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CVPR > CV week 3 > Flashcards

CV week 3 Flashcards

1
Q

Smoking and CAD risk

A

(50% increase in CAD risk) - cessation can normalize risk

  • Thrombogenic tendency, platelet activation, increased fibrinogen
  • Aryl hydrocarbon compounds promote atherosclerosis
  • Endothelial dysfunction, vasospasm
  • CO decreases myocardial oxygen delivery
  • Adverse effect on lipoproteins (decreased HDL)
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2
Q

HTN and CAD risk

A
  • Increased shear stress on arterial wall → endothelial cell injury and pathologic cell signaling (causes oxidant stress, cell proliferation)
  • Circulating hormones increased in HTN (angiotensin, aldosterone, NE) → adverse effects on arterial wall
  • LVH due to increased heart work → increased risk
  • Treatment reduces CV risk
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3
Q

Diabetes (and insulin resistance) and CAD risk

A

associated with inflammation, oxidative stress, dyslipidemia which predispose to atherosclerosis

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4
Q

Dyslipidemic triad

A

high LDL, low HDL, high triglycerides

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5
Q

LDL cholesterol

A

when oxidized, LDL = proinflammatory/atherogenic →

Injures vascular endothelium, impairs endothelial function

Deposited in arterial wall, taken up by macrophages → progressive increase in plaque volume

Activates inflammatory cells → progression/instability of lesions

Activates platelets, prothrombotic

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6
Q

HDL cholesterol

A
  • beneficial, opposes atherothrombosis
  • Inhibits LDL oxidation
  • Inhibits endothelial adhesion molecules
  • Inhibits tissue factor
  • Stimulates NO production
  • Enhances reverse cholesterol transport
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7
Q

Inflammation and CAD risk

A

key in initiation and progression of atherosclerosis

Lipid-laden macrophages (foam cels): in arterial wall plaque, highly pro-inflammatory

Extravascular inflammation (dental, respiratory, immunologic diseases): increase risk of athersclerotic CV events

Circulating markers of inflammation (e.g. CRP, IL-6): provide info about future CV risk
-Originate from inflammatory foam cells in arterial atheroma → IL-6 made by liver → CRP present in high concentrations in blood = amplified signal

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8
Q

Risk factors for CAD

A

smoking
HTN
diabetes
inflammation
dyslipidemia
Obesity, Psychological Stress, Sedentary Lifestyle
Obesity, Psychological Stress, Sedentary Lifestyle

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9
Q

Progression of atherosclerosis (3 steps)

A

1) Clinically silent
2) Effort angina claudication
3) Acute vascular events

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10
Q

Features of clinically silent CAD

A

fatty streak in vessel

Endothelial injury

Lipid deposition

Macrophage and T cell recruitment

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11
Q

Features of Effort Angina claudication

A

fibrous plaque → occlusive atherosclerotic plaque

Activated macrophages (foam cells)

Smooth muscle proliferation forms fibrous cap

Progressive lipid accumulation in core of plaque

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12
Q

Features of Acute Vascular events

A

plaque rupture/fissure and thrombosis → unstable angina, MI, stroke, critical leg ischemia

Plaque disruption

Thrombus formation

Vessel occlusion may occur

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13
Q

Distinguishing features of coronary circulation (3)

A

1) Myocardium depends on AEROBIC metabolism for energy supply
- Skeletal muscle adapted for burst energy production from anaerobic metabolism → lactate, H+ accumulation → fatigue
- Cardiac muscle requires sustained energy production, no fatigue

2) Under resting conditions a near-maximal amount of O2 is extracted from coronary arterial blood
- Must increase BLOOD FLOW RATE in order to increase O2 supply

3) The LV is perfused in diastole only (compression of intramural coronary vessels in systole)

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14
Q

Determinants of myocardial O2 supply

A

CORONARY BLOOD FLOW RATE

1) Perfusion pressure
2) Perfusion time (1/HR)
3) Vascular resistance

OXYGEN CONTENT

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15
Q

Determinants of myocardial O2 demand

A

1) Heart Rate
2) Wall Tension: determined by systolic BP, cardiac chamber dimensions (law of LaPlace T = (Ptm)(r)/u)
3) Inotropic State (contractility)

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16
Q

Coronary oxygen delivery = ______ x _______

A

CBF x O2 content

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17
Q

Perfusion pressure autoregulation

A

adaptive mechanism to maintain perfusion in face of altered perfusion pressure - at level of small arterioles

Provides protection from moderate changes in perfusion pressure

Dilation of downstream resistance vessels can compensate for pressure drop across stenosis (autoregulation) but only up to a point

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18
Q

Autoregulation of perfusion pressure and CHD

A

CHD → autoregulation exhausted when pressure drops across an epicardial coronary stenoses (downstream pressure lower than upstream pressure) → Ischemia

Pressure drop related to length and diameter of stenosis

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19
Q

Perfusion time is important why?

