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Cardiac Structure and Consequence of dysfunction > Pathogenesis of hypertrophy > Flashcards

Pathogenesis of hypertrophy Flashcards

a. Define cardiac hypertrophy and remodeling b. Define and describe morphologic patterns of pathologic cardiac hypertrophy c. Describe the adaptive response by a heart muscle cell to a prolonged increased workload d. Compare and contrast pathologic and physiologic cardiac hypertrophy

1
Q

What causes cardiac hypertrophy -general

A

Prolonged increase in workload

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2
Q

Hearts response to prolonged changes in workload

A

-remodels

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3
Q

Remodelling

A

The adaptive response of the heart to physiologic or pathologic stimuli

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4
Q

What does the process of remodeling involve

A
  • alterations at cellular, biochemical and molecular levels in the myocytes, vasculature and interstitium
  • ultimately leading to changes in size, shape and function of the heart
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5
Q

Causes of physiologic hypertrophy (2)

A
  • exercise

- pregnancy

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6
Q

Causes of pathologic hypertrophy (3)

A
  • hypertension
  • valve disease
  • infarction
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7
Q

Consequences of pathologic hypertrophy (4)

A
  • increase dysfunction after ischemia
  • increase infarct size
  • sudden death
  • heart failure
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8
Q

MOA normal heart –> pathologic hypertrophy

A

1) Pressure overload
2) Volume overload
3) Loss of contractile mass

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9
Q

Causes pressure overload

A
  • hypertension

- aortic stenosis

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10
Q

Causes volume overload

A
  • septal defects

- valvular regugitation

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11
Q

Causes of loss of contractile mass

A

-myocardial infarction

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12
Q

Law of laplace explanation of cardiac hypertrophy

A
  • Wall tension /stress is proportional to Pxr/h
  • if pressure increases due to a biomechanical stress (i.e. pressure overload) then to balance out and maintain wall tension thickness (h) of myocardial wall will increase = cardiac hypertrophy (negative feedback to wall tension/stress)
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13
Q

Two patterns of remodeling

A

1) pressure overload –> concentric remodeling

2) volume overload —> eccentric remodelling

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14
Q

Relative wall thickness

A

The ratio of LV wall thickness to diastolic diameter

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15
Q

Relative wall thickness in cocentric and eccentric hypertrophy

A
  • increase RWT in concentric (like wall growing in)

- decrease RWT in eccentric (like wall growing out)

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16
Q

MOA cardiac hypertrophy -what is happening to the cells

A

-increased cell size

17
Q

Pressure overload hypertrophy vs. volume overload hypertrophy

A

-difference in way the individual cells grow in
response to different stimuli
a) pressure overload
-increase length 5%
-increase x sectional area 150% (more like a square)
b) volume overload
-increase length 30%
-increase cross sectional area 50%
(which if look at the shape a rectangle - makes sense that it grows outwards)

18
Q

Cardiac hypertrophy response to a stimulus

- 2 changes included in growth

A

1) Quantitative changes
- structural changes i.e. size
2) Qualitative changes
- non structural changes (properties)
* * a hypertrophied heart is not just a big normal heart!

19
Q

Myocardial adaptations in pathologic cardiac hypertrophy

A
  1. decrease SR Ca2+ ATPase
  2. Increase ANP/BNP expression
    3) Expression NE/EPI receptors
    4) Increase glycolysis
    5) Decrease FA oxidation
    6) Increase beta MHC on contractile protein
    * many of changes in gene expression are reminiscent of the gene expression profile in fetal hearts
20
Q

MOA myocardial cell changes to get cardiac hypertrophy

A

1) Stimulus
-biomechanical stimuli
-neurohumoral stimuli
2) Receptors
activated by biomechanical stimuli
-stretch-sensitive receptors
activated by neurohumoral stimuli (hormones, cytokines, growth factors)
-surface receptors
3) Both stretch-sensitive and surface receptors activate the signal transduction pathway leading to..
a) gene transcription
b) protein synthesis/degradation
4) Net effect = cardiac hypertrophy

21
Q

Representative stimuli of cardiac myocyte hypertrophy

A

a) hormones
- Ang II
- endothelin-1
- norepinephrine/epinephrine
b) peptide growth factors
- insulin like growth factor 1
c) cytokines
- cardiotrophin-1

22
Q

Effects of prolonged exercise

A

Physiologic hypertrophy

23
Q

Hemodynamic response to acute exercise in endurance training (4)

A

1) increase o2 consumption
2) increase CO
3) Increase systolic bp
4) Decrease peripheral vascular resistance

24
Q

Hemodynamic response to acute exercise in strength training

A

1) Slight increase O2 consumption
2) Slight increase in CO output
3) Increase in systolic bp (more than endurance)
4) Increase peripheral vascular resistance

25
Q

Exercise induced morphologic changes -3 properties

A
  • majority in normal range
  • reversible with deconditioning
  • exact changes in morphology still depend on nature of stimulus
26
Q

Causes of physiologic concentric hypertrophy

A
  • still pressure overload = stimulus

- strength training (static/isometric)

27
Q

Causes of physiologic eccentric hypertrophy

A
  • still volume overload = stimulus

- endurance training (aerobic/isotonic)

28
Q

Energy substrate use in cardiac hypertrophy

A

1) In physiological hypertrophy
- fa utilization increased
- glucose utilization increased
2) In pathological hypertrophy
- fa utilization decreased
- glucose utilization increased

29
Q

Interstitial fibrosis changes in cardiac hypertrophy

A

-fibrous connective tissue level in left ventricle will be increased in pathologic cardiac hypertrophy

30
Q

Post ischemic recovery in cardiac hypertrophy

A

1) Will be decreased in pathologic hypertrophy

2) Will be increased in physiologic hypertrophy

31
Q

Pathologic vs. physiologic cardiac hypertrophy

a) fibrosis
b) fetal gene expression
c) cardiac function
d) association with heart failure
e) Reversible

A

a) yes, no
b) Increase, same?
c) decrease, increase
d) yes, no
e) “no”, yes

32
Q

What amount /intensity of exercise is the most beneficial

A

Greatest mortaility reduction with vigorous exercise for short period of time (i.e. around 30 min)

33
Q

Long-term consequences of intense, uninterrupted enducrance training in olympic atheletes

A

-not associated with deterioration in LV function, significant changes in LV morphology or occurence of CV symptoms or events

34
Q

Diverse patterns of myocardial fibrosis in lifelong veteran endurance athletes

A

-unexpectedly high prevalence of myocardial fibrosis observed in healthy asymptomatic, lifelong veteran male athletes

Cardiac Structure and Consequence of dysfunction (7 decks)

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