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1. HDS Cardiology > Pathology > Flashcards

Pathology Flashcards

1
Q

Atherosclerosis

A

Chronic progressive inflammatory process of multifactorial etiology affecting small and large arteries.

  • Formation of fibrofatty plaques
  • Stenosis of vascular lumen
  • Ass. degenerative changes in vascular media
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2
Q

Atherosclerosis

AHA Classification

A
  • Type I ⇒ fatty dot
    • Foam cells
  • Type II ⇒ fatty streak
    • Intracellular lipid
  • Type III ⇒ intermediate
    • Small extracellular lipid pools
  • Type IV ⇒ atheroma
    • Lipid core
  • Type V ⇒ fibroatheroma
    • Fibrotic layer, calcification, or fibrosis
  • Type VI ⇒ complicated lesion
    • Surface disruption
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3
Q

Fatty Streaks

A
  • 1st stage of atherosclerosis
  • Foam cells, T cells, and small amount of extracelluar lipids
  • Found in aorta of all children > 10 y/o
  • Not all will become plaques
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4
Q

Plaques

A
  • Cellular constiuents
    • Endothelial cells/ECM ⇒ injury starts process
      • ↑ Adhesion molecules
      • Becomes leaky
    • Lymphocytes, mainly T cells
      • Mediate chronic inflammation
      • Secrete IFN-𝛾 to activate MΦ
    • MΦ
      • Pro-inflammatory ⇒ IL-1, TNF
      • Oxidize LDL
    • Lipid core
      • Oxidized LDL toxic to endothelium and VSMC
      • Ingested by MΦ
      • ↑ Expression of adhesion molecules
      • Promotes/keeps MΦ there
    • Vascular smooth muscle cells (VSMC)
      • Migrate in from vascular media
      • Proliferate and secrete ECM proteins
  • Common places
    • Elastic arteries
      • Aorta, carotid, iliac
    • Large and medium muscular arteries
      • Coronary, popliteal
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5
Q

Complicated Lesions

A

Erosion, ulceration, rupture

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6
Q

Atherosclerotic

Thrombus Formation

A
  • Clot forms on the plaque surface
  • May lead to
    • ↑ Stenosis
    • Plaque rupture / fragmentation ⇒ embolization ⇒ distal ischemia
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7
Q

Plaque Hemorrhage

A
  • Bleeding can occur within the plaque
  • Results in rapid enlargement
  • If plaque does not rupture ⇒ blood clots and organizes over time
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8
Q

Aneurysmal Dilation

A
  • Results from thinning/weakening of arterial media
  • Weakened portion expands under arterial pressure
  • Creates an outpouching
  • Often leads to thrombus formation
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9
Q

Atherosclerosis

Pathogenesis

A

Response to injury hypothesis:

  1. Endothelial injury
  2. Inflammation
  3. Accumulaiton of lipoproteins
  4. Oxidation of lipoproteins
  5. Adhesion of monocytes and platelets
  6. Migration and proliferation of VSMCs
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10
Q

Endothelial Injury

A
  • Endothelial injury ⇒ endothelial cell activation
    • Multifactorial etiology
    • Turbulent blood flow
    • Hypercholesterolemia
  • Activated endothelial cells
    • ↑ Permeabiity
    • ↑ Leukocyte adhesion
    • ∆ Gene expression
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11
Q

Endothelial Dysfunction

A
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12
Q

Atherosclerosis

Role of Inflammation

A
  • Injured endothelium ⇒ adhesion molecule expression ⇒ recruitment of monocytes and T-cells
  • Monocytes ⇒ MΦ
  • MΦ remove lipids ⇒ foam cells
  • Lesion progression
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13
Q

Atherosclerosis

Role of Lipoproteins

A
  • Chronic HLD may impair endothelial cell function
  • Lipoproteins accumulate @ foci of ↑ EC permeability
  • Lipids + free radicals ⇒ oxidized LDL ⇒ ingested by MΦ ⇒ foam cells
  • Consequences
    • Stenosis
    • Thrombosis
    • Vasoconstriction
    • Acute plaque change
      • Rupture/fissuring ⇒ exposes highly thrombogenic plaque constituents
    • Erosion/ulcration ⇒ exposes thrombogenic subendothelial BM to blood
    • Hemorrhage into atheroma ⇒ expands volume
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14
Q

Atherosclerosis

Sequelae

A
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15
Q

Aneurysm

Formation

A

Most common location ⇒ abdominal aorta

(Distal to renal aa / Proximal to bifurcation)

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16
Q

Aneurysm

Classification

A

By shape and size:

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17
Q

Dissection

A

Occurs when blood seperates laminar planes of the media.

