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Pathology I > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

General heart facts

A
  • Consumes more energy than any other organ
  • Cycles 6kgs of ATP / day
  • Beats about 100,000 / day (over a billion times in a life time)
  • Pumps 10 tons of blood through the body
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2
Q

Heart failure

A
  • The heart is unable to pump blood at a rate commensurate with the requirements of metabolizing tissues
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3
Q

Prevalence of heart failure

A
  • 2 million patients
  • 400,000 new cases/yr
  • 200,000 deaths/yr
  • Most common DSC dx in patients > 65
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4
Q

Classifications of heart failure

A
  • Acute
  • Chronic
  • Systolic Dysfunction
  • Diastolic Dysfunction
  • Low / High Output Failure
  • Forward / Backward Failure
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5
Q

Systolic dysfunction

A
  • Progressive deterioration of myocardial contractile function
  • Left ventricular systolic dysfunction
  • Increased end diastolic volume (EDV)
  • Left ventricular dilatation
  • Ejection fraction < 45%
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6
Q

Diastolic dysfunction

A
  • Inability of the heart chamber to relax/expand
  • Increased stiffness of left ventricle
  • Inadequate filling of left ventricle
  • Diminished stroke volume (SV)
  • Ejection fraction > 45%
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7
Q

Hypertropic cardiomyopathy histological findings

A
  • Disarray of myocytes

- Interstitial fibrosis

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8
Q

Compensatory mechanisms in heart failure in maintaining perfusion

A
  • Frank Starling mechanism
  • Myocardial hypertrophy
  • Neurohormonal systems
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9
Q

Frank Starling mechanism

A
  • Increase venous return
  • Increases ventricular preload
  • Increases stroke volume
  • Stretching myocytes increases force generation (enhances contractility)
  • Heart ejects additional return
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10
Q

Neurohormonal regulatory systems

A
  • Release of neurotransmitters (such as NE)
  • Activation of the renin-angiotensin-aldosterone system
  • Release of atrial natriuretic peptide
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11
Q

Results of neurotransmitter release as a compensatory mechanism

A
  • Increases HR
  • Augment myocardial contractility
  • Increases vascular resistance
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12
Q

Precipitating causes of actue heart failure

A
  • Myocardial Infarction (LV)
  • Pulmonary Embolism (RV)
  • Malignant Hypertension
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13
Q

Precipitating causes of chronic heart failure

A
  • Systemic Hypertension (LV)
  • Valvular Heart disease (LV)
  • EtoH related DCM
  • COPD (RV)
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14
Q

Mitochondrial biogenesis and enzyme production

A
  • Peroxisome proliferator-activated receptor gamma coactivator - 1 alpha (PGC-1alpha) (Master Regulator)
  • Mitochondrial oxidative energy metabolism is regulated at the level of gene transcription
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15
Q

Physiological hypertrophy is associated with

A
  • Increased PGC-1 expression

- Expansion of mitochondrial volume density and oxidative capacity

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16
Q

Pathological hypertrophy is linked to

A
  • Decreased PGC-1

- Mitochondrial dysfunction

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17
Q

Transcriptional control of PGC-1

A
  • PGC-1 coactivators dock to transcription factor
  • Targets protein complexes that activate transcription
  • PPAR binds nuclear receptor response elements (NRRE)
  • PPAR recruits PGC-1
  • PGC-1 facilitates interactions with other coactivators with enzymatic activity
  • PGC-1 directly interacts with the transcription initiation machinery (TRAP/DRIP)
  • Provides a molecular bridge between the coactivator complex and RNA polymerase II (Gene Expression)
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18
Q

Early heart failure progression to heart failure

A
  • Perturbations in energy utilization (Glucose)
  • Metabolic shift due to:
  • Myocyte energy insufficiency
  • Reduced capacity of mitochondrial ATP production
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19
Q

Hypertrophic pathway activation (metabolic event precipitating heart failure)

