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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
Q

Pressure overloaded ventricles (concentric hypertrophy) results

A
  • Stimulates deposition of new sarcomeres (Parallel)
  • Hypertrophy of the left ventricle (concentric)
  • Reduction in cavity diameter
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26
Q

Volume overloaded ventricles

A
  • Ventricular dilation

- Dilated cardiomyopathy

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27
Q

Volume overloaded ventricles (eccentric hypertrophy) results

A
  • 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
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28
Q

Measure of hypertrophy

A
  • Heart weight
29
Q

Pressure vs. volume overload hypertrophy

A
  • Hypertrophy with and without dilation
30
Q

Characteristics of cardiomyopathic remodeling

A
  • Damaged and dysfunctional mitochondria
  • Energy-deficient state
  • Intra-myocellular lipid accumulation
  • Reactive oxygen species generation
31
Q

Hallmark of myocardial remodeling

A
  • Increased myocardial volume and mass with net loss of myocytes
  • Larger myocytes die
  • Increased load placed upon remaining myocytes
  • Progenitor cell stimulation
32
Q

Counter-regulatory effects that decline in myocyte and myocardial remodeling

A
  • Nitrous oxide
  • Prostaglandins
  • Bradykinin
  • Atrial natriuretic peptide and B-type
33
Q

Decline in counter-regulatory effects during myocardial remodeling results in

A
  • Reduction of cardiac output
34
Q

Consequences in reduction of cardiac output

A
  • Release of vasoconstrictors

- Vasoconstriction increases calcium concentrations in myocytes

35
Q

Vasoconstriction increasing calcium concentrations in myocytes causes

A
  • Contractility augmentation

- Impairment in relaxation

36
Q

Impairment of relaxation secondary to increased calcium concentration in myocytes results in

A
  • Increased β-adrenergic activity

- Activation of RAAS

37
Q

Peroxisome proliferator-activated receptors cause

A
  • Abnormalities in myocardial energy metabolism

- Maladaption

38
Q

Abnormalities in myocardial energy metabolism

A
  • Suppression of FA oxidation

- Increased glucose utilization

39
Q

Maladaptions caused by peroxisone proliferator-activated receptors

A
  • Lipid accumulation
  • Lactic acid accumulation
  • Diminished maximal ATP generation
40
Q

Systemic manifestations of left and right ventricular heart failure

A
  • Accumulation of excess fluid behind one or both ventricles
  • Activation of neurohormonal mechanisms
  • Organ dysfunction secondary to inadequate perfusion
41
Q

Left ventricular failure morphological findings seen in

A
  • Heart
  • Lungs
  • Kidneys
  • Brain
42
Q

Morphological findings of left ventricular heart failure in the heart

A
  • Hypertrophy and fibrosis in the myocardium

- Secondary enlargement of the left atrium with resultant atrial fibrillation

43
Q

Morphological findings of left ventricular heart failure in the lungs

A
  • Pulmonary congestion and edema
  • Widening of alveolar septa
  • Fluid in the alveolar spaces
  • Heart failure cells
44
Q

Pulmonary congestion and edema radiographic findings

A
  • Kerley B lines on x-ray

- Perivascular and interstitial transudate

45
Q

Clinical manifestations of left ventricular heart failure in the lungs

A
  • Dyspnea
  • Orthopnea
  • Paroxysmal Nocturnal Dyspnea
46
Q

Left ventricular heart failure morphology in the kidneys

A
  • Activation of the RAAS
  • Prerenal Azotemia
  • Manifestations of edema
47
Q

Left ventricular heart failure morphology in the brain

A
  • Hypoxic Encephalopathy
48
Q

Hypoxic Encephalopathy causes

A
  • Impaired judgement / memory
  • Inattentiveness
  • Confusion
  • Motor incoordination
49
Q

Causes of right ventricular heart failure

A
  • Consequence of left-sided heart Failure
  • Pure right-sided heart failure
  • Cor Pulmonale
50
Q

Morphological findings of right ventricular failure in the liver and portal system

A
  • Congestive Hepatomegaly (cardiac cirrhosis)
  • Centrilobular Necrosis
  • Congestive Splenomegaly
  • Ascites
51
Q

Morphological findings of right ventricular failure in the subcutaneous tissues

A
  • Peripheral dependent edema
  • Ankle (pedal) edema
  • Pretibial edema
  • Presacral
52
Q

Coronary circulation

A
  • Right coronary artery (RCA)
  • Left coronary artery (LCA)
  • Left anterior descending
  • Left circumflex
53
Q

Evolution of morphological changes in MI

A
  • 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
Q

Myocardial infarction laboratory findings

A
  • CK - MB (elevated)
  • Troponin T (elevated)
  • Troponin I (elevated)
  • LDH (elevated)
  • CK = Creatine Kinase
  • LDH = Lactate Dehydrogenase
55
Q

Complications associated with MI

A
  • Cardiac rupture (7-10 days)

- Arrhythmias

56
Q

Diabetic cardiomyopathy (DCM) is characterized by

A
  • Progressive cardiac hypertrophy
  • Dilation
  • Contractile dysfunction
57
Q

Causes of diabetic cardiomyopathy

A
  • Myocarditis
  • EtoH and toxins
  • Pregnancy associated
  • Genetic
  • Idiopathic
58
Q

Pathology of diabetic cardiomyopathy

A
  • Large flabby heart
  • Dilation of all chambers
  • Thinning of ventricular walls
  • Mural thrombi (source of thromboemboli)
59
Q

Mechanism of HF in DCM

A
  • Impairment of contractility (systolic dysfunction)
60
Q

Gross morphology of DCM

A
  • 4 chamber dilation
  • Mural thrombi
  • Functional regurgitation
61
Q

Clinical presentation of DCM

A
  • Commonly affects 20 – 60 yo individuals
  • Slow progressive congestive heart failure
  • End stage / ejection fraction < 25%
  • Cardiac failure
  • Arrhythmia’s
62
Q

Characteristics of Hypertrophic Cardiomyopathy (HCM)

A
  • Myocardial hypertrophy
  • Abnormal diastolic filling
  • Intermittent left ventricular outflow obstruction
63
Q

Pathogenesis of HCM

A
  • Familial disease

- Autosomal dominant

64
Q

Mutations of genes for cardiac contractile elements associated with HCM

A
  • β-myosin heavy chain (most frequently; 403 Arg –> Gln)
  • Cardiac Troponin T
  • α-Tropomyosin
  • Myosin binding protein C
65
Q

Pathology of HCM

A
  • Thickening of the ventricular septum (asymmetrical)
  • Thickening of anterior mitral leaflet
  • Myocyte hypertrophy
  • Haphazard disarray of myocyte bundles
  • Interstitial and replacement fibrosis
66
Q

Venturi Phenomenon

A
  • Outflow tract obstruction
67
Q

HCM is the most common cause of unexplained death in

A
  • Young athletes
68
Q

Clinical presentation of HCM

A
  • 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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