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Cardiology > Cardio TBL > Flashcards

Cardio TBL Flashcards

1
Q

Areteriosclerosis =

A

Hardening of Arteries

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2
Q

• Atherosclerosis: large and medium arteries;

A

INTIMAL CHANGES
—Lipid deposition, accumulation of macrophages + myointimal cells —>
plaque formation

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3
Q

• Arteriolosclerosis: Hypertension induced

A

hyperplasia/trophy of smooth muscle cells (Media)

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4
Q

• Endarteritis Obleterans:

A

Response to inflammation (syphilis); INTIMA

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5
Q

Arteritis:

A

• Arteritis: fibrinoid necrosis of arterial wall

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6
Q

Monkeberg’s:

A

Calcification of MEDIA

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7
Q

Areteriosclerosis Emphasis on Progression

A

• Intimal changes are persistent for decade(s), but then sclerosis can progress. Evidence shows lesions in same gross location, but different depth (in vessel wall) as individuals age.

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8
Q

Areteriosclerosis Presentation

A

• Presentation: 50 years of age

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9
Q

Arterial Structure Review Three Parts:

A

Intima:
Media:
Adventitia:

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10
Q

Arterial Intima:

A

Endothelium –> internal elastic lamella; contains myointimal cells in the sub-endothelial space

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11
Q

Arterial Media:

A

smooth muscle cells + Collagen I/III

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12
Q

Arterial Adventitia:

A

type I collagen + fibroblasts Vasa Vasorum not found in abdominal aorta –> more susceptible to athero.

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13
Q

CHRONIC ENDOTHELIAL DYSFUNCTION:

A
  • Platelet Microthrombi

* Fatty Streaks

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14
Q

Platelet Microthrombi -

A

Proposed theory because aggregates of plat are found incommon sites of athero

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15
Q

Fatty Streaks -

A

Subendothelial lipid (cholesterol/esters) + foamy cells

  • –No hemodynamic change
  • –Reversible (Lactating babies +, 4-5 y/o)
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16
Q

Bottom Line: Endothelial injury

A

↑permeability for lipids + ↑adhesions

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17
Q

Endothelial Injury occurs from:

A 
• Hyperlipidemia/hypercholesterolemia
• HTN
• Smoking
• Diabetes/Metabolic Syndrome
• Toxins/Viruses
• Homocysteine
Fatty streaks are reversible with lifestyle
change. if not --> Fibrous (Fatty) Plaque
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18
Q

Areteriosclerosis Pathophysiology:

A

• Because Atherosclerosis = chronic endothelial dysfunction; any disease that causes endothelial injury can lead to it.

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19
Q

Three Consequence of endothelial injury:

A
  1. ↑Endothelial adhesion to leukocytes and platelets
  2. Passage of lipids (LDL) into subendothelial space (Fatty streak)
  3. DAMAGE –> endogenous activation macrophages–> ↑cytokines + ↑Macrophage presentation to T-Cells –> ↑T-Cell Inflammation
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20
Q
  1. ↑Endothelial adhesion to leukocytes and platelets leads to?
A

Adhesion Accumulation of macrophages, myointimal cells and monocytes (future foamy cells) in subendothleial space

  • –Platelets on Fatty Streak –> ↑Cytokines –> ↑T Cell Activation
  • **Cytokines–> Smooth muscle proliferation / ECM deposition (smooth muscle from tunica media –> tunica intima)
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21
Q
  1. Passage of lipids (LDL) into subendothelial space (Fatty streak) leads to?
A
  • –LDL must be oxidized –> release inflammatory lipids
  • –Can be modified by homocysteine (MI in Homocysteinuria)
  • –Additional ↑Endothelial adhesion particles
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22
Q
  1. DAMAGE –> endogenous activation macrophages–> ↑cytokines +
    ↑Macrophage presentation to T-Cells –> ↑T-Cell Inflammation leads to?
A

—Inflammation –> ↑IL-6 –> ↑Acute Phase Proteins (SAA, CRP)
***CRP is best indicator of disrupted plaques; thus better than LDL for
predicting cardiovascular events

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23
Q

↑Endothelial adhesions leads to?

A

Macrophages and monocytes migrating: Lumen (L) to subendothelial space.
Once in subendothelial space,monocyte and macrophage ingests lipid –> Foamy Cell

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24
Q

Endothelial injury morphology?

A

• Fatty streaks: yellow streaks on
endothelium
• streaks occur at points of bifurcation
—Turbulent flow, likely place for injury

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25
Q

FATTY STREAK leads to?

A

FIBROUS PLAQUE

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26
Q

Proliferative lesion:

A

Monocyte, macrophage, myointimal cells proliferate===Intimal Thickening!

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27
Q

Fibrous Plaque =

A

• Amorpous central core: cholesterol + esters, acellular debris, foamy cells
• Fibrous cap: myointimal cells, collagen,
glycoproteins, PGs
—Provides stability
• Endothelium is intact (Continuous)
—But dysfunctional –> platelets!

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28
Q

Pathophysiology:

FATTY STREAK –> FIBROUS PLAQUE

A
  • Untreated fatty streaks allow ↑Lipid deposition + ↑Leukocyte adherence to dysfunctional endothelium
  • ↑Foamy Cells
  • ↑Stress –> ↑Smooth muscles changes –> ↑Myointimal cells
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29
Q

Veins and Pulmonary Circulation

A
  • VEINS ARE NOT AFFECTED

* Same with pulmonary circulation, EXCEPT IN PULMONARY ATHEROSCLEROSIS (DDx: Pulmonary Hypertension)

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30
Q

Morphology: “Fibrofatty Plaque”?