A

Increased HR → shorten cardiac cycle mostly by shortening diastole → tachycardia compromises coronary flow (esp. to LV)

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20
Q

Oxygen content of blood can be compromised by ______ and _______

A

Anemia → less Hgb per ml blood

Hypoxemia → incomplete saturation of Hgb

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21
Q

Pathophysiology of STABLE CAD

A

Obstructive coronary lesion limits coronary flow and causes myocardial ischemia, particularly when cardiac work and O2 demand increase

Ischemia = imbalance between coronary oxygen delivery and myocardial demand → angina pectoris

Characterized by EFFORT ANGINA

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22
Q

Treatment of stable CAD: improving supply decreasing demand how? 4 strategies for each

A

Supply:

1) Perfusion Pressure: prevent hypotension
2) Diastolic Time: rate slowing drugs (e.g B-Blockers)
3) Coronary Resistance: vasodilator drugs (nitrates, Ca channel blockers), coronary angioplasty, bypass surgery
4) Oxygen Content: treat anemia and hypoxemia

Demand:

1) Systolic Pressure: antihypertensive drugs
2) Heart rate: rate-slowing drugs (B-B, Ca channel blockers)
3) Wall tension: limit LV cavity size - limit excessive preload (diuretics, nitrates)
4) Inotropic state: negative inotropes to attenuate contractile state (B-B, Ca channel blockers)

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23
Q

Pathophysiology of unstable CAD (5 steps leading to cardiac dysfunction)

A

1) Inflammation of arterial wall (foam cell, T-lymphocyte)→ weakening of fibromuscular cap
2) → abrupt plaque fissure or rupture → thrombogenic components (lipids, TF) exposed to blood
3) Thrombosis with partial/complete vessel occlusion
4) Myocardial injury and/or necrosis → serum markers
5) Cardiac dysfunction, risk of arrhythmias, death

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24
Q

Markers of inflammation used in CAD

A

Inflamed arterial atheroma → inflammatory markers (CRP)

Downstream myocardial injury → cardiac markers (troponin, creatine kinase)

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25
Q

Unstable Angina

A
  • “Threatened” heart attack
  • Biomarkers usually negative (e.g troponin)
  • May not result in permanent myocardial damage if treated successfully
  • High risk of recurrent events in first year
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26
Q

Acute MI

A
  • Persistent and severe coronary flow reduction
  • Thrombus with complete vessel occlusion
  • Necrosis → cardiac dysfunction/failure
  • Biomarkers (troponin released from necrotic myocardial cells) elevated
  • Cardinal symptoms: severe unremitting chest discomfort at rest (30% of MIs are silent)
  • Early reperfusion key to tx but may also provoke additional injury (reperfusion injury)
  • High mortality (⅓ don’t get to hospital)
  • Late mortality related to extent of LV dysfunction
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27
Q

Within minutes of acute coronary occlusion what happens? (4)

within 1 hour?

A

1 minute:
1) Impaired Ca2+ re-uptake into SR during diastole → diastolic dysfunction (filling impairment) → increased LV filling pressures → pulmonary congestion and edema

2) Depletion of high energy phosphates, intracellular acidosis → systolic dysfunction (contractile failure)
3) ECG signs of myocardial injury
4) Symptoms (CP, dyspnea, arrhythmias)

1 hour:
myocardial necrosis and infarction

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28
Q

Treatment of unstable coronary heart disease (6)

A 
Hospitalization
IV NTG
B-Blockers
ASA and antiplatelet agents
Anticoagulation (heparin)
Catheterization and coronary intervention
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29
Q

Treatment of Acute MI with ST elevation

A
  • Tx initiated in the field
  • Immediate ASA, NTG, +/- B-blocker
  • Reperfusion therapy ASAP (coronary angioplasty)
  • thrombolytic therapy
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30
Q

Diagnosis of stable coronary artery disease: history and physical exam

A

History: CP, dyspnea, risk factors

Exam: may be normal or reveal evidence of cardiac dysfunction from prior myocardial damage (CHF) and evidence of atherosclerosis

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31
Q

Diagnosis of stable coronary artery disease: ECG

A

Resting ECG: ST segment changes (usually depression), T wave inversion, Q waves (indicate prior infarction)

Exercise ECG: dynamic ST segment changes

Ischemic response: horizontal/down sloping ST DEPRESSION with exercise → subendocardial ischemia

*Sensitivity of stress ECG questionable - use functional information, symptoms, and myocardial perfusion to improve sensitivity and specificity of stress ECG

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32
Q

Diagnosis of stable coronary artery disease: CT

A

noninvasive diagnosis of coronary atherosclerosis by coronary calcium on CT

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33
Q

Diagnosis of stable coronary artery disease: Coronary angiography

A

picture of vessel lumen (NOT vessel wall)

Good for diagnosis of coronary obstruction causing anginal symptoms, not good for predicting future events

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34
Q

How to estimate severity of coronary lesion on coronary angiography?

A

Distal pressure (Pd) with solid state catheter, compared to aortic pressure (Pa)

Infuse vasodilatory (adenosine) to have maximal dilation of resistance vessels

Allows you to assess under high flow and thus physiologic significance of stenosis
Ratio of distal coronary/aortic P

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35
Q

Treatment of stable CAD

A

1) Risk factor modification (for prevention and treatment of overt disease)
- Diet, exercise, smoking cessation

2) Drugs to treat angina, BP, lipids, platelets
- Lipid modifying (Statins)
- HTN treatment
- Antiplatelet (ASA, clopidogrel)
- Anti-anginal (nitrates, B-blockers, Ca channel blockers)
- LV dysfunction: ACEI, ARBs, B-blockers (if prior MI with reduced LV function)

3) Revascularization
- Coronary angioplasty
- Coronary artery bypass surgery

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36
Q

Coronary Angioplasty

A
  • tx of acute occlusion or restenosis
  • Balloon dilation of obstructed/narrowed vessel

Acute occlusion → stent and antiplatelet drugs

Restenosis → stents
-Fibrotic inflammatory reaction to stent = restenosis

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37
Q

Coronary Artery Bypass Grafting: (CABG)

A

Reduces mortality compared to medical therapy, may be better than angioplasty when there are multiple blockages

Used in chronic multi vessel coronary disease - not typically with acute MI (would do angioplasty because it’s faster)

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38
Q

Types of grafts used in CABG

A

Internal mammary artery (durability of arterial graft better than venous)
Saphenous vein
Prosthetic materials not successful as grafts