Forms a blood-filled channel within the vessel wall.

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18
Q

CVD

Risk Factors

A
  • HTN
  • HLD
  • Smoking
  • Obesity
  • DM
  • Age
  • Sex ⇒ estrogen protective
  • Genetics
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19
Q

Hypertension

Effects on Atherosclerosis

A

HTN associated with:

  • Hyaline arteriolosclerosis
    • Homogenous pink hyaline thickening and luminal narrowing
  • Hyperplastic arteriolosclerosis
    • Seen with malignant HTN
    • Lesion called ‘onion-skinning’
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20
Q

DM

Effects on Atherosclerosis

A
  • Causes macrovascular and microvascular disease
  • ↑ Risk of MI and stroke
  • 100x ↑ risk of atherosclerosis-induced gangrene of LE
  • Complex mechanism
    • Advanced glycation end products (AGEs) ⇒ accelerate endothelial injury
    • Intracellular hyperglycemia ⇒ ↑ susceptibility to oxidative stress
    • Insulin’s vasoprotective effects
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21
Q

Hypoxemia

A

Failure to deliver adequately oxygenated blood to tissues

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22
Q

Ischemia

A

Hypoxemia & inadequate removal of metabolites

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23
Q

Subendocardial MI

Pathogenesis

A
  • Subendocardium least well perfused
  • Relies on diffusion from ventricular space
  • Can be precipitated by shock from bleeding or sepsis
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24
Q

MI Pathology

Overview

A
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25
Q

2-4 Hours Post-MI

A

Can only see areas of infarction with TTC staining

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26
Q

12 Hours Post-MI

A
  • Micro
    • Wavy fibers
    • Pyknosis
    • Hyperesosinophilia
    • Hemorrhage
  • Gross
    • Mottling
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27
Q

24 Hours Post-MI

A
  • Left
    • Pyknosis
    • Hypereosinophilia
    • Few PMNs
  • Right
    • Dark contraction bands
    • Nuclei absent
    • Acute inflammation starting
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28
Q

2 Days Post-MI

A
  • PMNs infiltrate
  • Loss of striations
  • Loss of nuclei
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29
Q

3-4 Days Post-MI

A

Inflammatory cells including MΦ

Necrotic myocytes

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30
Q

3-7 Days Post-MI

A
  • Hyperemic border
  • Depressed sunken yellow area
  • Highest risk for rupture of the infarcted area
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31
Q

1 Week Post-MI

A

Very early granulation tissue

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32
Q

7-10 Days Post-MI

A

MΦ

Numerous capillaries

Immature collagen

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33
Q

2 Weeks Post-MI

A

More developed vessels

↑ Collagen

Maturing granulation tissue

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34
Q

2-4 Weeks Post-MI

A

Continued in-growth of capillaries

Fibroblasts w/ collagen deposition

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35
Q

2 Months Post-MI

A
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36
Q

Healed MI

A
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37
Q

Reperfusion Injury

A
  • Generally reperfusion beneficial
  • “New” cellular injury may occur
    1. Infiltrating WBCs generate oxygen free radicals
    2. Apoptosis
    3. Microvascular injury ⇒ hemorrhage and endothelial cell swelling
    4. Occlusion of capillaries ⇒ prevent reperfusion
    5. Contraction band necrosis
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38
Q

MI

Mortality

A
  • ½ of all deaths due to acute MI occur within 1 hour of onset
  • 30% overall mortality in the 1st year
  • Risk factors:
    • Advanced age
    • Female gender
    • DM
    • Previous MI
  • 75% have post-MI complications
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39
Q

Complications of MI

A
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40
Q

Myocardial Rupture

A

Full thickness hole through part of the heart

  • Ventricular free wall
    • Hemopericardium ⇒ cardiac tamponade
    • Highest risk 3-7 days post MI
  • Ventricular septum
    • L to R shunt ⇒ murmur and CHF
  • Papillary muscle
    • Acute, severe MR
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41
Q

Pericarditis 2/2 MI

A
  • Fibrinous or fibrino-hemorrhagic ⇒ bread and butter appearance
  • Usu. occurs 2-3 days post transmural MI
  • Usually resolves
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42
Q

Right Ventricular Infarct

2/2 MI

A

Usually seen with MI of the adjacent posterior LV and ventricular septum

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43
Q

Extension

A

New necrosis adjacent to an existing infarct

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44
Q

Expansion

A

Stretching, thinning, and dilation of the infarcted region.

