Pathology of CV system Flashcards

1
Q

Hypertrophy

A
  • Inc mechanical work from pressure or volume overload
    • causes myocytes to inc in size
  • Causes an inc in size and weight of heart
  • dependant on inc protein synthesis
  • requires healthy myocardium
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2
Q

Inc pressure (hypertension/aortic stenosis) causes

A
  • Pressure-overload hypertrophy
    • causes a concentric inc in wall thickness
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3
Q

Volume-overload hypertrophy

A
  • Ventricular dilation
  • wall thickness may be increased, normal, or less than normal
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4
Q

Cardiac Compensation

Dilation

A
  • Stretching myofibers
  • Maintain connections and architecture
  • Often degenerative in nature
  • Results from chronic volume overload
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5
Q

Result of Dilation

A
  • gradual inc in chamber pressures occurs as chamber volume increases
    • not as profound a change as seen with outflow obstructions
  • dilation dec pressures in chamber by increasing surface area
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6
Q

Supply of oxygen and nutrients to hypertrophied heart

A

More tenuous than the normal heart

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7
Q

Hypertrophy often accompanied by

A

deposition of fibrous tissue

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8
Q

Cardiac hypertrophy associated with

A
  • heightened metabolic demands due to
    • inc wall tension
    • inc heart rate and contractility
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9
Q

Hypertrophied heart vulnerable to

A
  • Decompensation
    • can evolve to cardiac failure => death
  • Sequence of compensation initially beneficial, later harmful
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10
Q

CHF characterized by

A
  • dec cardiac output
  • dec tissue perfusion (forward failure)
  • pooling of blood in the venous system (backward failure)
    • may cause pulmonary edema, peripheral edema, or both
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11
Q

Right-to-left shunts

A
  • Tetralogy of Fallot
  • Transposition of great arteries
  • Persistent truncus arteriosus

*Hypoxemia and cyanosis result because of mixture of poorly oxygenated venous blood w/ systemic arterial blood b/c it bypasses the lungs

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12
Q

Left-to-right shunts

A
  • ASD, VSD, PDA, septal defects
  • inc pulmonary blood flow
  • no cyanosis initially
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13
Q

Consequences of left-to-right shunts

A
  • raise flow and pressures in pulmonary circulation
    • normally low pressure system
    • right ventricular hypertrophy and pulmonary vasculature changes
  • When pulmonary vasculature approaches systemic levels
    • new right-to-left shunt introduces unoxygenated blood into systemic circulation
    • eventually cyanosis
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14
Q

PDA

A
  • shunt L to R, overloads R ventricle and inc pulmonary pressures
  • To compensate
    • total blood volume increases
    • left ventricle forced to increase output above normal levels
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15
Q

PDA Pathologic findings

A
  1. Compensatory hypertrophy of both LV & RV, with left atrial dilation due to inc pulmonary blood flow
  2. Dilation of PA and AA due to turbulence and altered pressure
  3. Slowly developing hypertrophy if the shunt is < 3mm, and pulmonary hypertension and congestive heart failure if its > 5mm
  4. Prone to thrombosis (Virchow’s triad)
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16
Q

Septal Defects

A
  • VSD most common
    • most common congenital defect in horses
  • Pulmonary hypertension from blood shunting L to R
    • R ventricular hypertrophy
    • Inc in pulmonary hypertension can lead to eventual compensatory R to L shunting
      • shunts blood past lungs
17
Q

Atrial septal defects

A
  • patent foramen ovale
    • may be probe patent but functionally closed
  • R ventricular hypertrophy and L to R shunts
  • Equalization of pressures may cause R to L shunts cyanosis
18
Q

Tetralogy of Fallot

A
  1. VSD
  2. R Ventricular Hypertrophy (secondary)
  3. Pulmonary Stenosis
  4. Dextroaorta
19
Q

Abnormalities of the Aortic Arch

A
  • May be incidental findings
  • Clinical signs are from compression of trachea and esophagus
    • Persistent right aortic arch - something about megaesophagus
    • Double aortic arch
    • Anomalous subclavian arteries
20
Q

Ectopia cordis

A
  • heart enclosed w/in pericardium outside of thorax
21
Q

Endocardial fibroelastosis

A
  • Left ventricle
  • Inc collagen and elastin
    • can affect conduction