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39
Q

Normal properties of endothelium (4)

A

1) anti-inflammatory
2) anti-thrombotic
3) vasodilatory
4) impermeable to large molecules

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40
Q

Nitric oxide normal expression

A
  • made by nitric oxide synthase + cofactors from L-arginine precursor
  • Expressed on luminal side of endothelium
  • Responds to multiple stimuli
  • Diffuses to vascular smooth muscle → cGMP-mediated vasodilation
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41
Q

Endothelium in inflammatory state (5)

A

1) Increased Permeability (to LDL)
2) Decreased NO (decreased vasodilation)
3) Decreased antithrombotic molecules
4) Expression of cytokines (IL-I, TNF)
5) Expression of cell adhesion molecules (CAMs, selectins)

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42
Q

Step 1 of atherosclerotic plaque formation:

Fatty Streak

A

precipitated by endothelial dysfunction (chemical or physical endothelial damage)

→ lipoprotein entry and modification, leukocyte recruitment, foam cell formation (full of LDL and pro-inflammatory molecules)

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43
Q

Step 2 of atherosclerotic plaque formation:

Plaque progression

A

smooth muscle cell migration into subendothelial space, altered matrix synthesis and degradation

-Foam cells produce MMPs that break down fibrous cap

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44
Q

Step 3 of atherosclerotic plaque formation:

Plaque Rupture

A

disrupted plaque integrity, thrombus formation

Fibrous rupture → Thrombosis → acute MI or healed rupture with narrowed lumen and fibrous intima

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45
Q

Common mechanisms of ischemic stroke (2)

A

1) Atheroembolism from carotid bifurcation lesion
- Breaks off and goes to brain
- Debris often goes to ophthalmic artery → loss of vision in one eye

2) Thromboembolization from LA appendage due to AFIB

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46
Q

Common mechanism of myocardial infarction

A

Thromboembolism

-ruptured plaque, in-situ thrombosis, not necessarily obstructive prior to rupture

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47
Q

Spectrum of severity of MI

A

1) Plaque rupture → NONOCCLUSIVE thrombosis, some flow, intermittent occlusion or embolization → stabilize with anticoagulation/vasodilators
- Unstable angina or NSTEMI (ST depression and/or T wave inversion)
2) Plaque rupture → OCCLUSIVE thrombus → no flow → clinical emergency → recanalize
- STEMI - emergency (prevention of irreversible myocardial necrosis)

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48
Q

Claudication

A

Leg pain induced by exertion

Manifestation of peripheral arterial disease (PAD)

-OBSTRUCTIVE (>70% diameter reduction), stable plaque

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49
Q

Acute Limb ischemia

A
  • Manifestation of peripheral arterial disease (PAD)
  • Acute event obstructs blood flow without prior development of collaterals
  • Atheroembolization or thromboembolization
  • Rarely in-situ thrombosis
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50
Q

Stable plaque

A

rich in fibrous tissue, calcified, less lipid content, less inflammation, less apoptosis → Angina

  • Less biologically active
  • Cause angina and claudication (exertional ischemia) if obstructive (>70% diameter reduction)
  • Less likely to cause thrombotic and embolic events
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51
Q

Unstable/Vulnerable plaque

A

less fibrous tissue, less calcified, more lipid content, more inflammation/inflammatory cells, more apoptosis → plaque rupture, thrombosis

  • More biologically active
  • Cause MI and stroke
  • More likely via thrombotic and embolic mechanisms
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52
Q

Venous vs. arterial thrombus

A

Venous = DVT, PE

  • Fibrin rich, RBC rich, area of stasis, genetic predisposition, environmental predisposition
  • Treat with anticoagulation

Arterial =

  • Platelet rich, plaque rupture, areas of high flow, atherosclerosis, trauma, APLA
  • Treat with antiplatelet therapy
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53
Q

What information can be obtained from an ECHO

A

chamber size, function, and structure, wall motion, valves, pressure and hemodynamics, shunts, murmurs, intracardiac masses, bacterial endocarditis, pericardial disease

-Can use micro-bubbles that are too large to pass through pulmonary capillaries - If you see bubbles in L heart → intracardiac shunt, intrapulmonary shunt

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54
Q

Cardiac Catheterization and Coronary Angiography

A

Catheter inserted into artery or vein, advanced to heart or coronary arteries

Measurements of: pressure, gradients, saturation, intracardiac shunt

Inject contrast for angiography

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55
Q

Contraindications for stress testing

A

Unstable angina, untreated life-threatening arrhythmias, uncompensated heart failure, advanced AV block, acute myocarditis/pericarditis, critical aortic stenosis, significant HOCM, uncontrolled HTN, acute systemic illness

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56
Q

Pharmacologic agents used in stress testing

A

Vasodilator (Dipyridamole, Adenosine, Regadenoson)

Dobutamine (B-agonist)

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57
Q

Radionuclide Stress Test General Concepts

A

Tracer deposited based on blood flow

  • Thallium-201 = continuous exchange across cell membrane
  • Technetium-99m-Sestamibi (Cardiolite) = one pass
  • Imbalance between supply and demand results in relative decreased perfusion
  • Compare perfusion during increased demand (stress) and decreased demand (rest)
  • Reversible perfusion defects indicate reversible ischemia
  • Fixed perfusion defects indicate infarction, scar
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58
Q

Stress ECHO General Concepts

A
  • Imbalance between supply and demand results in wall motion abnormality
  • Compare increased demand (stress) wall motion to decreased demand (rest) wall motion
  • Normally LV should beat faster and thicken more with exercise or dobutamine
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59
Q

BNP

A

32-aa peptide found only in ventricles of heart

-Released in response to stretch, and increased ventricular volume

BNP levels correlate with:

