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SYSTEMIC PATHOLOGY - 1 > 1 – Introduction and Heart Failure > Flashcards

1 – Introduction and Heart Failure Flashcards

1
Q

3 layers of the heart:

A

-pericardium
-myocardium
-endocardium

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2
Q

Pericardium: epidcardium

A

o Parietal and visceral pericardium
 Thin layer of mesothelium and connective tissue
 Pericardial space contains small amounts of clear lubricant fluid

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3
Q

Myocardium: heart muscle

A

o Striated, connected by intercalated disks
o Lots of mitochondria

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4
Q

Endocardium: atria, ventricles, valves

A
  1. Endothelium (superficial)
  2. Basal lamina
  3. Sub-endothelial connective tissue
    *Purkinje fibres
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5
Q

AV valves

A
  • Attached to papillary muscles by chordae tendinea
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6
Q

Postmortem examination of the heart

A
  • Check in situ (relative size)
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7
Q

Most important compensatory mechanisms of the heart:

A
  • Activation of neurohumoral systems (NE/RAA
  • Cardiac dilation and hypertrophy
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8
Q
  • Activation of neurohumoral systems (NE/RAA)
A

o Vascular redistribution of blood
o Increase HR
o Increase in blood volume
o *all leads to atrial natriuretic peptide secretion (counter mechanism)

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9
Q

o Cardiac dilation

A

 Increased stroke (blood) volume
 Myocardial fibers stretch=increase contractile force
* Limit to stretch (too far=decrease tension)
 Chronic dilation through addition of sarcomeres (lengthening of myocytes)
 *acute overload=dilation, chronic overload=hypertrophy

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10
Q

o Myocardial hypertrophy

A

 Greater contractility and ejection force
* Pump more blood (volume overload)
* Pump at a higher pressure (pressure overload)
 Due to sustained increase in cardiac workload OR due to trophic signals (ex. hyperthyroidism)
 *reversible if workload demand is corrected

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11
Q

Eccentric hypertrophy:

A
  • Accompanied by dilation
  • *thin wall and distended ventricle
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12
Q

Concentric hypertrophy:

A
  • Reduced volume of ventricular chamber
  • *thick wall and reduced ventricular space
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13
Q

Cellular stages in cardiac hypertrophy:

A
  1. Initiation
  2. Compensation
  3. Deterioration
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14
Q
  1. Initiation
A

a. Increase cell size (sarcomeres/mitochondria)

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15
Q
  1. Compensation
A

a. Stable hyperfunction with no clinical signs

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16
Q
  1. Deterioration
A

a. Degeneration of hypertrophied cardiomyocytes
b. Loss of contractility followed by heart failure

17
Q

Gross changes in cardiac hypertrophy/dilation: Right side

A

o Broad base
o Ex. pulmonic stenosis, brisket disease

18
Q

Gross changes in cardiac hypertrophy/dilation: left side

A

o Increased length
o Ex. aortic stenosis, feline hyperthyroidism

19
Q

Gross changes in cardiac hypertrophy/dilation: bi-ventricular

A

o Globose (rounded)
o Ex. hypertrophic cardiomyopathy

20
Q

Cardiac failure

A
  • Heart unable to pump blood at a sufficient rate to meet metabolic demands of tissues
  • Cardiac dysfunction is NOT properly compensated
  • Retrograde and anterograde component
21
Q

Anterograde component of cardiac failure

A
  • Decreased CO via the aorta and/or pulmonic arteries
  • Leads to:
    o Hypotension
    o Depression
    o Lethargy
    o Syncope: temporary loss of consciousness
22
Q

Pathophysiological mechanisms in heart failure: pump failure

A
  • Weak contractility and emptying of chambers caused by myocardial degeneration, fibrosis, inflammation and/or neoplasia
23
Q

Retrograde component of cardiac failure

A
  • Inability to adequately empty the venous reservoirs
  • Leads to
    o Swollen abdomen (ascites)
    o Tachypnea
    o Dyspnea
    o *due to pleural effusion and pulmonary edema
24
Q

Pathophysiological mechanisms in heart failure: outflow obstruction

A
  • Vascular or valvular stenosis
  • Systemic or pulmonic hypertension
25
Q

Pathophysiological mechanisms in heart failure: blood flow regurgitation

A
  • Valvular insufficiency
  • Endocardiosis
  • Endocarditis
  • Volume overload
26
Q

Pathophysiological mechanisms in heart failure: shunting of blood

A
  • Congenital hear defects
  • Persistence of fetal circulation
27
Q

Pathophysiological mechanisms in heart failure: restriction of atrial/ventricular filling

A
  • Cardiac tamponade
  • Pericarditis
  • Tumor
28
Q

Pathophysiological mechanisms in heart failure: conduction disorders

A
  • Arrhythmias caused by functional or structural abnormalities in the conduction system
29
Q

Congestive heart failure

A
  • Unilateral (left or right) or bilateral
  • Acute or chronic
30
Q

Right sided heart failure due to

A
  • Pulmonic stenosis
  • Pulmonary hypertension
  • Brisket disease
  • Hardware disease
  • Pulmonary fibrosis
31
Q

Left sided heart failure due to

A
  • Aortic stenosis
  • Systemic hypertension
  • Mitral endocardiosis
  • Mitral dysplasia
  • Feline hyperthyroidism
32
Q

Bilateral heart failure due to

A
  • Tetralogy of Fallot
  • Hypertrophic
  • Cardiomyopathy
33
Q

Extra cardiac lesions in right-sided heart failure

A
  • Systemic venous and portal congestion and hypertension
  • LUNGS are the target
  • Generalized edema
  • Hydrothorax
  • Passive liver congestion
34
Q

Cor pulmonale

A
  • Pulmonary hypertension and R. heart failure secondary to PULMONARY disease
35
Q

Extra cardiac lesions in left-sided heart failure

A
  1. Pulmonary venous congestion
  2. Pulmonary edema and intra-alveolar hemorrhage
  3. Red cells phagocytized by alveolar macrophages
  4. Iron pigment in alveolar macrophages=’heart failure cells’
36
Q

Specific animal diseases causing R and L heart failure

A
  • High altitude
  • Brisket disease in cattle
  • Mitral endocardiosis in dog
37
Q

High altitude

A
  1. Pulmonary hypertension
  2. Hypertrophy RV
  3. R. heart failure
  4. Ascites and subcutaneous edema
38
Q

Brisket disease in cattle

A
  • Extensive subcutaneous edema caused by R. sided heart failure
  • Nutmeg liver
    o Chronic passive congestion
    o Zonal pattern caused by congestion/necrosis/fibrosis of centrilobular regions
39
Q

Mitral endocardiosis in dog

A
  • Mitral insufficiency
    1. Passive congestion of lung
    2. Pulmonary edema
    3. Intra-alveolar hemorrhages
    4. ‘heart failure cells’

SYSTEMIC PATHOLOGY - 1 (24 decks)

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