Atherosclerosis/MI/Peripheral Artery Diseases Flashcards Preview

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Flashcards in Atherosclerosis/MI/Peripheral Artery Diseases Deck (184):
1

Fatty Streak

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

2

what is endothelial dysfunction?

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.

3

What happens with lipoprotein entry?

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

4

What cells are recruited to the fatty streak?

macrophages and T-cells

5

What T cells contribute to Atherosclerosis?

TH1 and Th17

6

TH1 produces what cytokines

IFNy

7

TH-17 produces what cytokines

IL17a, IL21, IL22

8

what cytokines are triggered with oLDL

TNFalpha, IL1, IL6, IFN

9

what T cells inhibit atherosclerosis?

Tregs which produce TGF beta and IL10

10

What helps in leukocyte recruitment?

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.

11

Reversible Risk Factors for Atherosclerosis

Smoking, hypertension, hyperlipidemia

12

Questionable whether effective treatment to decrease risk of atherosclerosis

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

13

non alterable changes for atherosclerosis risk

Male, Males >45, Females >55, genetics

14

what are non traditional markers of atheroscelrosis?

ApoB, lipoprotein A, CRP, homocystein

15

Plaque Progression

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.

16

what weakens the fibrous cap?

increased expression of IFNy, MMPs and TF
MMPs activate collaginase and gelatinases

17

What causes plaque to rupture?

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

18

what makes a stable vs. an unstable plaque

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

19

plaque rupture or thrombosis causes

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

20

Complications of atherosclerosis

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

21

how is smoking a risk factor for atherosclerosis?

Increased Platelet activation, increased fibrinogen
hydrocarbons, increased endothelial dysfunction and decreased HDL

22

Why is hypertension a risk factor of atherosclerosis?

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

23

why is DM a risk factor for atherosclerosis?

Inflammation, oxidative stress, dyslipidemia

24

NO synthesis is triggered by..

ACh, Bradykinin, thrombin, serotonin, shear stress

25

Cofactors of NO synthesis

Calmodulin, NAPDH, BH4

26

what is NO synthesized from

Arginine

27

Cholesterol normal function

synthesis and repair of membranes.
Precursor to steroid hormones

28

Triglyceride normal function

Fuel for muscles, forms adipose tissue

29

Lipoprotein structure

Hydrophobic core of TG and CE
Hydrophilic surface of phospholipids, cholesterol, and apoprotein.

30

Chylomicron

Packaged dietary lipids
Mostly made up for TGs

31

VLDL

Liver Lipid Structure
55% TG, 20% cholesterol, 15% PL, 10% Protein

32

LDL

Created from LDL
50% cholesterol

33

HDL

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

34

what lipid structure is mostly triglycerides

Chylomicron > VLDL

35

what structure is mostly cholesterol

LDL

36

what structure is mostly protein

HDL

37

what is the difference between Chylomicron and VLDL?

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

38

what makes up total cholesterol?

LDL + HDL + VLDL

39

VLDL =

TG/5 if TG

40

LDL =

Total Cholesterol - HDL - (TG/5)

41

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

160 below

42

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

130 blow (100)

43

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

100 below (70)

44

Path for exogenous lipids

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

45

Endogenous LIpids

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

46

HDL path

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

47

when are statins recommended?

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%

48

High does statins

Atorvastatin and Rosuvastatin

49

Low dose statin

Sminvastatin, Pravastatin, Lovastatin, fluvastatin, Pitavastatin

50

how much fat should be in a heart healthy diet?