  • LV EDP
  • NYHA classification
  • Objective heart failure diagnosis in pts 55 or older
  • Levels higher in women, elderly, renal insufficiency
  • Negative predictive value
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60
Q

Troponin I and T

A
  • Regulatory proteins involved in actin-myosin interaction
  • Specific to heart
  • Released into bloodstream with myocyte necrosis
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61
Q

Troponin timeline

A

Released within 3-12 hrs
Peak 18-24 hrs
Remains elevated for 7-10 days

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62
Q

Exacerbating factors in coronary atherosclerosis

A

1) Coronary artery vasospasm
2) Platelet aggregation +/- coronary vasospasm
3) Hypotensive episode e.g. shock, massive hemorrhage in presence of critically stenosed coronary artery

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63
Q

Reperfusion Injury

A

-damage that occurs to myocytes following restoration of blood flow

-Mitochondrial dysfunction
Influx of Ca2+ → myofibril hypercontracture

  • Free radical damage to membrane proteins and phospholipids
  • Leukocyte aggregation
  • Platelet and complement activation
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64
Q

Myocardial Infarction Evolution

A

-Start in subendocardial region (most poorly perfused and thus vulnerable)
Progress towards epicardial region over several hours (intervention may limit progression)

-Myocardial ischemia due to hypoxia AND low blood flow has more detrimental effect than hypoxia alone due to added detrimental metabolic problems

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65
Q

Myocardial Infarction:

Size/Extent determined by…(4)

A

1) Site of occlusion
2) Duration of ischemia
3) Extent of collateral circulation
4) Metabolic needs of myocardium

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66
Q

Myocardial infarction typical location

A
  • Majority involve LV and septum (more prone to ischemia due to larger mass, higher workload and oxygen demand)
  • Only 1-3% involve RV
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67
Q

Collateral Circulation

A

preferentially supplies outer myocardium, thus can limit infarcts to subendocardial area

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68
Q

Pathology Evolution of Infarcts:

0-30 min

A

0-30 min: reversible ultrastructural/biochemical changes

  • ATP levels fall, cessation of contractility
  • depletion of ATP, cellular edema, decreased membrane potential and susceptibility to arrhythmias

20-24 min: IRREVERSIBLE CELL INJURY

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69
Q

Pathology Evolution of Infarcts:

1-2hrs

4-12hrs

A

1-2 hr: irreversible ultrastructural changes
-sarcolema disruption, release of intracellular proteins and ion gradient disruption

4-12 hr: wavy myofibers (noncontractile ischemic fibers stretched with each systole)
-No gross changes

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70
Q

Pathology Evolution of Infarcts:

18-24 hrs

24-72 hrs

A

18-24hr:

  • coagulation necrosis (pyknotic nuclei with eosinophilic cytoplasm)
  • PMN infiltration
  • GROSS CHANGES PRESENT (pallor, contraction bands at edge of infarct

24-72 hours:

  • max coagulation necrosis (no nuclei or striations, rimmed by hyperemic tissue)
  • neutrophils infiltration peaks
  • monocytes appear
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71
Q

Pathology Evolution of Infarcts:

4-7 days

A
  • macrophages with disintegration of myocytes (max softening)
  • Gross changes = pallor with hyperemic border
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72
Q

Pathology Evolution of Infarcts:

10 days

4-8 weeks

A

10 days: granulation tissue
-Gross changes = yellow, soft with dark border

4-8 wks: fibrosis
-Gross changes = firm and gray

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73
Q

Complications associated with MI

A

1) Arrhythmias
2) LV failure with pulmonary edema
3) Cardiogenic shock (if >40% LV infarction)
4) Pericarditis (CP, friction rub)
5) Infarction/rupture of papillary muscle with mitral valve incompetence
6) Ventricular aneurysm can rupture, or develop mural thrombus
7) Rupture of LV free wall or septum
8) Mural thrombus (+/- embolism) may occur early or late

74
Q

Rupture of LV free wall or septum

A
  • May occur within first 3 weeks, usually within 2-10 days post infarction
  • Due to max softening and macrophage activity at 4-7 days
  • 10% of deaths post MI in hospitalized patients
75
Q

Hypertensive Heart Disease

A
  • Pressure overloaded states → add new sarcomeres → increase diameter of muscle fibers → concentric hypertrophy → increased O2 requirements → vulnerable to ischemic injury since myocardial capillary bed does not expand in step with increased myocardial mass
  • Predisposition to atherosclerosis and problems in other organs due to HTN
76
Q

Aneurysm

A

localized, congenital, or acquired vessel dilation (saccular, fusiform, berry) secondary to weakening of the wall

77
Q

Atherosclerotic Aneurysm

A

Pathogenesis:

  • plaque→compress media→degeneration/ thinning wall
  • Inflammation → ECM degradation → weaken wall
  • Most common type of aneurysm (elderly males)
  • Often due to severe atherosclerosis of abdominal aorta below renal arteries
  • Often asymptomatic
78
Q

Aneurysms can form due to…(4)

A

1) Systemic diseases: atherosclerosis, HTN, vasculitis
2) Developmental defects
3) Infection: mycotic aneurysms secondary to septic emboli from infective endocarditis
4) Congenital diseases: marfan syndrome (defective synthesis of fibrillin)

79
Q

Berry aneurysms

A
  • congenital defect in media of arteries at bifurcation of cerebral vessels → subarachnoid hemorrhage
  • Berry aneurysms associated with polycystic renal disease
  • severe rapid onset headache
80
Q

Vessel Dissection

A

Most often in aorta

-Blood dissects into media of vessel wall (often due to intimal defect)