A
  • Gross: elevated lesions at points of turbulent flow
  • Micro: (image) see foamy cells (F) (in and out of core), fibrous cap, and central core (necrotic material and cholesterol crystals)
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31
Q

Complex Atheromatous Lesions

A

FIBROUS PLAQUE + SOMETHING ELSE

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32
Q

Complex Atheromatous Lesions Maintains Components of Fibrous Plaque

A
  • Necrotic debris
  • Cholesterol deposits
  • Foamy cells/fibrous cap
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33
Q

Complex Atheromatous Lesions + New Process:

A 
• Calcification (breaks off with pulse flow)
• Hemorrhage (capillary ingrowth)
• Ulceration/Fissure (abdominal aorta)
• Ruptured Plaque (Coronary Syndrome)
• Luminal Thrombosis (platelets)
Progression from Fibrous Plaque -->
Complex Lesions is NOT mandatory
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34
Q

Complex Atheromatous Lesions Pathophysiology:

A
  • Again, lack of treatment/intervention allows fatty streak –> fibrous cap –> addition of new process
  • Recall abdominal aorta is more susceptible to atherosclerosis because lack of vasa vasorum
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35
Q

Myocardial Infarction from CAD requires?

A

100% occlusion

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36
Q

Most patients with CAD have?

A

Multiple plaques along their entire coronaries

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37
Q

Because ATHEROsclerosis =

A

Intima of CA is thickened

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38
Q

Effect of Pre-Existing Collaterals:

A

• Men have ↑↑ collateral circulation
• Premenopausal women have ↓collaterals, but ↓atherosclerosis
• Immediately post-menopausal women CA occlusion = DEVESTATING
—Enter “accelerated atherosclerosis” and have ↓collateral circulation

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39
Q

Coronary Artery Disease Etiology:

A

• Coronary arteries especially at risk because intimal thickening naturally takes place at points of bifurcation (turbulent flow)

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40
Q

Coronary Artery Disease Areas at Risk

A

• LAD: anterior LV, IV-Septum, Apex
• Circumflex A: Wall of LV
• RCA: Posterior wall of LV, IV septum,
RV, and Right wall of Heart

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41
Q

Coronary Artery Disease Pathophysiology:

A
  • 80% of lumen can be narrowed without myocardial necrosis
  • Recall from acute coronary syndrome that endothelial dysfunction –> atherosclerosis, but damage does not occur until plaque ruptures
  • Acute episode (plaque rupture, fissure, hemorrhage, thrombosis) —-> dislodge plaque + expose endothelium –> platelets aggregate (thrombus) —> TXA2 = VASOCONSTRICTION
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42
Q

Stary’s Classification of Coronary Artery Disease

A
  • Type 1: Adaptive Thickening
  • Type 2: Macrophageic Foam Cells
  • Type 3: Extracellular Lipid = preatheroma
  • Type 4: Necrotic Core = atheroma
  • Type 5: Fibrous cap = fibroatheroma
  • Type 6: Atheroma + addition = complicated lesion
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43
Q

Myocardial Infarction =

A

100% Occlusion of Coronary Artery

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44
Q

Myocardial Infarction Area of Risk vs. Area of Necrosis

A

• Area of risk: area irrigated by coronary
artery if occluded for long time
• Area of Necrosis: area of actual tissue
death
Big Point: quicker perfusion occurs –>
less area of necrosis

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45
Q

Myocardial Infarction: 10 hours:

A

no gross/micro change

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46
Q

Myocardial Infarction: 10-20 hrs:

A

Dead cells (white) cell surrounded by hypereosinophilic + some edema +/- PMN (Coagulative necrosis)

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47
Q

Myocardial Infarction:1-3 days:

A

↑eosinophilia, pyknosis, karyorrhexis, ↑edema + ↑PMNs

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48
Q

Myocardial Infarction: 4-7 days:

A

Macrophages + PMNS remove dead cells –> risk for rupture; granulation tissue begins to form around necrotic area

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49
Q

Myocardial Infarction: 7-10 days:

A

Gross yellowish color; ↑collagen + granulation tissue

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50
Q

Myocardial Infarction: 11-21 days:

A

Dead cells gone (macro w/ lipofuschin); granulation tissue

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51
Q

Myocardial Infarction: 4-10 weeks:

A

Granulation tissue —> non-contractile scar

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52
Q

Post-MI Complications Reperfusion Injury:

A 
• Fibers at edge of MI are hypereosinophilic
bands with distortion,
pyknosis, and interstitial edema
===Contraction Bands
• During MI, ↑Ca++ accumulation.
• When reperfused --> massive sustained
contraction
• Also free radical damage
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53
Q

Post-MI Complications Pathophysiology:

A

During reperfusion post MI, lots going on:

  1. Mitochondria come back, but not quick enough to stop ROS
  2. pH is changing drastically (back up)
  3. Ca++ overload
  4. Inflammation
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54
Q

Myocardial Hypercontracture –>

A

↑Pores in Mito. Membrane = DAMAGE

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55
Q

Reperfusion ↓Infarction size, but do it after cardioprotection to prevent cardiac hypercontracture:

A
  • Rx preventing mitochondrial membrane pore formation

* Rx activating reperfusion injury salvage kinase (RISK) pathway

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56
Q

Post-MI Complications Mural Thrombosis

A

Area over infarct thickens and is

abnormal –> attracts platelets

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57
Q

Post-MI Complications Consequences Mural Thrombosis

A
  • Embolism

* Occupy LV volume —> ↓CO

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58
Q

Post-MI Complications Ventricular Aneurysms

A

Ventricular Aneurysms
• Common in transmural infarcts
Mechanism:
• While scarred area has ↑strength, during contraction it remains
stationary and healthy myocardium contracts, creating an anuerysm

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59
Q

Ventricular Aneurysms

A

Common in transmural infarcts

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60
Q

Ventricular Aneurysms Mechanism:

A

While scarred area has ↑ strength, during contraction it remains stationary and healthy myocardium contracts, creating an anuerysm

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61
Q

Myocardial Rupture Occurs

A

Days 4-7 (max removal of tissue)

—60% during this time period; 30% in 24 hr

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62
Q

Myocardial Rupture Risk Factors:

A
  • Hypertension
  • Diabetics
  • Women in early menopause
  • Psychiatric Patients
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63
Q

Myocardial Rupture Pathophysiology - Two Required Conditions

A

• Transmural infarct - full thickness of wall must be necrotic — Makes sense, or else blood would not seep out
• ↑↑ intraventricular pressure — Push blood out, dissecting through the wall
Rupture pushes blood into pericardial sac (TAMPONADE) or can rupture a papillary

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64
Q

Septal Rupture

A

Acquired A-V Defect Less common than rupture of the free wall.
Free wall > septal > papillary

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65
Q

Aneurysm =

A

Sac formed from dilation of vascular wall (cardiac, arterial, venous) —Call venous aneurysm “Varicose / Varices”

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66
Q

Thoracic aneurysms =

A

Dissecting unless proven otherwise.