5-6% saturated fats, no trans fat

51

Hypertriglyceridemia

If moderate: risk factor of atherosclerosis
If severe - risk of acute pancreatitis

52

Primordial Prevention

Steps before development of risk factors

53

Primary Prevention

Steps before development of disease

54

Secondary Prevention

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

55

Tertiary Prevention

Steps to reduce disability and minimize suffering

56

Pharmacologic Secondary Prevention

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

57

Class 1 post ACS or PCI

P2Y12 inhibitor + aspirin for 1 year

58

Class 1 Post Bypass

Aspirin 1 year

59

Class 1 Post Stroke

Aspiring +/- Clopidogrel chronically

60

Class 1 PAD symptomatic

Aspirin or Clopidogrel

61

Class 1 beta blockers

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

62

Class 2a Beta Blockers

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

63

Class 1 for ACEI

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

64

Class 1 for ARBs

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

65

Class I for AA

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

66

Recommendations for BP

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

67

are non statin cholesterol lowering effective?

not really because they don't have vasodilation effects

68

Class I DM management to lower CV risk

Lifestyle changes with PCP

69

Class IIa and IIb DM management to lower CV risk

IIA: metforming
IIB: HbA1C

70

Depression and Class IIa

assessment of depression

71

Class IIb depression

Treat depression, but does not lower CV risk.

72

Lifestyle modifications CLass I

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

73

Primary Prevention

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

74

If 10 year risk factor is greater than 7.5%

Cholesterol lower, obesity, lifestyle changes

75

If 10 year risk factor is less than 7.5%

Assess 30 Year or lifetime risk

76

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

LD aspirin

77

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

Individual decision about apirin

78

Primary Prevention for adults 70

No recommendation

79

Depression and CV disease

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

How is depression related to CV disease

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

81

Depression treatment and CV disease

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

Percentage of CV patients with undiagnosed depression

75.5%

83

What contributes to Oxygen supply

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

84

What determines perfusion pressure

is approximately aortic diastolic pressure

85

what determines coronary blood flow

perfusion pressure, perfusion time, vascular resistance

86

Myocyte Oxygen Delivery =

CBF * O2 content (intrinsic control)

87

Autoregulation

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

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

prevent hypotension

89

If diastolic time is low, what can you do?

rate slowing drugs

90

is coronary resistance is high, what can you do?

vasodilators or angioplasty

91

if oxygen content is low, what can you do?

tx anemia and hypoxemia

92

what contributes to O2 demand

HR, wall tension, inotropic state

93

when does troponin I rise?

3-4 hours, peaks at 18-36 hours

94

when does CK-MB rise?

3-8 hours, peaks 24 hours

95

Functional Flow measurement in CV

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

what populations is BNP naturally higher?

Women, elderly, renal insufficiency

97

A type B type C type BNP

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

98

Stroke is due to...

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

99

MI is due to..

Rupture plaque, in situ thromobsis
Stable obstructive plaque

100

Claudication is due to..

obstructive stable plaque

101

Acute Limb Ischemia is due to..

Atheroembolization or thromboembolization (rarely in situ thrombosis)

102

Venous vs Arterial Thrombosis

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

Arterial vs venous thrombosis treatment

Arterial: antiplatelet
Venous: anticoagulation

104

stress testing with left main a. or 3 vessel CAD

75-95% sensitive

105

Sensitivity of stress testing with 1 Vessel CAD

only 25-70%, LAD>RCA>circumflex

106

expected results of a stress tests

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

107

pharmacologic vasodilators for stress tests

dipyradimole, adenosine, regadenoson, dobuatmine (HR dependent)

108

Imaging of stress test

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

Thallium 201

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

110

Tecnetium 99m

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

111

what happens with exercise to the wall thickness and motion

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

112

Tx of stable angina - basic regimen

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

113

Tx of unstable angina - basic regimen

Hosptialization
IV nitroglycerin
Beta blockers
Antiplatelet
anticoagulation
Catheterization

114

Tx of Acute MI - basic regimen

ASAP repurfusion with angioplastly or thrombolytic of no cath lab.

115

Problems with baloon angioplasty

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

116

PAD

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

117

Epidemiology of pAD

10-12% of adults have it
20% are over 70 yo or younger with smoking and diabetes

118

risk factors of PAD

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

119

How many factors does PAD increase CV death

6X

120

what arteries are affected with PAD?

aortoiliac, superficial femoral, tibial a.