81
Q

Outcomes of dissection

A

1) Rupture into the mediastinum or retroperitoneum
2) Back into pericardial cavity → tamponade
3) Double barreled aorta

82
Q

Symptoms of dissection and predisposing factors of dissection

A

Symptoms:

1) Sudden onset severe CP radiating to back
2) Hypotension, shock
3) CT scan shows double lumen

Men 40-60 with HTN (younger if CT abnormalities - marfan)

83
Q

Infectious Vasculitis

A

Direct invasion of arteries by bacteria or fungi (aspergillus/mucor)

Vascular invasion as part of generalized infection (e.g. abscess, pneumonia)

84
Q

Giant Cell (temporal arteritis)

A

Most common type of arteritis

  • Segmental granulomatous inflammation of branches of carotid arteries (esp. Temporal artery)
  • Sometimes involves ophthalmic artery, can cause blindness
  • Most commonly elderly females

DX: clinical (headache, localized tenderness, visual symptoms), ESR, biopsy

TX: steroids

85
Q

Polyarteritis Nodosa

A

Acute segmental necrotizing vasculitis of small/medium arteries with coexisting different stages of inflammation

  • Involves gut, NOT lungs
  • most common in middle-aged males

TX: steroids, immunosuppressive drugs

86
Q

Wegener’s Granulomatosis

A
  • Necrotizing granulomatous inflammation of small to medium vessels
  • Cell mediated hypersensitivity response directed against inhaled infectious or environmental antigens
  • LUNG AND KIDNEY INVOLVEMENT
  • Males more than females
  • positive for PR3-ANCA (neutrophil granule)
87
Q

Churg Strauss Syndrome

A
  • Allergic (assoc. with fever, asthma, increased eosinophils)
  • Granulomatous necrotizing vasculitis of small arteries and veins
  • more common in young adults
88
Q

Leukocytoclastic / Hypersensitivity Vasculitis

A

Involves arterioles, venules, and capillaries of skin mucosa

  • Self limited
  • Skin (palpable purpura)
  • Often hypersensitivity to drugs/infectious organisms
89
Q

Granuloma Pyogenicum

A

benign vascular lesion

-polypoid granulation tissue nodule on skin or mucosa

90
Q

Capillary hemangioma

A

benign vascular lesion

-Affects skin, mucosal surfaces, occasionally deep organs
In newborns may grow rapidly, but 80% will spontaneously regress

91
Q

Cavernous hemangioma

A

benign vascular lesion

  • Affects skin, mucosa, or organs
  • Associated with von Hippel Lindau Disease
  • Associated with Sturge Weber Syndrome when in 5th nerve distribution
92
Q

Kaposi Sarcoma

A
  • Intermediate grade vascular lesion
  • Malignant tumor with skin, mucosa, or deep visceral involvement -start with skin/mucosa, progress to internal organs
  • Associated with AIDS and HHV-8
93
Q

Angiosarcoma

A
  • malignant skin lesions
  • Rare sarcoma involving skin, soft tissue, breast, liver
  • Most common in elderly caucasians
94
Q

Unfractionated Heparin

Mechanism of action

A

indirect thrombin-10a inhibitor

-Binds ATIII and accelerates activity –> inactivates 2 and 10

95
Q

Unfractionated Heparin

Pharmakokinetics

A

given IV or SC (not absorbed from GI)

  • Does NOT cross placenta (safe in pregnancy)
  • Requires IV loading dose for immediate anticoag effect
  • Continuous infusion preferred (less bleeding complications)
96
Q

Heparin

Uses (3)

A

1) prevention and treatment of venous thromboembolism (PE, DVT)
2) prevention of cardioembolic events (stroke) in patients with AFIB
3) Tx of UA, acute MI (NSTEMI, STEMI)

97
Q

Heparin

Adverse reactions (4) and OD

A

1) Hemorrhage
2) Hypersensitivity rxns to contaminants
3) Thrombocytopenia (heparin more than LMWH, NOT with fondaparinux)
4) Osteoporosis

Overdose:

  • Nosebleeds, hematuria, tarry stools, bruising
  • TREATMENT → PROTAMINE (neutralizes heparin within 5 min)
98
Q

Heparin Drug-Drug interactions (1)

A

1) drugs that interfere with platelet aggregation

- ASA, indomethacin, ibuprofen, dextran

99
Q

LMW Heparin

Mechanism of action

A
  • bind ATIII, inactivate Xa but not IIa (thrombin)

- renal elimination

100
Q

LMW Heparin

benefits over UF Heparin

A
  • Less tendency for bleeding complications
  • Less effects on platelets (less thrombocytopenia)
  • No effect on aPTT
  • less monitoring
101
Q

Fondaparinux

mechanism of action

A

activates ATIII, inactivates Xa only

102
Q

Warfarin (Coumadin)

Mechanism of Action

A

-acts in liver to block vitamin K-dependent clotting factor synthesis (2, 7, 9, 10, protein S, protein C) by blocking vitamin K reactivation (carboxyglutamic rxn)

103
Q

Warfarin (Coumadin)

Pharmakokinetics (6)

A

1) 100% oral absorption
2) Crosses placenta, contraindicated in pregnancy
3) CYP2C9 metabolism → drug interactions
4) VKORC1 enzyme has genetic polymorphisms = different warfarin sensitivity among patients
5) Protein C inhibition can result in early procoagulant effect
6) Onset of anticoag effect delayed to allow turnover of existing clotting factors (dependent on half life - 2=60hrs, 7=6hrs, 9=24hrs, 10=40hrs)

104
Q

Warfarin (Coumadin)

Uses (2)

A

1) AFIB: prevention of thromboembolic complications

2) Prophylaxis of thromboembolism (from valve replacement)

105
Q

Warfarin (Coumadin)