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67
Q

Abdominal aneurysms =

A

Atherosclerotic unless proven otherwise.

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68
Q

Aneurysms Morphological Classification:

A

Fusiform, Saccular, Cylindrical, Fistula

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69
Q

Laplace’s Law :

A

Tension = (Pressure)(Radius)/(2xHeight)

• Dilation –> ↑Radius –> ↓Wall Thickens (↓H) –> –>

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70
Q

What causes symptoms of aneurysms?

A
  • Compression of surrounding organs
  • Ischemia distal to aneurysm
  • Hemorrhage due to rupture
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71
Q

Dissecting (Thoracic) Aneurysm =

A

Intimal tear in Aorta –> Blood in MEDIA

• Intimal tear ~ 6cm from aortic valve.

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72
Q

Dissecting (Thoracic) Aneurysm Etiology:

A 
• Poorly controlled hypertension***
• Marfan’s Syndrome (presents early)
• Bicuspid Aortic Valve
• Familial Thoracic Aortic Aneurysm Syn
• Coarctation of Aorta (HTN proximal)
• Ehlers Danlos Syndrome (Type IV)
• Loey’s Dietz Syndrome (TGF B)
• Iatrogenic (catheters, surgery)
• Turnuer’s Syndrome (coarctation)
Ascending/thoracic aorta has > 30 elastic
lamella, it has vasa vasorum blood supply.
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73
Q

Dissecting (Thoracic) Aneurysm Presentation

A

Presentation
• Age: 50-70; males > females (2:1); >50% mortality
• Pain to back b/c adventitia is stretched (has pain receptors)

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74
Q

Dissecting (Thoracic) Aneurysm

Fate of Dissection

A

• Rupture —> hemorrhage OR false lumen (↑BP)
• Re-entry (best prognosis)
• No rupture —> thrombosis of false lumen (note normal BP)
• Collapse of Aorta
–hemocardium –> cardiac tamponade with retro-grade flow only

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75
Q

Dissecting (Thoracic) Aneurysm Morphology:

A

• Dissection occurs and blood flows to specific location
• 80% have Cystic Medial Necrosis
—No cysts; pools of PG (cystic) displacing smooth muscle and elastic
lamellae (necrosis) in media (medial) = Creates points of weakness

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76
Q

Vasa vasorum penetrates?

A

Adventitia and divides ~1/3 way into media; at this junction (inner 2/3 from outer 1/3 of media) is least resistance path for
blood being forced through intimal tear

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77
Q

Atherosclerotic (Abdominal) Aneurysm =

A

Weakening of Aortic Wall –> Leakage

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78
Q

Atherosclerotic (Abdominal) Aneurysm Etiology:

A

Atherosclerosis***

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79
Q

Atherosclerotic (Abdominal) Aneurysm Mechanism:

A 
• Atherosclerosis ---> weakening of wall
• ↑Dilation --> ↑Pressure (Laplace)
• ↑Pressure --> Endo damage (↑ather)
• Cycle continues; eventually endothelial
damage ---> ↑Thrombus/Platelets
• ↑Thrombus --> damage --> leakage
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80
Q

Atherosclerotic (Abdominal) Aneurysm Presentation:

A

• 33% die <10 years
• Usually asymptomatic until late
∝ size + diagnosis + rate
Leakage/Rupture most common COD

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81
Q

Atherosclerotic (Abdominal) Aneurysm

Consequence of Dissection

A
  • Narrow/occlude renal and mesenteric arteries
  • Pressure = ↑Bone Damage + ↑Viscera Damage + ↑Neuron Damage
  • Rupture –> hemorrhage
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82
Q

Atherosclerotic (Abdominal) Aneurysm Morphology:

A

TONS of atherosclerosis and thrombi (mura/transmural)

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83
Q

Pseudoaneurysms (Thrombus)

A

Trauma induced bleed –> thrombus –>

dilation –> looks like aneurysm

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84
Q

Pseudoaneurysms (Thrombus) Presentation:

A

Knife, bullet wound, Carson Rider post-Wiz concert

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85
Q

Pseudoaneurysms (Thrombus) Morphology:

A

Hemorrhage –> clot –> dense fibrous tissue

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86
Q

Mycotic Aneurysm:

A

Bacterial Arteritis (Septic Emboli)
Vessel wall weakening from infection
Misnomer, caused more by bacterial
rather than from bacteria

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87
Q

Mycotic Aneurysm Presentation:

A
  • Thrombosis +/- infarction

* Rupture

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88
Q

Most common cause of Sudden Cardiac Death?

A

Ventricle Fibrillation (1,000 Americans/day)

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89
Q

Ventricle Fibrillation most common in patients with?

A

MI + Heart Disease

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90
Q

Ventricle Fibrillation Treat with?

A

AICD (Automated Implantable

Cardioverter Defibrillator)

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91
Q

Ventricle Fibrillation Iatrogenic undetectable cause?

A

↑potassium

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92
Q

Most common cause of stroke?

A

Atrial Fibrillation (atrial stasis –> thrombus –> stroke)

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93
Q

Atrial Fibrillation Prophylaxis with?

A

Warfarin

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94
Q

Atrial Fibrillation interpret ECG?

A

• HR = 300 / (#Big boxes between peaks) = # total peaks x 6
• LV Hypertrophy: (V1 Depth of S-Wave) + (V5 Depth of R Wave) —If >35 mm = LV Hypertrophy
• Rhythm: look for normal P wave before each complex (normal~60)
• Axis: Determined by Lead I and aVF
+Lead 1 and +Lead aVF = normal
+Lead 1 and -Lead aVF = Left Axis Deviated (opposite is RAD)
-Lead 1 and -Lead aVF = Indeterminate Axis

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95
Q

Mechanisms Arrhythmia Types?

A
  1. Enhanced Automaticity

2. Re-Entry

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96
Q

Enhanced Automaticity Two things can change the slow depolarization?