Seen most often in anteroseptal infarcts.

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45
Q

Mural Thrombus

A

Focal abnormal in contraction ⇒ stasis

Endocardial damage ⇒ thrombogenic surface

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46
Q

Ventricular Aneurysm

A
  • Late complication
  • Bounded by scarred myocardium
  • Usually from large anteroseptal MI that has undergone expansion
  • Bulges during systole
  • Rupture does not occur
  • Complications
    • Mural thrombus
    • Arrhythmias
    • Heart failure
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47
Q

Chronic Ischemic Heart Disease

(CIHD)

A

“Progressive late heart failure”

  • Exhaust compensatory hypertrophy of viable myocardium ⇒ cardiac decompensation
  • Slow progressive onset of CHF s/p MI
  • Accounts for ~ 50% of cardiac transplants
  • Enlarged, heavy heart with LV hypertrophy and dilation
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48
Q

Sudden Cardiac Death

A
  • 80-90% due to IHD
  • Typically due to a lethal arrhythmia
  • Increased cardiac mass is an independent risk factor
  • Prognosis improved w/ automatic defibrillators
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49
Q

Atrial Natriuretic Peptide

(ANP)

A
  • Produced by atrial cells
  • Causes:
    • Vasodilation
    • Natriuresis
    • Diuresis
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50
Q

Cardiac

Gap Junctions

A
  • Ensure synchronous contraction through electrical coupling
  • Ischemia and myocardial disease ⇒ abnl spatial distribution of gap junctions
    • Contributes to electromechanical dysfunction and heart failure
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51
Q

Cardiomyopathy

Structural Changes

A
  • Chambers
    • ↑ LA cavity size
    • ↓ LV cavity size
    • Sigmoid septum
  • Valves
    • AV calcification
    • MV annular calcification
    • Fibrosis of leaflets
    • Buckling of mitral leaflets towards LA
    • Lambl excrescences ⇒ small filiform processs on the closure lines of aortic and mitral valves
  • Epicardial coronary arteries
    • Tortuosity
    • ↑ Cross-sectional luminal area
    • Calcification
    • Atherosclerosis
  • Myocardium
    • ↑ Mass
    • ↑ Subepicardial fat)
    • Brown atropy
    • Lipofuscin deposition
    • Basophilic degeneration (by-product of glycogen metabolism
    • Amyloid deposits
  • Aorta
    • Dilated ascending aorta with rightward shift
    • Elongated thoracic aorta
    • Sinotubular junction calcification
    • Elastic fragmentation and collagen accumulation
    • Atherosclerosis
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52
Q

Heart Failure

Pathophysiology

A

6 principal mechanisms underlie heart failure:

  1. Pump failure
  2. Obstruction to flow
  3. Regurgitant flow
  4. Shunted flow
  5. Conduction abnormalities
  6. Rupture of heart or major vessel
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53
Q

Cardiomyopathy

A

A primary abnormality of the myocardium.

  • Primary vs secondary
  • Classified based on morphology
    • Dilated
    • Hypertrophic
    • Restrictive
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54
Q

Dilated Cardiomyopathy

A

“Congestive cardiomyopathy”

  • Progressive dilation and contractile dysfunciton
  • Most common form ⇒ 90%
  • Onset 20-50 y/o
55
Q

Etiology of Dilated Cardiomyopathy

A
  • Familial ⇒ 25-35%
    • Most AD w/ variable penetrance
    • Typically affect cytoskeleton
      • Also proteins of sarcomere, mitocondria, nuclear envelope
    • X-linked form
      • Mutation in dystrophin gene
      • Presents in teens to early 20’s
      • Rapidly progressive
  • Acquired
    • Toxin-induced
      • ETOH and acetaldehyde directly toxic to myocardium
        • Thiamine deficiency may contribute
      • Chemotherapeutic agents like doxorubicin
    • Inflammatory ⇒ myocarditis
      • Coxsackie B virus and other enteroviruses
    • Pregnancy associated
      • Occurs in late pregnancy or weeks-months postpartum
      • HTN, volume overload, nutritional deficiencies, immune rxn may be involved
56
Q

Dilated Cardiomyopathy

Appearance

A
  • Gross
    • Enlarged globular heart
    • Usu. all chambers dilated
  • Micro
    • Myocyte hypertrophy and stretching
    • Nulcear enlargement
    • Interstitial fibrosis
    • Inflammatory infiltrates
57
Q