A
  • Ca2+ / Calcineurin / Nuclear Factor of Activated T Cells
  • Myocardial G-protein–coupled receptors (GPCRs)
  • Adrenergic, angiotensin, and endothelin (ET-1) receptors
  • Phosphoinositide 3-Kinase / Akt / Glycogen Synthase
  • Myocyte Enhancer Factor-2 / Histone Deacetylases
  • Small G Proteins
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20
Q

Myocardial G-protein coupled receptors serve a fundamental role in

A
  • Cardiac hypertrophy by activating hypertrophic gene program activation
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21
Q

Pathology of heart failure sequence (1st half)

A
  • Increased mechanical load = increased subcellular components
  • Increased myocytes (sarcomeres) without increase in capillary nuumber
  • Increased intercapillary distance = increased oxygen consumption (hypertrophy)
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22
Q

Pathology of heart failure sequence (2nd half)

A
  • Enlarged muscle mass with increased metabolic demands
  • Increased wall tension
  • Heart rate increases
  • Increased contractility (inotropic state, or force of contraction)
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23
Q

Patterns of hypertrophy

A
  • Pressure overloaded ventricles

- Volume overloaded ventricles

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24
Q

Pressure overloaded ventricels

A
  • Essential hypertension

- Aortic stenosis

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25
Pressure overloaded ventricles (concentric hypertrophy) results
- Stimulates deposition of new sarcomeres (Parallel) - Hypertrophy of the left ventricle (concentric) - Reduction in cavity diameter
26
Volume overloaded ventricles
- Ventricular dilation | - Dilated cardiomyopathy
27
Volume overloaded ventricles (eccentric hypertrophy) results
- New sarcomere deposition (in series) - Increased cell length and width - Dilation with increased ventricular diameter - Wall thickness may be increased, normal or less than normal
28
Measure of hypertrophy
- Heart weight
29
Pressure vs. volume overload hypertrophy
- Hypertrophy with and without dilation
30
Characteristics of cardiomyopathic remodeling
- Damaged and dysfunctional mitochondria - Energy-deficient state - Intra-myocellular lipid accumulation - Reactive oxygen species generation
31
Hallmark of myocardial remodeling
- ***Increased myocardial volume and mass with net loss of myocytes*** - Larger myocytes die - Increased load placed upon remaining myocytes - Progenitor cell stimulation
32
Counter-regulatory effects that decline in myocyte and myocardial remodeling
- Nitrous oxide - Prostaglandins - Bradykinin - Atrial natriuretic peptide and B-type
33
Decline in counter-regulatory effects during myocardial remodeling results in
- Reduction of cardiac output
34
Consequences in reduction of cardiac output
- Release of vasoconstrictors | - Vasoconstriction increases calcium concentrations in myocytes
35
Vasoconstriction increasing calcium concentrations in myocytes causes
- Contractility augmentation | - Impairment in relaxation
36
Impairment of relaxation secondary to increased calcium concentration in myocytes results in
- Increased β-adrenergic activity | - Activation of RAAS
37
Peroxisome proliferator-activated receptors cause
- Abnormalities in myocardial energy metabolism | - Maladaption
38
Abnormalities in myocardial energy metabolism
- Suppression of FA oxidation | - Increased glucose utilization
39
Maladaptions caused by peroxisone proliferator-activated receptors
- Lipid accumulation - Lactic acid accumulation - Diminished maximal ATP generation
40
Systemic manifestations of left and right ventricular heart failure
- Accumulation of excess fluid behind one or both ventricles - Activation of neurohormonal mechanisms - Organ dysfunction secondary to inadequate perfusion
41
Left ventricular failure morphological findings seen in
- Heart - Lungs - Kidneys - Brain
42