A

Increasing rate of depolarization OR raising the threshold potential (less negative)

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97
Q

What causes ↑ In Phase 4 Slope?

A 
↑SNS Tone / ↓PS Tone
↑CO2 / ↓O2
↑Stretch
↑Digoxin
↓Potassium
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98
Q

Re-entry occurs requiring?

A

Slow conduction + re-excitable

cell

99
Q

Re-entry causes?

A

Circular movement produces a rapid series of APs with ↑ Frequency
===TACHYCARDIA
===ARRHYTHMIA

100
Q

Most common cause of SCD (Sudden Cardiac Death)?

A

Ventricular Fibrillation (1,000 Americans/day)

101
Q

Ventricular Fibrillation ECG Features

A
  • Complete erratic rhythm

* No Identifiable waves

102
Q

AICD - Automated Implantable Cardioverter Defibrillator does what?

A
  • Device is given preset HR

* Monitors rate and rhythm of heart and alters via shock delivery

103
Q

Atrial Fibrillation ECG Features:

A
  • Chaotic baseline = Irregularly irregular = not consistently weird
  • NO DISCRETE P WAVES
104
Q

Atrial Fibrillation Treatment:

A
  • B-Blocker
  • Ca++ Channel Blocker
  • Digoxin
105
Q

Atrial Flutter ECG Features:

A
  • Rapid back-back atrial depolarization waves

* SAW TOOTH PATTERN

106
Q

Ventricular Hypertrophy:

A 
Ventricular Hypertrophy
• ↑Mass of ventricle
• ↑Mass --> Delayed Depolarization
• Common with CHF
• Common with valvular disease
• LV Hypertrophy puts patient at ↑Risk for
Coronary Heart disease
• Equal risk factor for MI as smoking, etc
107
Q

Ventricular Hypertrophy ECG Features:

A
  • ↑QRS Complex Peak —> steep QRS Segment
  • S in V1 + R in V5 or V6 (whichever is larger) ≥ 35 mm
  • May see tall P-wave
  • T-Wave Reversal
108
Q

Bundle Branch Block:

A
  • Conducting tissues is “blocked”
  • Delayed activation of ventricle
  • Always abnormal, but not specific
109
Q

Bundle Branch Block ECG Features:

A

↑ QRS width –> prolonged QRS Segment

110
Q

P waves –>

A

Look at for atrial / supraventricular origin

111
Q

QRS –>

A

Widened in ventricular origin; can be narrowed in atrial

112
Q

Tombstone ST =

A

STEMI

113
Q

Depressed ST =

A

Ischemia

114
Q

Automaticity Disease:

A

Sinus tachycardia, sinus arrest, VPB, etc.

*Both mechanisms can cause most arrhythmias; these are common groupings

115
Q

Re-Entry Disease:

A

VTAC, PSVT, WPW, AFIB

*Both mechanisms can cause most arrhythmias; these are common groupings

116
Q

Pathogenetic Mechanisms of Vasculitis

A
  1. Immune Complex Deposition in Vessel Wall
  2. ANCA-Mediated
  3. Ab Directed at Vessel Wall (endothelial, GBM)
  4. Cell Mediated Immune Reaction (Granuloma)
  5. Component of Other Immune Disorders
117
Q

Vasculitis ANCA-Mediated:

A
  • –Pathogenic from activating PMNs (↑adhesion via B2 integrin, Fcgamma)
  • –Target Endothelia–> ANCA-PR3 + Endothelia –> lost thromboresistance
118
Q

Vasculitis Ab Directed at Vessel Wall (endothelial, GBM):

A
  • –In anti-endothelial, Ab levels == disease activity

- –Ab usually bind to cytoplasmic components, not surface

119
Q

Immune Complex Pathogenicity Criteria

A
  • Circulating immune complex
  • Hypocomplementemia
  • IgG (or other) deposition in vessel wall
  • Complement deposition in vessel wall
120
Q

Vasculitis has to be diagnosed with?

A

Biopsy

121
Q

Vasculitis Infectious:

A

From pathogen directly invading wall.

Recognize that infectious can generate an immune-mediated inflammation.

122
Q

Vasculitis Non-infectious

A

Non-infectious from immune-mediated inflammation.

123
Q

Variability in Non-Infectious Vasculitis

A

Disease occurs from complexes; presentation is location-dependent

124
Q

Vasculitis =

A

Vessel Wall Inflammation with necrosis of vessel walls, narrow/occlusion +/- aneurysms

125
Q

Kawasaki’s Disease

A

Kawasaki’s Disease Vasculitis
• Exact etiology is uknown
• Most likely delayed hypersensitivity T
cell reaction

126
Q

Kawasaki’s Disease Presentation:

A
  • Asian children < 4 years old
  • “strawberry tongue”
  • Lymphadenitis, conjunctivitis
  • High association with developing coronary aneurysms
127
Q

Buerger’s Disease

Thromboangitis Obliterans

A
  • SMOKING, SMOKING, SMOKING

* Treat: smoking cessation!

128
Q

Buerger’s Disease
(Thromboangitis Obliterans)
Presentation:

A
  • Heavy smokers
  • Males < 40
  • Intermittent claudication –> gangrene + autoamputation of digits
  • Radial arteries often affected –> Raynaud’s Phenomenon
129
Q

Temporal (Giant-Cell) Arteritis:

A 
• Exact etiology unknown
• Most likely T-cell mediated response
against vessel antigen
• Affects arteries neck and up
• Most common vasculitis in elderly people
(females)
130
Q

Temporal (Giant-Cell) Arteritis Presentation:

A
  • Female patients > 50 y/o
  • Unilateral headache + jaw claudication
  • Irreversible blindness (opthalmic artery occlusion)
  • Associated with polymyalgia rheumatica
131
Q

Temporal (Giant-Cell) Arteritis Morphology

A
  • Affects branches of carotid artery

* Focal granulomatous inflammation

132
Q

Temporal (Giant-Cell) Arteritis Labs

A

↑ ESR

133
Q

Temporal (Giant-Cell) Arteritis Treatment

A

High Dose Steroids

134
Q

Fats have two functions:

A
  1. P-lipids + cholesterol = structural part of all cell membranes
  2. Triglycerides (TG) and FFA = energy sources of body
135
Q

General Flow of Transport Fats:

A
  1. TG in Liver/Gut —-> Muscle (energy) and Fat (storage)
  2. Cholesterol across tissue —> Liver
    - –All cells make cholesterol; they have excess; rarely deficient
136
Q

Lipoprotein Functions:

A
  1. Carry p-lipids, free cholesterol, cholesterol esters, TG, and apolipoproteins
    - –Apo’s have structural, cofactor, and receptor roles
  2. Allow easy circulation of fat throughout body
137
Q

Lipoprotein Pathophysiology Disease Overview

A
  1. Genetic disease: think mutation in apo, apo-receptor, or enzymes
  2. Environmental disease: think overproduction of certain component
138
Q

CM + VLDL =

A

TG Rich Lipoproteins

139
Q

CM made in?

A

GI

140
Q

VLDL made in?

A

Liver

141
Q

CM has?

A

apoB-48 (no LDL receptor)

142
Q

VLDL has?

A

apoB-100

143
Q

• TG removed from and via?

A

CM or VLDL via LPL

144
Q

LPL hydrolyses?

A

TG –> FFA + Monoglyc.

145
Q

VLDL =

A

↑TG + ↑Cholesterol

146
Q

Post LPL =

A

IDL/LDL w/↑Cholesterol

147
Q

ApoE =

A

Liver, Macrophages, CNS
—Macrophages w/cholesterol secrete
apoE with the cholesterol; important b/
c macrophages are involved in athero

148
Q

Hypobetalipoproteinemia =

A

trunc apoB ↓ApoB Production
• Truncated apoB secreted ↓, excreted ↑
by renal tubule

149
Q

Hypobetalipoproteinemia Genetics Heterozygotes:

A

Heterozygotes: 25-50% of LDL; steatosis

150
Q

Hypobetalipoproteinemia Genetics Homozygotes:

A

Homozygotes: ↓↓↓LDL and CM

  • –Fat malabsorption –> ↓Vit A,D,E, K
  • –Acanthocytosis
  • –Neuromuscular Degeneration (↓VIt E)
151
Q

Hypobetalipoproteinemia - Physiology

A

Intestine and liver REQUIRE apoB to export TG
• ApoB = hydrophobic; remains in membrane of ER and grabs p-lipids,
TG, esters and free cholesterol = forming lipoprotein
• Secreted; acquire additional apo-proteins from HDL in blood

152
Q

Hypobetalipoproteinemia Pathophysiology:

A

• Partial (heterozygotes) or full (homozygote) truncation of apoB –>
inability to export TG from gut (48) or liver (100) in CM + VLDL
• Expect to see ↓CM and ↓LDL levels (↓Synthesis and ↓Secretion)

153
Q

Abetalipoproteinemia =

A

Deficient MTP

↓CM + ↓VLDL production (RECESSIVE)

154
Q

Abetalipoproteinemia Heterozygotes:

A

No abnormal values.

155
Q

Abetalipoproteinemia Homozygotes:

A

↓CM + ↓LDL

  • –Similar sympotoms as hypo-beta
  • –↓ApoB containing lipoproteins (DDx)
156
Q

Abetalipoproteinemia Physiology:

A

MTP = Manages Transport & Particle formation
• Shuttles TG and cholesterol esters: membranes lipoproteins
• Controls lipid particle / droplet formation for apoB to attach

157
Q

Abetalipoproteinemia Pathophysiology

A
  • If apoB does not accumulate lipoprotein components –> degrades
  • ↓MTP –> ↓Shuttling of TG + ↓Lipoprotein Particle –> apoB degrade
158
Q

Familial Combined Hyperlipidemia (FCHL) =

A 
• Some patients have ↑ApoB Production
---B/c one gene cluster causing FCHL also
involved in apoB/LDL metabolism
• ↑Risk of CVD
---↑## of small dense particles -->
↑atherogenic risk of LDL
• Family with varying lipid phenotypes,
• Consistent ↑VLDL of NORMAL
COMPOSITION
159
Q

Familial Combined Hyperlipidemia (FCHL)

Physiology

A

apoB is key in forming lipoproteins CM and VLDL

160
Q

Familial Combined Hyperlipidemia (FCHL)

Pathophysiology

A
  • ↑ApoB synthesis —> ↑VLDL synthesis by liver (normal composition)
  • ↑VLDL —> ↑LDL
161
Q

Familial Combined Hyperlipidemia (FCHL)

Consequences of ↑LDL

A
  1. ↑VLDL Production + ↓LDL Clearance –> ↑Normal LDL –> ↑Cholesterol (b/c TG is removed via LPL)
  2. ↑VLDL Production + ↓Cholesterol Accumulation –> ↑LDL apoB (low TG and low cholesterol) –> HYPERAPOBETA
  3. ↑VLDL production + ↑LDL Clearance –> normal/↓LDL apoB and cholesterol
162
Q

Familial Dysbetalipoproteinemia

Type III Hyperlipidemia

A 
• ↑Beta-VLDL in plasma = ↑Risk Athero
---Cholesterol rich
---Labs: ↑TG + ↑Cholesterol
• Called “Broad-Beta” Disease
• E2/E2 genotype
---Normal VLDL, but...
---Post-delipidation, cannot bind to LDL-R
---Accumulates cholesterol via HDL CETP
• Analysis will look like ↑VLDL, but these
are composed of ↑cholesterol
163
Q

Familial Dysbetalipoproteinemia
(Type III Hyperlipidemia)
Possible Genotypes

A 
• E2/E2 = ↓+ charge in ApoE LDL-R
binding domain
• E2/E2 genotype is 1%, but frequency of
this disease ~ 10,000 (rare)
---B/c mutation not inside AA 140-160
• 1-2 E2 alleles = ↓LDL + ↑TG
---Even without Type III HLP
• 1-2 E4 alleles = ↑LDL + ↑TG
---↑LDL b/c better IDL--> IDL conversion
164
Q

Familial Dysbetalipoproteinemia
(Type III Hyperlipidemia)
Alzheimer’s Risk

A
  • ApoE4 best predictor for Alzheimer’s

* ApoE2 protects against Alzheimer’s

165
Q

Familial Dysbetalipoproteinemia
(Type III Hyperlipidemia)
Physiology:

A

• AppE clears remnants of TG rich lipoproteins = CM/VLDL remnants
• ApoE gets into circulation via HDL or LDL, b/c these come from liver
—CM never has ApoE before plasma b/c ApoE not made in intestine
• Reservoir of ApoE is in HDL; new VLDL/CM particles get ApoE when they enter plasma from HDL transfer
• Post-lipolysis (TG removal via LPL), the ApoE donation to CM/VLDL allows them to bind to both B-E receptors on liver
—B-E receptors = LDL-R that bind both ApoB (LDL) and ApoE (IDL)
—Remnants are atherogenic; important to remove!