Hypertrophic Cardiomyopathy

A

“Idiopathic hypertrophic subaortic stenosis (IHSS)”

  • Symmetic and asymmetrical patterns
    • 30% w/ outflow obstruction
  • Loss of compliance ⇒ diastolic dysfunction
  • Systolic function usually hyperdynamic
  • Etiology:
    • Familial ⇒ 50%
    • Friedreich ataxia
    • Storage diseases
    • Infants of diabetic mothers
  • Pathophysiology: mutations in structural proteins of scarcomere ⇒ diastolic dysfunction, myocyte hypertrophy, and disarray
58
Q

Familial Hypertrophic Cardiomyopathy

A
  • Mutations in structural proteins of sarcomere
    • β myosin heavy chain most common
  • Autosomal dominant
59
Q

Hypertrophic Cardiomyopathy

Mimics

A
  • HTN heart disease w/ age related subaortic septal hypertrophy
  • Aortic stenosis
  • Amyloidosis
60
Q

Hypertrophic Cardiomyopathy

Morphology

A
  • LVH affects septum most
  • Endocardial fibrosis
  • Myocyte hypertrophy and disarry with interstitial fibrosis
61
Q

Restrictive Cardiomyopathy

A
  • Loss of compliance ⇒ diastolic dysfunction
  • Least common type
  • Often associated with systemic disease
  • Causes:
    • Direct
      • Toxic
        • Methylsergide
        • Anorectic agents
        • Radiation
      • Infectious
      • Infiltration
      • Genetic
      • Idiopathic
    • Indirect: infiltration by something other than cardaic muscle
      • Glycogen storage diseases
      • Amyloidosis
      • Hemachromatosis
      • Sarcoidosis
62
Q

Secondary Causes of Cardiomyopathy

A
  • Often d/t compensatory changes in the heart
    • CO doesn’t meet demand
      • ↑ Peripheral resistance
      • Volume overload
      • Cardiac dysfunction
63
Q

Compensatory Cardiac Hypertrophy

A

Pattern dependent on etiology.

  • Concentric hypertrophy ⇒ seen with conditions that ↑ afterload
    • HTN
    • Aortic stenosis
  • Non-concentric / Eccentric hypertrophy ⇒ seen with volume overload
    • ↓ Capillary to myocyte ratio
    • ↑ Fibrous tissue
    • Abnormal protein synthesis
64
Q

Cardiac Hypertrophy & Dilation

Pathophysiology

A
65
Q

Heart Failure

Pathophysiology

A

CO insufficient to meet requirements of peripheral tissues.

  • HTN, valvular disease, MI, etc ⇒ ↑ cardiac work
    • ↑ Wall stretch ⇒ hypertrophy and/or dilation
  • ↓ Renal perfusion ⇒ RAAS activation ⇒ sodium and salt retention
  • Down regulation of neurohumoral receptors
  • May be due to:
    • Loss of blood, arrhythmia, obstructed flow, regurg, or primary pump failure
66
Q

Heart Failure

Clinical Presentation

A
67
Q

Left-sided Heart Failure

A
  • Causes:
    • Ischemic heart disease
    • HTN
    • AV or MV disease
    • Non-ischemic myocardial diseases
  • Effects:
    • Congestion of pulmonary vasculature
    • ↓ Peripheral blood pressure and flow
  • Sequelae of left HF:
    • Secondary atrial enlargement
    • Pulmonary congestion and edema
    • ↓ Renal perfusion
    • Cerebral hypoxia
68
Q

Pulmonary Edema

A
  • Leakage of congested capillaries into alveolar spaces
  • Results in hemosiderin deposition in MΦ ⇒ siderophages (“Heart failure cells”)
69
Q

Right-sided Heart Failure

A
  • Causes:
    • Left-sided HF ⇒ most common
    • Cor pulmonale
    • Chronic pulmonary HTN
  • Effects:
    • Passive congestion of liver
    • Renal congestion
    • Pleural effusions
    • Anasarca
    • RVH
70
Q

Biventricular Heart Failure

A
  • Many pts have right and left HF
  • Treatment
    • Diuretics ⇒ ↓ fluid overload
    • ACEi ⇒ ⊗ RAAS
    • β-blockers ⇒ ↓ systemic vascular resistance
71
Q

Farmingham Criteria

Dx CHF

A
72
Q

CHF

Diagnostic Tests

A

Important for management, diagnosis is clinical.