Adverse Reactions (3) and OD

A

1) Hemorrhage
2) GI
3) Osteoporosis

Overdose:

  • Hematuria, excessive menstrual bleeding, gum bleeding, bruising
  • Must closely monitor INR
  • Use IV infusion of vitamin K
106
Q

Warfarin (Coumadin)

Drug interactions - increased warfarin effect

A 
Increased effect:
Inhibit CYP2C9:
1) amiodarone
2) cimetidine
3) fluconazole
4) fluoxetine
5) metronidazole
6) rosuvastatin

Interfere with platelets: ASA

Interfere with Vitamin K function: oral abx (eliminate intestinal bacteria)

107
Q

Warfarin (Coumadin)

Drug interactions - decreased warfarin effect

A

Increased CYP2C9 activity:

1) barbiturates
2) phenytoin
3) rifampin
4) St. John’s Wort
5) Carbamazepine
6) Vitamin K from diet

108
Q

Dabigatran (Pradaxa)

Mechanism of action

A

directly inhibit activity of thrombin (2a)

  • More rapid onset than warfarin
  • Steady state levels in 2-3 days
  • Renal excretion
109
Q

Dabigatran (Pradaxa)

Benefits (4)

A

1) Does NOT require monitoring and dosage adjustments (but more expensive to assess bleeding risk if you need to)
2) No dietary restrictions
3) Has reversal monoclonal ab (Praxbind)
4) Not a CYP450 substrate → fewer drug/food interactions

110
Q

Dabigatran (Pradaxa)

Disadvantages (2)

A

Twice daily dosing

Shorter acting → missed doses = increased risk thrombosis

111
Q

Dabigatran (Pradaxa)

Uses

A

Non-valvular AFIB

112
Q

Rivaroxaban (Xarelto), Apixaban (Eliquis), Edoxaban (Savaysa)

Mechanism of action

A

directly inhibit factor 10a

113
Q

Rivaroxaban (Xarelto), Apixaban (Eliquis), Edoxaban (Savaysa)

Benefits/disadvantages

A

No monitoring, no dietary restrictions

NO REVERSAL AGENT

Shorter acting → missed doses = increased thrombosis risk

114
Q

Rivaroxaban (Xarelto), Apixaban (Eliquis), Edoxaban (Savaysa)

Uses

A

1) Non valvular AFIB

2) Rivaroxaban (Xarelto) the only one approved for VTE and treatment of DVT/PE

115
Q

Aspirin

A

inhibit COX-1 synthesis of thromboxane in platelets, effect for 8 days (irreversible)

GI bleeding risk

116
Q

Clopidogrel (Plavix)

A

ADP receptor antagonist, interfere with ADP-induced platelet aggregation (irreversible)

117
Q

Dipyridamole

A

block PDE break down of cAMP potentiating prostacyclin’s anti-aggregatory action

-Minimal antithrombotic benefit

118
Q

Abciximab (Reopro), Eptifibatide (Integrilin), Tirofiban (Aggrastat)

A

block IIb/IIIa receptors on platelet → prevent integrin and fibrinogen binding and platelet aggregation

Continuous IV infusion

119
Q

Antiplatelet Agent usage:

1) Acute MI (STEMI)
2) Unstable Angina (UA) and NSTEMI
3) Percutaneous coronary interventions
4) Secondary prevention of MI and ischemic stroke

A

1) Acute MI (STEMI): ASA + ADP antagonist
2) Unstable Angina (UA) and NSTEMI: ASA +/- ADP antagonist
3) Percutaneous coronary interventions: ASA + ADP antagonist +/- GIIb/IIIa inhibitors
4) Secondary prevention of MI and ischemic stroke (ASA)

120
Q

Tissue Plasminogen Activator (tPA)

Mechanism of action

A

binds fibrin, activates bound plasminogen

Increases formation of plasmin from plasminogen → lytic state

121
Q

Tissue Plasminogen Activator (tPA)

Uses

A

1) Acute MI (STEMI): emergency treatment of coronary artery thrombosis (use within 2 hours)
- PCI may be preferred to thrombolytic therapy in some cases

2) DVT
3) Multiple PE

122
Q

Venous thrombi vs. arterial thrombi

A

Venous Thrombi = fibrin and trapped RBCs with relatively FEW PLATELETS

Arterial thrombi = platelet aggregates with SMALL AMOUNT of FIBRIN

123
Q

Spectrum of acute coronary syndrome due to…

A

supply/demand mismatch

124
Q

Complete vessel occlusion

A

STEMI

Transmural ischemia: spans entire thickness of myocardium

Most often due to complete coronary block

125
Q

Partial coronary vessel occlusion with myocardial necrosis

A

NSTEMI

126
Q

Partial coronary vessel occlusion, escalating symptoms, without myocardial necrosis

A

Unstable angina

Subendocardial ischemia: involves innermost layers of myocardium

a.Most often due to partial occlusion

127
Q

Pathophysiology of ACS: ___ + ____ + ____ = ______

A

dysfunctional endothelium + coagulation + platelet aggregation = coronary thrombosis

128
Q

Pathophysiology of ACS (4)

A

i. Inflammation + risk factors promote atherosclerosis
ii. Atherosclerosis promotes dysfunctional endothelium
- Decreased vasodilator effect, decreased antithrombotic effect compared to normal endothelium
iii. Inflammatory mediators weaken atherosclerotic fibrous cap → cap bursts → thrombogenic, TF released → activates coagulation cascade, creates platelet aggregation
iv. All leads to coronary thrombus

129
Q

Serum markers in NSTEMI and STEMI

A

Necrosis of myocardial tissue causes intracellular leak of molecules into bloodstream (in STEMI and NSTEMI)

a. Cardiac troponin (Troponin I and T) = sensitive and specific for myocardium, important for diagnosis of MI
b. Creatine Kinase-MB isoenzyme (not as specific for heart)