166
Q

Familial Dysbetalipoproteinemia
(Type III Hyperlipidemia)
Pathophysiology

A 
• AppE normally binds E-LDL-R via charge interaction (ApoE is ++++)
• If + charge is lost --> binding is disrupted
---Note charge mutation has to exist AND it has to be in the LDLReceptor
binding region (AA 140-160)
• IEF Gel for ApoE Shows
---ApoE-3 = normal charges
---ApoE-2 = ↓+ or ↑- charge
---ApoE-4 = ↑+ or ↓- charge
167
Q

Why is Beta-VLDL Bad?

A

Beta-VLDL, like LDL, is taken up by macrophages, but does not need to be oxidized first –> ↑foam cell formation

168
Q

Changes in ApoA1 Production Cause:

A 
• Mutated ApoA1 --> ↓HDL Levels
• Most likely responsible for
hypoalphalipoproteinemia (↓HDL) and
hyperalphalipoproteinemia (↑HDL)
• Most have ↑atherosclerosis
Exception
• ApoA1 Milano == Rapid RCT
• Still have ↓HDL levels
169
Q

LCAT Deficiency / Fish Eye Disease =

A 
↓HDL Cholesterol
• No LCAT = no FC --> CE in pre-HDL
• HDL particles don’t acquire spherical
shape b/c no hydrophobic ester
• +/- Poor RCT; could be fine or terrible
170
Q

LPL Deficiency Causes

A 
↓ HDL Cholesterol
• LPL genetic defect, ↓ApoC2, ↑ApoC3,
↓Insulin (DKA)
• LPL delipidizes VLDL and gives extra
superficial material to the growing HDL3
particle --> HDL2
• Ability to grow HDL3 w/CE is important for
ccn-gradient transfer into liver via SR-B1
171
Q

Abnormal ↑Hepatic Lipase Activity Causes:

A 
↑HDL Clearance = ↓HDL Cholesterol
• HL can ↑HDL uptake in liver, but does not
recycle HDL/ApoA1
↑HL From:
• Hyperinsulinemia
• Hyperthyroidism
• Hyperandrogenism
↓HL From:
• Estradiol
• Adiponectin (cytokine in thin people)
172
Q

Physiology - Reverse Cholesterol Transport (RCT)

A
  1. ApoA1 from liver/GI –> adds to disc-shaped nascent pre-beta HDL
  2. Cholesterol Efflux from Cells
  3. Free Cholesterol –> Cholesterol Esters (FC–>CE)
  4. HDL2 Uptake from Liver
  5. Cholesterol Ester Transfer Protein (CETP)
    CETP levels don’t determine activity; CETP-Inhibitor levels do!
173
Q

CETP Deficiency Yields:

A

↑CETP-I / ↑LTIP === (6-Fold)↑HDL2 Cholesterol

174
Q

The real goal of cholesterol should be LDL

A

LDL<70 in those with other risk factors-not on test…

175
Q

Stenosis:

A

Narrowing of orifice –> valve doesn’t open correctly

176
Q

Regurgitation (=insufficiency):

A

Leakage in opposite direction –> valve doesn’t

close correctly

177
Q

Cardiac Adaptation

Concentric Hypertrophy:

A

Pressure Overload = STENOSIS (+HTN)

—↑Thickness (thick walls) but normal volume - “LV Hypertrophy”

178
Q

Cardiac Adaptation

Eccentric Hypertrophy:

A

Volume Overload = REGURGITATION

—↑Dilation of Chamber (more volume + thin walls) —> ↑Output (Starling’s Law)

179
Q

Valvular Heart Disease Acute

A

In acute scenarios, there is no time to adapt; pt presents severely ill. Murmur heard, but no concentric/eccentric hypertrophy
• Thus, expect to see ↑↑ΔP in acute scenarios with ↓structural heart changes.

180
Q

Valvular Heart Disease Chronic

A

↓↓ΔP with ↑structural heart changes in chronic

181
Q

Diseased Aortic Valve Rheumatic:

A

Micro-vegetation (not as much as infective endocarditis) + FUSION of COMMISURES

182
Q

Diseased Aortic Valve Calcification/Bicuspid:

A

Sinus of Valsalva calcification + NO FUSION

183
Q

Symptoms of Stenosis

A

Syncope, Angina, Heart Failure, Arrhythmias

184
Q

Types of Stenosis

A

Supravalvular Stenosis
Valvular Stenosis
Subvalvular

185
Q

Supravalvular Stenosis:

A

Above the valve; congenital (ex: narrowing of aorta).

186
Q

Valvular Stenosis:

A

At the valve; congenital or acquired.

187
Q

Subvalvular:

A

Below the valve, congenital or acquired ex: IV septum pushing into one ventricle.

188
Q

When is stenosis TOO severe?

A

Valve area depends on two things:

  1. Gradient - pressure drop across LV and Aorta in systole (normally 0)
  2. Flow Across Stenosed Valve approximated by CO
189
Q

Stenosis Evaluation:

A

ECHO – view diseased valves, hypertrophy and blood flow.

190
Q

Stenosis Pathology Basics:

A

Valves = AVASCULAR endothelial-lined (endocardium)

—Core of PG, GP, Collagen (Type 1) Fibers, and Fibroblasts

191
Q

Post-Streptococcal Molecular Mimicry?