  • Kidney function
  • Electrolytes
  • CXR
  • BNP
  • ECHO
73
Q

Left-sided HF

Classification

A
  • Diastolic HF
    • LVEF > 50%
    • Thickened and stiff chambers
    • Heart can’t fill
  • Systolic HF
    • LVEF < 40%
    • Dilated and thin chambers
    • Heart can’t pump
74
Q

Diastolic Heart Failure

A

“CHF w/ preserved systolic function”

  • More common
  • Seen in older pts with hx of HTN
  • Stiff ventricles with impaired filling leading to inadequate pumping
  • Sensitive to HR and volume overload
  • Acute presents with similar sx to systolic HF
    • SOB, orthopnea, PND, edema
  • Management
    • Acutely treat with diuresis
    • Long-term goal to control BP
75
Q

Systolic Heart Failure

A

“CHF with reduced LVEF”

  • Generally due to cardiomyopathies
  • Different types
    • Ischemic heart disease
      • CAD
      • MI
      • CABG
    • Non-ischemic cardiomyopathies
      • Familial
      • Viral
      • Drug and ETOH
      • Hypo or hyper thyroid disease
      • Chemotherapy (Doxorubicin and Herceptin)
      • Toxins (cobalt)
      • Infections like HIV
      • Valvular heart disease
76
Q

Heart Failure

Long-term Management

A
  • Manage modifiable factors
  • Medications
    • Beta-blockers
    • ACEi
    • Mineralocorticoid inhibitors
  • Patient education
    • Avoid NSAIDS
77
Q

Heart Failure

Causes of Decompensation

A
  • Non-compliance ⇒ leading cause
  • Ischemia
  • Inadequate treatment
  • Arrhythmias
  • Miscellaneous
  • HTN
  • No definite factor
78
Q

Cardiac Teratogens

A
  • Maternal rubella infection ⇒ PDA
    • Environmental acquired congenital heart defect
  • ETOH
  • Thalidomide
  • Maternal DM
79
Q

Trisomy 21 (Down’s) is associated with…

A
  • Atrioventricular septal defects (endocardial cushion defect)
  • VSD
  • ASD
  • PDA
80
Q

Trisomy 18 (Edwards) is associated with…

A
  • VSD
  • Double outlet right ventricle
  • PDA
81
Q

Trisomy 18 (Patau) is associated with…

A

VSD, ASD, PDA

82
Q

Turner syndrome (XO) is associated with…

A

aortic coarctation

83
Q

Marfan’s syndrome is associated with…

A

Mitral valve prolapse

Aortic root dilatation

84
Q

DiGeorge Syndrome is associated with…

A

Truncus arteriosus

85
Q

Thrombocytopenia Absent Radius Syndrome (TAR) is associated with…

A

Tetralogy of Fallot

86
Q

William’s Syndrome is associated with…

A

Supravalvar aortic and pumonary stenosis

87
Q

Cyanosis Tardive

A

Congenital heart defects with initial L→R shunt and later development of a R→L shunt

88
Q

Eisenmenger’s Complex

A

VSD with reversal of flow due to pulmonary HTN

Occures when pulmonary pressure = systemic pressure

89
Q

Atrial Septal Defect

(ASD)

A
  • Abnormal opening in atrial septum allowing communication between left and right atria
  • 3 types classified by location on septum
    • Secundum ASD ⇒ 90%
      • @ Fossa ovale
    • Primum ASD ⇒ 5%
      • Near AV valves
      • Usually ass. w/ cleft anterior mitral leaflet
    • Sinus venous ASD ⇒ 5%
      • Near entrance of SVC
      • Usu. w/ anomalous connections of right pulmonary veins
  • Pulmonary blood flow 2-4x nl
  • Most isolated well tolerated ⇒ asymptomatic till 30 y/o
  • Mumur often present
90
Q

Ventricular Septal Defect

(VSD)

A
  • Most common congenital cardiac anomaly
  • Described by location and size
    • Membranous vs muscular
  • 50% of small muscular VSD close spontaneously
  • Large defects usu. membranous or infundibular
    • Stay open with sign. shunt
  • L to R shunt ⇒ RV dilation and hypertrophy
  • Eisenmenger’s syndrome
91
Q

PDA

A
  • 90% are isolated
  • Most w/o functional difficulties @ birth
  • Harsh “machine-line” murmur
  • Initial L to R shunt ⇒ Eisenmenger
  • Close ASAP
  • Sometimes need to keep open ⇒ Prostaglandin E
92
Q