130
Q

CK-MB time to initial elevation

A

4-6 hours

131
Q

CK-MB time to peak elevation

A

18 hours

132
Q

CK-MB time to return to normal

A

2-4 days

133
Q

cTnI time to initial elevation

A

4-6 hours

134
Q

cTnI time to peak elevation

A

12 hours

135
Q

cTnI time to return to normal

A

3-10 days

136
Q

cTnT time to initial elevation

A

4-6 hours

137
Q

cTnT time to peak elevation

A

12-48 hours

138
Q

cTnT time to return to normal

A

7-10 days

139
Q

ECG: acute STEMI

A

ST elevation

140
Q

ECG: STEMI hours after infarction

A

ST elevation
Small R wave
Q wave begins

141
Q

ECG: STEMI, days 1-2

A

T wave inversion

Q wave deeper

142
Q

ECG: STEMI, days later

A

ST normalizes

T wave inverted

143
Q

ECG: STEMI, weeks later

A

ST and T normal

Q wave persists

144
Q

Stable vs. Unstable angina

A
  1. Stable angina: present when there is increased demand for myocardial O2 in a reproducible fashion
    a. NOT on ACS spectrum
  2. Unstable angina: change in chest symptom - discomfort, new onset or increased duration, frequency or intensity with less exertion or at rest compared to previous episodes of discomfort
145
Q

Treatment of STEMI

A

Artery occluded → open it!

i. Within 90 minutes go to cath lab to open vessel mechanically with cardiac catheterization
ii. Outside of 90 min:
1. Consider fibrinolytics
2. Hemodynamically stable → oral B-Blockers, nitrates → decrease myocardial oxygen demand

146
Q

Treatment of NSTEMI and unstable angina (3)

A

artery partially occluded → halt thrombotic process from completely occluding the artery (halt propagation of clot)

i. Anticoagulants (1): unfractionated heparin, LMW heparin, fondaparinux
ii. Antiplatelets (2):P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor), GIIb/IIIa inhibitors PLUS ASPIRIN
iii. If hemodynamically stable consider oral B-Blockers, nitrates → decrease myocardial oxygen demand

147
Q

Development of Atherosclerosis and progression to ASCVD: (7 Steps)

A

1) LDL infiltrates subendothelial space
2) LDL modified (oxidized, glycosylated)
3) Release of proinflammatory cytokines (TNFa, IL-1, IL-6, IFN), increased expression of cell adhesion molecules (CAMs), monocyte chemotactic protein-1 (MCP-1) and IL-8
4) Monocytes recruited to clean up oxidized LDL
5) Phagocytosis of LDL → foam cell formation
6) Foam cells and T-lymphocytes within the plaque cause MMP secretion and activation of tissue factors
7) Plaque rupture occurs in “unstable” lesions → vessel thrombosis and acute coronary events

148
Q

Lipoproteins

5 different classes

A

ferry water-insolible fats through the blood stream

-hydrophilic phospholipid + free cholesterol + apolipoproteins

5 different classes:

1) Chylomicrons
2) Very Low Density Lipoproteins (VLDL)
3) Intermediate-density Lipoproteins (IDL)
4) LDL
5) HDL

149
Q

Exogenous Lipid Metabolism Pathway:

1) Fats absorbed in _________ –> repackaged as ________ with apo _____
* (HDL adds _____ and ____)
2) Chylomicrons enter circulation via the ____________
3) _________ cleaves fatty acids from chylomicrons and stores FFA in ______, used as energy in ______ or _______ muscle
4) _________ removed from circulation by ______ via remnant receptor and apo-____
5) Cholesterol in liver can be incorporated into ______ –> exported to _______

A

1) Fats absorbed in small intestine –> repackaged as chylomicrons with apo B-48
* (HDL adds ApoE and ApoC)
2) Chylomicrons enter circulation via the lymphatic system
3) Lipoprotein lipase (LPL) cleaves fatty acids from chylomicrons and stores FFA in adipose tissue, used as energy in cardiac or skeletal muscle
4) Chylomicron Remnants removed from circulation by liver via remnant receptor and apo-E
5) Cholesterol in liver can be incorporated into bile acids –> exported to intestine
* Normal is no chilomicrons in blood if you haven’t eaten in 8-10 hours

150
Q

Endogenous Lipid Metabolism Pathway:

1) Liver packages cholesterol and triglycerides into _____ particles with apo-_____
* (HDL adds ____ and ____)
2) VLDL broken down by _____ –> release fatty acids to muscle and adipose tissue –> _____
* some _____ cleared in liver via hepatic receptors that recognize _____
3) LPL and hepatic lipase (HL) hydrolyze _____ –> ______
4) _____ cleared from plasma via _____ receptor-mediated endocytosis in the liver and peripheral cells, directed by LDL’s apo-____ and apo____

A

1) Liver packages cholesterol and triglycerides into VLDL particles with apo-B100
* (HDL adds apoC and apoE)
2) VLDL broken down by LPL –> release fatty acids to muscle and adipose tissue –> IDL
* some IDL cleared in liver via hepatic receptors that recognize apoE
3) LPL and hepatic lipase (HL) hydrolyze IDL –> LDL
4) LDL cleared from plasma via LDL receptor-mediated endocytosis in the liver and peripheral cells, directed by LDL’s apo-B100 and apoE

151
Q

HDL transfers lipids to VLDL and Chylomicrons via ________

A

Cholesteryl Ester Transferase Protein (CETP)