121

Intermittent claudication vs. critical Leg ischemia

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

Symptoms of CLI

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

123

Signs of PAD

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

124

ABI

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

125

Tx of PAD

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

126

what does PAD cause pallor when elevated

stenosis cant work against gravity.

127

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

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

128

arterial aneurysm

extansion of all three layers of the vessel.

129

Normal aortic side

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

130

Definition of AAA

>3cm or increase in 50%

131

Fusiform vs. Saccular Aneurysm

Fusiform in all around, saccular is only one side.

132

Pseudoaneurysism

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

133

Epidemiology of AAA

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

134

Pathophysiology of AAA

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

135

Inflammation in AAA

B and T lymphocytes
Macrophages
Cytokines
autoantigens

136

Proteolysis in AAA

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

137

Biochemical Stress in AAA

Elastin distrubance, Turbulance, mural thrombus

138

clinical Presentation of AAA

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

Diagnosis of AAA

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

140

Tx of AAA

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

141

Aortic Dissection

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

142

Aortic dissection epidemiology

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

Risk factors of aortic dissection

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

144

A type Aortic dissection

involves the asscending aorta

145

B type aortic dissection

does NOT involve ascending aorta

146

Symptoms of Aortic Dissecion

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

147

Symptom differences in Aortic dissection vs Aortic aneurysm

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

148

Diagnosis of Aortic Dissection

CT, trans esophageal ECHO, angiography

149

Tx of Aortic Dissection

Decreased BP meds, Nitrates, ACEI, CCB, Pain relief
Surg: repair, stent, synthetic graft

150

Venous Thromboembolic Disease

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

151

how many hospital deaths are due to VTE?

5-10%; 58% were not treated prophylactically

152

Risk factors of no anticoagulant prophylaxis

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

153

Post Phebotic Syndrome

in 40-80% of untreated VTE Disease
Valvular damage due to persistent occlusion by DVT to cause chronic leg swelling, stasis pigmentation, ulceration

154

Virchows Triad

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

155

Thrombophilia

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

156

Severe thrombophilia

is due to inherited Protein C/S deficiency

157

Mild Thrombophilia is

inherited due to factor V leiden

158

Acquired Thrombophilia is due to..

infection, inflammaion, drugs (estrogen)

159

what contributes to increase stroke volume in exercise

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

160

what is the respiratory pump in exercise

negative thoracic pressure in exercise increases venous return

161

what preserves ventricular filling in exercise

increased Venous Return, increase distensibility, pericardial constraint.

162

how much does strove volume increase in exceris

40-60%

163

stroke volume in upright vs supine exercise

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

164

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

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

165

standard rule for increasing CO during exercise

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

166

Increasing HR and SV

167

>50% VO2 max is determined by

only increased HR

168

CO athletes vs. sedendary

same at rest

169

Rest CO for men vs women

Men: 5 L women 4.5 L

170

Men CO during exercise Athlete vs. Sedenary

Sed: 22 L Ath: 34

171

Women CO during exercise Athlete vs. Sedendary

Sed: 18 L Ath 24

172

Athlete vs Sedenary increase in CO in exercise

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

173

Coronary Vein O2 saturation in rest vs. exercise

Rst; 25%
Exercise: lower than 10%

174

what happens to blood pressure in excercise

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

175

Mean arterial pressure:

average BP of the cardiac cycle

176

Redistribution during exercise.

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

Autoregulation of vasodilation in exercise

increase PCO2, NO, K, Acidosis, Adenosine
Decrease PO2

178

Capillary recruitment

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

179

Skeletal muscle blood flow in exercise

15-20% --> 80-85%

180

Brain blood flow in exercise

Increased flow from 5 L/min --> 25 L/min
but decrease in total CO% from 15-3-4%

181

O2 extraction in exercise

increased extraction, but most due to increase CO.
Rest: change in O2 is 5, but 15 in exercise

182

O2 extraction VO2 =

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

183

Rate Pressure Product

is myocardial workload = HR * SBP = mVO2

184

RPP is more dependnet on

HR^2*SV*SVR