Atrioventricular Septal Defect (AVSD)

A
  • From abnl development of embryologic AV canal
    • Superior and inferior cushions fail to fuse
    • Incomplete closure of AV septum
    • Inadequate formation of tricuspid and mitral valves
  • In complete form ⇒ all 4 chambers freely communicate
  • > ⅓ with complete AVSD have Downs
93
Q

Tetralogy of Fallot

A
  • Most common cyanotic congenital heart disease
    • 10% of all CHD
  • Features:
    • VSD ⇒ membranous, malaligned
    • RV outflow tract obstruction
      • Most severe form is pumonary valve atresia
    • Aorta overriding septal defect ⇒ dextroposition
    • RVH ⇒ compensatory
  • Clinical manifestations
    • R to L shunt ⇒ cyanosis
    • Pulmonary arteries hypoplastic
    • Aorta enlarged
    • Subpulmonary stenosis protects pulmonary vasculature from pressure overload ⇒ RV failure rare
94
Q

Truncus Arteriosus

A
  • Persistent presence of one arterial trunk arising from the ventricles
    • Due to failure of separation into pulmonary artery and aorta
  • Single great artery receives blood from both ventricles
  • Accompanied by underlying VSD
  • Blood from RV and LV mix ⇒ early systemic cyanosis
  • ↑ Pulmonary blood flow ⇒ risk of irreversible pulmonary HTN
95
Q

Transposition of the Great Vessels

A
  • Discordant ventriculo-arterial connections
  • LV ⇒ pulmonary artery / RV ⇒ aorta
  • Need mixing of systemic venous and arterial blood to live
    • VSD (35%)
    • PFO and PDA (65%)
  • RVH, LV atrophy
  • Fix with arterial switch operation
    • Need to consider abnl of coronary arteries
96
Q

Aorta Coarctation

A

A narrowing, or constriction, in a portion of the aorta.

  • Infantile form
    • Tubular hypoplasia of aortic arch proximal to PDA
    • Sx early in life
  • Adult form
    • Ridge of proliferative intimal tissue usually in a post-ductal position
    • Ass. with male sex except for Turner’s syndrome
    • Bounding pulses in BUE
    • Can develop collaterals via enlarged intercostal and internal mammary arteries
      • Visible erosions “notching” on underside of ribs on CXR
97
Q

Pulmonary Stenosis and Atresia

A
  • Obstruction @ pulmonary valve
    • Varied severity
  • Isolated or part of complex
  • Clinical manifestations:
    • RVH
    • ± Post-stenotic dilation of pulmonary artery
    • ± Pulmonary trunk hypoplasia
  • Complete atresia of PA ⇒ no communication b/t RV and lungs
    • See hypoplastic RV and ASD
98
Q

Aortic Stenosis and Atresia

A
  • Valvular AS
    • Cusps hypoplastic, dysplastic, or abnl #
    • Less severe forms compatible with life
    • 80% isolated
    • May see dense, porcelain-like endocardial fibroelastosis of LV
  • Subaortic stenosis
    • Thickened band (discrete type) or collar (tunnel type) of dense endocardial fibrous tissue
    • Below level of the cusps
  • Supravalvular AS
    • Ascending aortic wall thickened ⇒ luminal constriction
    • May be related to developmental d/o affecting multiple organ systems
      • Includes hypercalcemia of infancy (Williams syndrome)
    • Can be caused by elastin mutations
99
Q

Hypoplastic Left Heart Syndrome

A

Constellation of findings:

  • Severe congenital valvular aortic stenosis/atresia
  • LVOT obstruction ⇒ LV and ascending aorta hypoplasia
  • PDA ⇒ allows flow into aorta and coronary arteries
  • Nearly always fatal in first week of life when ductus closes
100
Q

Causes of Myocarditis

A

Most cases are viral.

101
Q

Dallas Criteria

A

Classifies myocarditis based on endomyocardial biopsy findings.