152
Q

HDL beneficial effects

2 possible mechanisms

A

HDL “removes” cholesterol from periphery

HDL has antioxidant and anti-inflammatory effects

153
Q

Cholesterol and progression of atherosclerosis

A

Atherogenic lipoproteins (LDL, VLDL, IDL) are central to initiation and progression of atherosclerosis

Cholesterol lowering stabilizes plaque and reduces ASCVD-related events

154
Q

Hypertriglyceridemia puts patients at risk for…(3)

A

Acute pancreatitis
ASCVD
Metabolic syndrome

155
Q

Calculating LDL

A

LDL = total cholesterol - HDL - (TG/5)

156
Q

Stable Angina

A

lumen narrowed by plaque, inappropriate vasoconstriction

Exertional angina - myocardial oxygen demand increases → supply unable to increase in response (autoregulation coronary artery dilation ineffective)

Fixed, stenotic, endothelialized atheromatous plaque

157
Q

Treatment of stable angina (3)

A

Goal: reduce O2 demand

Nitrates, Ca2+ channel blockers, B-blockers

158
Q

Unstable Angina

A
  • plaque rupture, platelet aggregation, thrombus formation, unopposed vasoconstriction
  • MI from occlusive thrombus generally imminent
  • Angina at rest, change in frequency, character, duration, and precipitating factors
159
Q

Treatment of Unstable Angina (acute)

A

Clot: ASA, heparin, GPIIb/IIIa inhibitors, PTCA/CABG, fibrinolytics

Arrhythmias: B-blockers

Pain: NTG, morphine

160
Q

Treatment of UA post MI (5)

A

ACEI, Statin, B-blocker, ASA, clopidogrel (if post stent)

161
Q

Variant Angina

A

coronary vasospasm with or without atheromatous plaque

Oxygen supply decreases due to reversible coronary vasospasm

-occurs at rest, NOT associated with exercise

162
Q

Treatment of variant angina (2)

A

Goal: reverse/prevent vasospasm

Vasodilators (Ca2+ channel blockers, nitrates)

163
Q

Nitrates

Mechanism of action

A

nitrates → NO → activate GC → cGMP increased in VSM → relaxation of VSM

  • Primary target is venous capacitance vessels → reduce preload (LVEDP) → reduce myocardial O2 demand
  • Dilate coronary artery vessels → increase myocardial O2 supply
164
Q

Nitrates

Pharmacokinetics

A

Sublingually, transdermally, parenterally

Isosorbide Mononitrate (PO, chronic treatment)

Nitroglycerin (rapid onset, sublingual or translingual spray)

165
Q

Nitrates

uses

A

Treatment of acute angina

Prophylaxis for stable angina (long acting nitrates)

166
Q

Nitrates

side effects (4)

A

Due to VASODILATION →

1) Throbbing headache
2) **orthostatic hypotension
3) **reflex tachycardia
4) facial flushing

Can get tachyphylaxis (tolerance) with continuous exposure - recommended to have nitrate free interval (6-14 hrs daily)

167
Q

Nitrates

drug interactions

A

sildenafil, vardenafil or tadalafil (viagra) → unsafe drop in BP

168
Q

Propanolol vs. metoprolol/atenolol

A

Propranolol = non selective B1 and B2

Metoprolol, Atenolol = B1 selective (cardioselective)
-Selectivity at low doses only

169
Q

B-blockers mechanism of action

A

target B-adrenergic receptors to decrease HR, BP, contractility → reduce O2 requirements

170
Q

VSM:

A1 adrenergic receptor activation –> ?

B2 adrenergic receptors –> ?

A

A1 adrenergic receptors → increased Ca2+ intracellularly → VSM contraction

B2 adrenergic receptors → increased cAMP → VSM relaxation

171
Q

B-blocker uses (2)

A

NOT vasodilatory → No role in variant (vasospastic) angina

  • First-line therapy for stable angina
  • Used in acute and post-MI therapy for unstable angina
172
Q

B-blocker contraindications

A
  • asthma
  • severe bradycardia
  • peripheral vascular disorder
  • abrupt withdrawal precipitates sympathetic overreactivity
173
Q

Nifedipine and Amlodipine are ______ LTCC blockers

A

DHP class

174
Q

DHP class (Nifedipine, Amlodipine)

A

more vascular relaxation than cardiac actions (contractility, SA node impulse generation, AV nodal conduction)

**DO NOT use short acting DHPs (Immediate-Release Nifedipine) - too rapid of BP lowering → **Reflex activation of SNS (tachycardia, worsening of angina)

175
Q

Diltiazem and Verapamil

A

more effect on cardiac nodal tissue, SA and AV, (phase 0) and cardiac muscle (phase 2)

Verapamil has the highest risk of negative inotropic effect

176
Q

Adverse reactions associated with DHPs (4)

A

1) Edema
2) Hypotension
3) Flushing
4) Reflex tachycardia with short acting Nifedipine

177
Q

Adverse reactions associated with non-DHPs

A

1) Cardiac depression (bradycardia, AV block, arrest) - more likely with verapamil and diltiazem
2) Dizziness
3) Constipation (more with verapamil)
4) Gingival hyperplasia

178
Q

LTCC blocker uses (DHP and non DHP)

A
  • Vasospastic angina
  • Stable angina
  • Arrhythmias
  • HTN
  • Inhibition of premature labor
  • Subarachnoid hemorrhage
179
Q

Ranolazine mechanism of action

A

-block Na+ channel that mediate late current in cardiac AP

Late Na+ current can cause intracellular Na+ overload → NCX Ca2+in/Na+ out → intracellular Ca2+ overload → more myocardial O2 demand

180
Q

Ranolazine adverse reaction

A

prolong QT interval (do not use with other QT prolonging drugs)

CVPR (12 decks)

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