A

2-3 weeks post strept infection form Ab:

cross react with cytoskeletal proteins

192
Q

What valve is affected?

A

Mitral > Aortic > Tricuspid > Pulmonary
—Mitral valve experiences the most pressure
in the entire heart.

193
Q

Possible exam topic?

Fusion of commisures?

A

Occurs in RF, but not in calcified aortic stenosis.

194
Q

Rheumatic Fever Presentation:

A

• 2-3 Weeks Post-Streptococcal Infection
• “Dog that licks the joint, but bites the heart” === TRANSIENT
(except long term pericarditis effects)

195
Q

Mitral Valve Stenosis

Rheumatic Fever

A

↑P behind the mitral (stenosed) valve
—Concentric hypertrophy + dilation of the LA
—Pulmonary Hypertension-> Atherosclerosis
—Concentric hypertrophy of RV!
—Thrombi (stasis) from damaged + dilated
LA –> Ball/Valve + Emboli

196
Q

Mitral Valve Stenosis
Rheumatic Fever
Presentation:

A
  • SOB (pulmonary HTN –> ↑Pressure in Pulmonary Capillaries –> Capillary Congestion –> ↑fluid in alveolar space)
  • Alveolar Fluid w/fibrinous material, RBC (+macrophages if chronic)
  • Hemoptysis (if chronic)
  • Right Heart Failure
  • Atrial Fibrillation –> Brain emboli –> Stroke
  • Dysphagia (atria compresses back on esophagus)
197
Q

Mitral Valve Regurgitation Causes:

A
  1. MITRAL VALVE PROLAPSE
  2. Left Ventricular Dilation
    - –Left sided heart failure dilates ring of MV
  3. Rheumatic Fever
198
Q

Mitral Prolapse Leaflets replaced by?

A

Myxomatous (spongy) tissue

199
Q

Mitral Valve Regurgitation Presentation:

A
  • Can be asymptomatic with murmur
  • Sudden rise in Atrial pressure
  • ↑Preload (from atrium) + ↓Afterload (from venting) = ↑↑SV
200
Q

Mitral Valve Regurgitation
Acute vs. Chronic: EXAM QUESTION
• Acute =

A

No change in RA volume (adaptation), ↑Pulmonary Capillary Wedge Pressure (large pressure build up)

201
Q

Murmur For MV Regurgitation

A

Systolic murmur= pansystolic: S1——S2

202
Q

Aortic Valve Stenosis Causes:

A
  1. Age-Related Calcification
    - –Calcified aortic stenosis from wear/tear
    - –Calcification in Sinuses of Valsalvas
    - –”Arthritis of the aortic valve”
  2. Bicuspid Aortic Valve
    - –Congenital Failure of Apoptosis
    - –Prone to calcification –> stenosis
203
Q

Aortic Valve Stenosis Pathophysiology:

A

In both, ↑P in LV —> LV Concentric

Hypertrophy –> HTN, Angina, Syncope

204
Q

Aortic Valve Stenosis Presentation:

A
  • Pt > 60 = Calcified
  • Pt ~ 35-40 = Bicuspid Aortic Valve
  • Delayed/Absent Arterial Pulse
  • Heart Failure
  • Angina = O2 demands from ↑work
  • Syncope = ↓supply (fixed CO)
  • Arrhythmia
  • Sudden death
205
Q

Aortic Valve Stenosis Murmur:

A

Systolic diamond shape murmur S1 –<>– S2

206
Q

Mitral Valve Stenosis Murmur

A

Diastolic murmur: S1——S2 OS⤷S1

207
Q

Aortic Valve Regurgitation Disease of?

A

Aorta/Aortic Cusps

208
Q

Disease of Aorta/Aortic Cusps Pathophysiology:

A
  • ↑LV Volume == ↑Preload + ↑Eccentric Hypertrophy (dilation) == ↑SV (Starling)
  • ↑SV + aortic venting = ↑pulse pressure
209
Q

Infective Endocarditis Two Requirements:

A
  1. BUGS in BLOOD
    - –Any pathogen (virus, bacteria, fungi)
  2. Abnormal Heart Valve
210
Q

Infective Endocarditis Pathology:

A

• ↑Velocity blood across abnormal valve
• Platelets adhere –> thrombus formation
• Bacteria bind to injured endothelium
(direct contact / fibronectin mediated)

211
Q

Infective Endocarditis Consequences

A 
• Valve vegetation, regurge, destruction
• Metastatic infection (Osteomyelitis)
• Immune Reaction (Arthritis, nephritis)
• Local spread (myocarditis, pericarditis)
• Septic Embolus (Mycotic Aneurysm)
---Coronary vessels (MI), kidney, hand
212
Q

Bacteremia =

A

Living bacteria in blood.

213
Q

Septicemia =

A

↑invasion + replication in blood stream.

214
Q

Infective Endocarditis Source of Infection

A
  • –IVDU (polymicrobial); Prosthetic Valves (PVE)
  • –Dental procedures involving gingiva/gums
  • –Catheters/iatrogenic.
215
Q

Infective Endocarditis Treatment:

A
  • Recall –> VALVES = AVASCULAR
  • Fibrin verruca forms colonies of bacteria; because avascular valves high dose of abx needed to kill bacteria via passive diffusion.
216
Q

Infective Endocarditis Microbiology:

A 
Gram + is most common EXAM*
• Acute IE = Staph Aureus
• Subactue = Strep Viridans
• Non-enterococcal Group D (S.Bovis -- look for GI disease)
Gram - in Key Patient Profiles
• Pseudomonas Aeruginosa in IVDU
and PVE
Fungal
• Also in IVDU and immuno-deficient
Culture Negative?
• Prior ABX most common cause
217
Q

Infective Endocarditis Presentation:

A
  • IV Drug abusers (polymicrobial)
  • Immune compromised (Fungal)
  • Age: 30 (pre-antibiotic, more women); 50% >50 (last decade, men)
  • Subacute = nonspecific symptoms; ACute = ill + stroke/arthritis
  • Splinter Hemorr – embolization ≠ 100% diagnostic septic emboli
  • Roth Spots (eye)
  • Janeway Lesions (septic emboli in palms of hands)
  • Osler Nodes (immune complexes in fat pads)
218
Q