102
Q

Types of Myocarditis

A
  • Lymphocytic myocarditis
  • Hypersensitivity myocarditis
  • Giant cell myocarditis
  • Sarcoid myocarditis
  • Infectious myocarditis
103
Q

Lymphocytic Myocarditis

A
  • Most common form
  • Associated with myocyte injury
  • Most cases are viral
  • Focal, patchy, or diffuse pattern
  • Gross appearance
    • Normal ⇒ Enlarged and dlidated with mottling
  • Dx with clinical findings, serology, histopathology, ISH, molecular probes, and PCR
104
Q

Lymphocytic Myocarditis

Causes

A
105
Q

Hypersensitivity Myocarditis

A
  • Etiologies
    • Typically caused by drugs
      • Sulfonamides, methyldopa, PCN
    • Parasitic infections
      • Taenia, Echinococcus, Schistosoma, Tricinella, Toxoplasma, Trypanosomiasis
    • Hypereosinophilic syndromes
    • Asthmatic bronchitis
  • Eosinopril-rich inflammatory infiltrate in myocardium
106
Q

Infectious Myocarditis

A
  • Chagas disease due to Trypanosoma cruzii
  • Toxoplasma
  • Diphtheria
  • Trichinosis
107
Q

Granulomatous Myocarditis

A

Characterized by infiltrates of histiocytes and lymphocytes with granuloma formation.

  • Idiopathic
  • Sarcoidosis
  • Granulomatous infections
    • Mycobacteria and fungi
    • See necrotizing granulomas
  • Hypersensitivity
  • Rheumatoid disases
  • Rheumatic fever
108
Q

Giant Cell Myocarditis

A
  • Unknown etiology
  • Rapidly progressive
  • Frequently fatal
  • Mixed inflammatory infiltrate including multinucleated giant cells
  • Multifocal myocyte necrosis
  • No granulomas
109
Q

Neutrophilic Myocarditis

A
  • Causes
    • Bacteria and some fungi
    • Due to generalized sepsis or direct spread from infective endocarditis
    • Early viral and idiopathic myocarditis
    • Ischemia/Infarct
110
Q

Myocarditis

Clinical Features

A
  • May be asymptomatic with no sequelae
  • May result in acute heart failure, arrhythmia, or sudden death
  • Most have fatigue, dyspnea, palpitations, precordial discomfort, fever
  • Dilated cardiomyopathy may result over time
111
Q

Pericardial Disease

A
  • Pericardial disorders can cause
    • Fluid accumulation
    • Inflammation
    • Fibrous constriction
  • Usually associated with disease elsewhere in the heart or systemic disease
  • Isolated pericardial disease rare
112
Q

Pericardial Effusion

A
  • Most often develop d/t pericarditis
  • Exceptions include cardiac rupture and myxedema (hypothryoidism)
  • Pericardium may be distended by:
    • Serous fluid
    • Blood ⇒ hemopericardium
    • Pus ⇒ purulent pericarditis
    • Gas/air ⇒ pneumopericardium
113
Q

Chronic Pericardial Effusion

A

Slowly accumulating effusions dilate the pericardium.

  • Can reach > 500 ml and remain asymptomatic
  • CXR ⇒ globular enlargement of the heart shadow
  • EKG ⇒ low-voltage QRS complexes in all 6 limb leads
114
Q

Acute Pericardial Effusion

A

Rapidly developing fluid collections.

  • 200-300 ml may cause cardiac tamponade
    • Compress atria and venae cavae
    • Can compress ventricles
    • Cardiac filling restricted
  • Seen with
    • Hemopericardium d/t ruptured MI site
    • Proximal aortic dissection
115
Q

Cardiac Tamponade

Etiologies

A
  • Hemopericardium d/t ventricular wall rupture s/p MI
  • Proximal aortic dissection
  • Bacterial or fungal infections
  • HIV-associated infections
  • Neoplastic involvement
    • ~ 20% of large effusions with no obvious cause constitute the initial presentation of unrecognized cancer
116
Q

Cardiac Tamponade

Pathogenesis

A

Unless intrapericardial pressure immediately decreased, pulmonary blood flow stops and cardiac arrest follows.

117
Q

Cardiac Tamponade

Clinical Presentation

A
  • Dyspnea and tachypnea
  • Pericardial pain
  • Diaphoresis
  • Peripheral cyanosis
  • Beck’s triad ⇒ hypotension, muffled heart sounds, JVD
  • Paradoxical pulse ⇒ abnormally large drop in systemic arterial pressure during inspiration
  • Varying degrees of reduced CO and shock
    • Diaphoresis, cool extremities, depressed sensorium
118
Q

Electrical Alternans

A
  • Occurs with pericardial effusion and tamponade
  • Beat-to-beat shift in QRS axis
  • Associated with mechanical swinging of the heart
  • Electrical alternans + sinus tach virtually dx of cardiac tamponade
119
Q