Morphological findings of left ventricular heart failure in the heart
- Hypertrophy and fibrosis in the myocardium | - Secondary enlargement of the left atrium with resultant atrial fibrillation
43
Morphological findings of left ventricular heart failure in the lungs
- Pulmonary congestion and edema - Widening of alveolar septa - Fluid in the alveolar spaces - Heart failure cells
44
Pulmonary congestion and edema radiographic findings
- Kerley B lines on x-ray | - Perivascular and interstitial transudate
45
Clinical manifestations of left ventricular heart failure in the lungs
- Dyspnea - Orthopnea - Paroxysmal Nocturnal Dyspnea
46
Left ventricular heart failure morphology in the kidneys
- Activation of the RAAS - Prerenal Azotemia - Manifestations of edema
47
Left ventricular heart failure morphology in the brain
- Hypoxic Encephalopathy
48
Hypoxic Encephalopathy causes
- Impaired judgement / memory - Inattentiveness - Confusion - Motor incoordination
49
Causes of right ventricular heart failure
- Consequence of left-sided heart Failure - Pure right-sided heart failure - Cor Pulmonale
50
Morphological findings of right ventricular failure in the liver and portal system
- Congestive Hepatomegaly (cardiac cirrhosis) - Centrilobular Necrosis - Congestive Splenomegaly - Ascites
51
Morphological findings of right ventricular failure in the subcutaneous tissues
- Peripheral dependent edema - Ankle (pedal) edema - Pretibial edema - Presacral
52
Coronary circulation
- Right coronary artery (RCA) - Left coronary artery (LCA) - Left anterior descending - Left circumflex
53
Evolution of morphological changes in MI
- ½ - 4hr: waviness of fibers - 4 - 12hr: coagulation necrosis, edema, hemorrhage - 1 - 3days: loss of nuclei, coagulative necrosis, neutrophil infiltrate - 3 - 7days: dead myofibrils, phagocytosis by macrophages - 7 - 10days: Fibrovascular, granulation tissue - > 2mo: collagenous scar
54
Myocardial infarction laboratory findings
- CK - MB (elevated) - Troponin T (elevated) - Troponin I (elevated) - LDH (elevated) - CK = Creatine Kinase - LDH = Lactate Dehydrogenase
55
Complications associated with MI
- Cardiac rupture (7-10 days) | - Arrhythmias
56
Diabetic cardiomyopathy (DCM) is characterized by
- Progressive cardiac hypertrophy - Dilation - Contractile dysfunction
57
Causes of diabetic cardiomyopathy
- Myocarditis - EtoH and toxins - Pregnancy associated - Genetic - Idiopathic
58
Pathology of diabetic cardiomyopathy
- Large flabby heart - Dilation of all chambers - Thinning of ventricular walls - Mural thrombi (source of thromboemboli)
59
Mechanism of HF in DCM
- Impairment of contractility (systolic dysfunction)
60
Gross morphology of DCM
- 4 chamber dilation - Mural thrombi - Functional regurgitation
61
Clinical presentation of DCM
- Commonly affects 20 – 60 yo individuals - Slow progressive congestive heart failure - End stage / ejection fraction < 25% - Cardiac failure - Arrhythmia's
62
Characteristics of Hypertrophic Cardiomyopathy (HCM)
- Myocardial hypertrophy - Abnormal diastolic filling - Intermittent left ventricular outflow obstruction
63
Pathogenesis of HCM
- Familial disease | - Autosomal dominant
64
Mutations of genes for cardiac contractile elements associated with HCM
- β-myosin heavy chain (most frequently; 403 Arg --> Gln) - Cardiac Troponin T - α-Tropomyosin - Myosin binding protein C
65
Pathology of HCM
- Thickening of the ventricular septum (asymmetrical) - Thickening of anterior mitral leaflet - Myocyte hypertrophy - Haphazard disarray of myocyte bundles - Interstitial and replacement fibrosis
66
Venturi Phenomenon
- Outflow tract obstruction
67
HCM is the most common cause of unexplained death in
- Young athletes
68
Clinical presentation of HCM
- Reduced chamber size - Reduced stroke volume - Impaired diastolic filling - Ventricular outflow obstruction - Focal myocardial ischemia - Exertional dyspnea - Atrial fibrillation

Pathology I (9 decks)

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