Infective Endocarditis Morphology:

A
  • Note large friable vurruca (vegetation) on mitral valve
  • Valves often erode and perforate
  • Fungal vegetations larger than bacterial, though less common
  • Tricuspid valve commonly infected in Drug users.
219
Q

Infective Endocarditis Tests:

A
  • CULTURE, CULTURE, CULUTRE

* TEE - closer to the heart

220
Q

Non-Infective Endocarditis (NBTE)

“Marantic”

A 
Non-Infective Thrombotic Endocarditis
• Aseptic vegetations = thrombotic
deposits on endocardium
• Often in Libman-Sacks Disease (SLE),
DIC, Paraneoplastic
221
Q

Non-Infective Endocarditis (NBTE)
“Marantic”
Morphology:

A

• Like infective, there are vegetations on valves, CT, and mural endocardium; unlike infective, there are vegetations on papillaries
(no septal defects here)
• NO INFLAMMATION = STERILE

222
Q

Pericardial Disease is?

A

• Disease of fluid accum., inflammation, fibrous constriction of pericardium
• Disease of DIASTOLE
—Prevents heart from relaxing (expanding)

223
Q

Pericardial Disease Characteristic Findings:

A
  1. Gets better when they lean forward

2. Friction rub from serous/parietal layers rubbing together.

224
Q

Pericardial Response to Injury Acute:

A

Congestion, Transudate, Exudate (fibrin, inflammation).

225
Q

Pericardial Response to Injury Chronic:

A

Exudate –> Fibrosis (adhesions + calcifications)

226
Q

Pericarditis + Pericardial Effusion?

A

Go hand in hand.

227
Q

Pericardial effusion:

A

Abnormal accum of serosal fluid in pericardial sac—If chronic accumulation (even though large) –> sac dilates –> asymptomatic
but w/↑Halo on Chest Xray

228
Q

Cardiac Tamponade:

A 
MEDICAL EMERGENCY (rapid accumulation) --> pulsus paradoxus
---Volume is less important than RATE (heart can accumulate 600 ml/mo without tamponade, but not 300 ml/min)
229
Q

Pulsus Paradoxus

A

• Loss of heart beat on inspiration
• Inspiration –> ↓Intrathoracic Pressure –> ↑Blood to RA (but cannot expand b/c of pericardial disease/effusion) –> ↑Volume distorts IV septum into LV –> ↓Preload (↓LVEDV) –> ↓SV –> HYPOTENSION
• Starling Curve (Pressure/Volume) –> Results in ↑ΔP for small ΔLVEDV, but
overall ↓Pressure

230
Q

Pericarditis Etiology (more often secondary than primary):

A

• Infectious: viral (primary), bacterial (lung infection), fungal, protozoal
• Immune Mediated: secondary to systemic inflammatory disease (SLE, RF, Scleroderma, PAN, RA) —Often see polyserositis (serosa attacked)
• Other: MI (Dresslers), Renal Failure
(Uremia - metabolites from urine damage pericardium), Trauma, Pancreatitis

231
Q

Pericarditis Key to DDx:

A 
Pericardial Fluid 
• Heart/Kidney Failure = Serous (clear/
straw colored)
• Viral Infection = Sero-sanguinous
• Bacterial Infection = Purulent + Serosanguinous
• Mycoardial Rupture = Sanguinous
• Trauma = sero-sanguinous
• Drugs = serous
232
Q

Pericarditis: Acute Pericarditis:

A

• Serous: mild inflammation + exudate
• Fibrinous: inflammation + fibrin strands in pericardial fluid
—”Shaggy” or “Bread and Butter” = PMN, Fibrin, RBC
—MOST COMMON
• Purulent: INFLAMMATION + PMNs
—Bacterial –> extension of nearby lung infection
—Often organizes –> granulation tissue w/capillaries and myofibro’s
—Gran tissue can lead to pericardial layer adhesion that may develop
into constrictive endocarditis
—Exudate –> Fibrosis = adhesions, restrictions
• Caseous: TB
• Hemorrhage: inflammatory exudate with RBC

233
Q

Pericarditis: Chronic Pericarditis:

A
  • Adhesions: chronic infections, repeated acute pericarditis (fibrosis)
  • Constriction: fibrosis + calcification fuse the pericardial layers.
234
Q

Pericarditis Labs/Tests:

A
  • Silhouette/halo on CX-Ray

* Friction rub (fibrinous pericarditis especially)

235
Q

Pericardial Effusion

Acute and Chronic Fluid Accumulation

A

• Acute vs. Chronic: recall that rate of
↑volume > amount of volume
• Mesothelial cells don’t offer passage to
fluid –> effusion during pericardial injury

236
Q

Acute Pericardial Effusions

A

Ruptured MI, trauma, etc.

237
Q

Chronic Pericardial Effusions

A
  1. Heart Failure, Myocarditis, RF
  2. Collagen Vascular Diseases
  3. Chronic Infections
  4. Chronic Renal Disease
  5. Neoplasms
    - –Breast and lung seen the most (common)
    - –Melanoma and lymphoma (preference)
  6. Radiotherapy
238
Q

Pericardial Effusions Presentation:

A
  • If chronic, can be asymptomatic

* If acute (hemopericardium) –> pulses paradoxus –> EMERGENCY

239
Q

Pericardial Effusions Types:

A
  1. Hydropericardium (Transudate)
  2. Hemopericardium (Blood)
  3. Chylopericardium (Lymph)
240
Q

Chylopericardium (Lymph)

A

= Rare

—Lymph from thoracic duct

241
Q

Hydropericardium (Transudate):

A
  • –Associated with anasarca

- –NO INFLAMMATION

242
Q

Hemopericardium (Blood):

A

—Blood accumulates over wks/months –> ↑intrapericardial P –> ↓SV
and ↓CO
—Ruptured MI (Req. transmural, ↑ventricular Pressure)
—Ruptured dissecting hematoma
—Aortic dissection
—Trauma
—Iatrogenic

243
Q

Pericardial Effusions Labs/Tests

A

Silhouette/halo on CX-Ray

Cardiology (10 decks)

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