Pneumopericardium

A
  • Air within the pleural cavity
  • Can lead to cardiac tamponade
  • Causes
    • Complication of respiratory therapy in infants
      • Seen with pneumothorax and pneumomediastinum
    • Spontaneously in asthma
    • Blunt chest trauma
    • S/p pericardiectomy
120
Q

Causes of Pericarditis

A
121
Q

Pericarditis

Clinical Presentation

A
  • Severe pleuritic pain in anterior chest
    • May radiate to arms and back
  • Pericardial friction rub
    • Best heart at the left sternal border at end expiration
  • EKG ⇒ diffuse ST elevations in all leads
122
Q

Acute Pericarditis

A
  • Most common types:
    • Fibrinous ⇒ “dry’, little or no serious effusion
    • Serofibrinous ⇒ “wet”, ass. w/ serous effusion
  • Causes:
    • Noninfectious inflammatory diseases
      • Rheumatic fever
      • Dressler syndrome
      • Uremia
      • SLE, Scleroderma
      • Tumors
    • Infection of contiguous tissues
      • Preceding viral infection
    • Other causes:
      • 1-3 days post MI
      • Radiation
      • Post-surgical
123
Q

Purulent/Suppurative Pericarditis

A
  • Due to infection of pericardial space
    • Direct extension from adjacent tissues
    • Hematogenous or lymphatic spread
    • Inoculation during procedure
  • Up to 500 ml of exudate
  • Serosa reddened and granular
  • Extension ⇒ mediastinopericarditis
  • Usu. results in organization and scarring ⇒ constrictive pericarditis
124
Q

Hemorrhagic Pericarditis

A
  • Most often caused by malignancy
  • Bacterial infections esp. Tb
  • Pts w/ bleeding diathesis
  • S/p cardiac surgery
125
Q

Caseous Pericarditis

A
  • Presumed to be Tb until proven otherwise
  • Rarely fungal infections
  • Occurs by direct spread from Tb foci
  • Frequently progresses to disabling, fibrocalcific, chronic constrictice pericarditis
126
Q

Chronic Pericarditis

A
  • Can develop from any type of acute pericarditis
  • Fibrous thickenings ⇒ soldier’s plaque
  • Delicate, stringy adhesions may damage pericardial sac ⇒ adhesive pericarditis
  • Rarely interferes with cardiac function
127
Q

Adhesive Mediastinopericarditis

A
  • Obliteration of pericardial sac with adherence of outer pericardium to surrounding structures
  • Pulls during systole ⇒ cardiac strain
  • Inc. workload ⇒ hypertrophy and dilation
128
Q

Constrictive Pericarditis

A
  • Fusion of visceral and parietal layers ⇒ thick fibrous scar
  • Compresses the heart
  • Prevents hypertrophy & dilation
  • Heart cannot respond to inc. peripheral demand
  • See DOE, weight loss, fatigue, ankle edema
  • May require pericardiectomy
  • Most common w/ pericardial disease d/t:
    • Tb
    • Radiation therapy
    • Prior cardiac surgery
    • Chest trauma
    • Uremia
    • Metastatic tumor
  • Develops months to years after acute insult
129
Q

Cardiac Tumors

A
  • Primary tumors
    • Much lower incidence
    • Myxoma most common
  • Metastatic tumors
    • Far more common
    • Can originate from anywhere
    • Sarcomas and germ cell tumors common
130
Q

Myxoma

A
  • Most common primary tumor in adults
    • 90% in atria
    • L:R = 4:1
  • Derived from multipotent mesenchymal cells
  • Gelatinous “myxoid” consistency with soft, irregular surface
131
Q

Myxoma

Histology

A
  • Abundant myxoid matrix
  • Stellate, endothelia, SM, and undiff. cells
  • Inflammation and hemorrhage may be present
132
Q

Lipomas

A
  • Occur in subepicardium or subendocardium > myocardium
  • Most in LV, RA, or atrial septum
  • Lipomatous hamartoma of cardiac valves ⇒ rare
  • Gross and micro appearance of adipose tissue
133
Q

Rhabdomyoma

A
  • Most common primary cardiac tumor in kids
  • Protrude into ventricle
  • Often seen with tuberous sclerosis
  • May cause outflow obstruction
  • Composed of skeletal muscle dervied cells
    • Spider cells
134
Q

Angiosarcoma

A
  • Malignant vascular tumor
  • Anastomosing vascular channels lined by atypical cells
  • Hemorrhage and necrosis common

1. HDS Cardiology (7 decks)

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