.
2/3 are asymptomatic of undiagnosed.

151
Q

how many hospital deaths are due to VTE?

A

5-10%; 58% were not treated prophylactically

152
Q

Risk factors of no anticoagulant prophylaxis

A

24% MI get VTE, 60% paralytic stroke get VTE, 75% of hip survey patients get VTE

153
Q

Post Phebotic Syndrome

A

in 40-80% of untreated VTE Disease

Valvular damage due to persistent occlusion by DVT to cause chronic leg swelling, stasis pigmentation, ulceration

154
Q

Virchows Triad

A

1) stasis (decreased laminar flow)
2) hypercoagulability
3) vascular damage

155
Q

Thrombophilia

A

hypercoagulability state due to increased thrombin, increase platelet activation and aggregate and mediates endothelail damage and fibrinolytic inhibition.

156
Q

Severe thrombophilia

A

is due to inherited Protein C/S deficiency

157
Q

Mild Thrombophilia is

A

inherited due to factor V leiden

158
Q

Acquired Thrombophilia is due to..

A

infection, inflammaion, drugs (estrogen)

159
Q

what contributes to increase stroke volume in exercise

A

Vasodilation and increased venous return due to venoconstriction, muscle pumps, and respiratory pump to preserve ventricular filling.

160
Q

what is the respiratory pump in exercise

A

negative thoracic pressure in exercise increases venous return

161
Q

what preserves ventricular filling in exercise

A

increased Venous Return, increase distensibility, pericardial constraint.

162
Q

how much does strove volume increase in exceris

A

40-60%

163
Q

stroke volume in upright vs supine exercise

A

Increased basal stroke volume supine, but only 20-40% increase in exercise.

164
Q

why is there a continual increase in SV with athletes and not sedentary during exercise

A

continual rise due to increased EDV and increased contractility at lower ESV.

165
Q

standard rule for increasing CO during exercise

A

6L/min required for every 1 L/min in O2 uptake increase.

166
Q
A

Increasing HR and SV

167
Q

> 50% VO2 max is determined by

A

only increased HR

168
Q

CO athletes vs. sedendary

A

same at rest

169
Q

Rest CO for men vs women

A

Men: 5 L women 4.5 L

170
Q

Men CO during exercise Athlete vs. Sedenary

A

Sed: 22 L Ath: 34

171
Q

Women CO during exercise Athlete vs. Sedendary

A

Sed: 18 L Ath 24

172
Q

Athlete vs Sedenary increase in CO in exercise

A

Sedentary is 4-5x; Athletes in 6-7X

173
Q

Coronary Vein O2 saturation in rest vs. exercise

A

Rst; 25%

Exercise: lower than 10%

174
Q

what happens to blood pressure in excercise

A

Increase Mean Arterial Pressure, Increase in systolic BP, same Diastolic BP.

175
Q

Mean arterial pressure:

A

average BP of the cardiac cycle

176
Q

Redistribution during exercise.

A

Vasoconstriction of non-exercising tissues via ergoreceptors and cardiovascular control center in medulla.
Vasodilations of arterioles and small a. via autoregulation
Increase capillary recruitment

177
Q

Autoregulation of vasodilation in exercise

A

increase PCO2, NO, K, Acidosis, Adenosine

Decrease PO2

178
Q

Capillary recruitment

A

increased recruitment in exercise 5-10% at rest, but 100% in exercise

179
Q

Skeletal muscle blood flow in exercise

A

15-20% –> 80-85%

180
Q

Brain blood flow in exercise

A

Increased flow from 5 L/min –> 25 L/min

but decrease in total CO% from 15-3-4%

181
Q

O2 extraction in exercise

A

increased extraction, but most due to increase CO.

Rest: change in O2 is 5, but 15 in exercise

182
Q

O2 extraction VO2 =

A

CO * a-v(O2) in exercise CO (increased by 5) a-v(O2) (increased by 3)
OR {Hgb} 1.34O2 saturation

183
Q

Rate Pressure Product

A

is myocardial workload = HR * SBP = mVO2

184
Q

RPP is more dependnet on

A

HR^2SVSVR

CVPR (12 decks)

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