Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Physiology > Ischaemic reperfusion injury and HF > Flashcards

Ischaemic reperfusion injury and HF Flashcards

1
Q

After infarction, dead muscle is replaced by what kind of tissue?

A

Fibrous tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

After infarction, the remaining functional part of the heart undergoes ____ to compensate for muscle death.

A

Hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The size of the damage zone from original and ischaemic reperfusion injury (IRI) is determined by what factor?

A

The site of vessel occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List the four consequences of IRI

A
  • Myocardial stunning
  • Reperfusion arrhythmias
  • Endothelial dysfunction
  • Irreversible cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is meant by ‘myocardial stunning’?

A

Failure to recover contractile function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the result of endothelial dysfunction after IRI

A

Impaired endothelial-mediated vasodilatory mechanisms and hyper-responsiveness to vasoconstriction results in the NO flow phenomenon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List some of the ways IRI leads to irreversible cell death

A
  • Maintained hypoxia
  • Inflammatory responses
  • ROS
  • Ca toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the mechanism of the oxygen paradox

A
  • ROS generated from endothelial cells and the inflammatory response upon reperfusion leads to cell death
  • Ischaemic endothelial cells upregulate xanthine oxidase after reperfusion which generates super-oxide radicals (hydrogen peroxide, super-oxide anion, hydroxyl radical)
  • Oxygen radials damage lipid membranes and proteins, leading to permeable ‘leaky’ membranes. This causes cellular oedema and massive Ca influx (calcium paradox), causing cell lysis
  • ROS reacts with and destroys NO (nitric oxide); NO is a vasodilator and is cardio-protective (inhibits neutrophils). This leads to the NO flow effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the mechanism of the calcium paradox

A

Abrupt increase in Ca++ released from dying cells causes overwhelming cytoplasmic and mitochondrial Ca++ overload. This causes hyper-contraction of myocardial cells (which are already swelling due to odema and ion influx), resulting in cell death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the mechanism of the pH paradox

A
  • Absence of O2 during ischaemia increases anaerobic metabolism, causing lactate build-up which decreases pH
  • Rapid restoration of normal physiological pH by reperfusion triggers cell death by removing the protective mechanism (driven by acidosis) that was helping to prevent hyper-contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

List some potential therapies to combat oxygen paradox

A
  • Allopurinol (inhibits xanthine oxidase activity)
  • Anti-inflammatory drugs (ineffective so far)
  • Anti-oxidants (e.g. vitamin E)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name a potential therapy to combat calcium paradox

A

Calcium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What can be done to combat pH paradox?

A

Experimentally reperfusing ischaemic tissues with acidic buffers has had a significant cardio-protective effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name the four mechanisms of HF

A
  • Myocardial remodelling
  • Venous congestion
  • Worsening renal function
  • Endothelial dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pathogenesis of HF after MI is closely linked with development of what?

A

Post-infarct remodelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

True or false: structural and functional alterations involve both infarcted and non-infarcted myocardial tissue.

A
17
Q

Cardiac remodelling can result in what two kinds of long term effects?

A

Dilative and fibrotic effects

18
Q

Cardiac remodelling with dilative effects causes what kind of dysfunction?

A

Systolic dysfunction

19
Q

Cardiac remodelling with fibrotic effects causes what kind of dysfunction?

A

Diastolic

20
Q

What factors may influence development of dilative or fibrotic effects after cardiac remodelling?

A

Genetics and comorbidities

21
Q

Describe the progression of cardiac remodelling

A
  • Myofibroblasts are recruited to damaged area and secrete large amounts of extracellular matrix to preserve structural integrity of the region
  • In the myocardium, preservation of geometry and function are dependent on balance between matrix degrading and replacement
  • Overactive matrix degradation triggered by excessive prolonged inflammation leads to ventricle dilation and systolic dysfunction
22
Q

What function of the inflammatory response is crucial to prevent excessive damage and remodelling?

A

Timely regression

23
Q

What is acute decompensated heart failure?

A

Sudden worsening of pre-existing CHF

24
Q

Describe the development/effect of LHF

A
  • Too much blood in the L) ventricle; fluid backs up into the lungs, causing:
    • Pulmonary oedema (crackles)
    • Dyspnoea
    • Orthopnoea (worsens when supine)
    • Narrow pulse pressure (difference between systolic and diastolic BP)
25
Q

Describe the development/effect of RHF

A

Blood backs up into venous circulation, causing peripheral oedema and JVD

26
Q

On which side does hypertrophy primarily occur, the failing side or the adequate side?

A

Primarily the failing side

27
Q

What is the role of the sinoatrial (SA) node?

A

Impulse (heartbeat) generation

28
Q

What is the role of the atrioventricular (AV) node?

A

To delay the impulse as it passes from atria to ventricles

29
Q

The AV node and Bundle of His together form what pathway?

A

The pathway from atria to ventricles

30
Q

Describe the process of excitation in the heart

A
  • SA node generates impulse
    • Atrial excitation begins
  • Impulse is delayed at AV node
  • Impulse passes to heart apex along bundle branches
    • Ventricular excitation begins
  • Impulse travels along Purkinje fibres; ventricular excitation is complete
31
Q

List the sympathetic effects on the heart via the cardiac nerve

A
  • Increased HR
  • Increased force of contraction
  • Increased blood flow to the heart
32
Q

List the parasympathetic effects on the heart via the vagus nerve

A
  • Slows HR
  • Decreases force of contraction
33
Q

Which region of the brain controls cardiac function?

A

The medulla oblongata (in the brainstem)

34
Q

List some effects of the sympathetic division of the autonomic nervous system

A
  • “Fight or flight”
  • Pulmonary
    • Brochodilation
    • Increased pulmonary blood flow
  • Cardiac
    • HR increases
    • Increased strength of cardiac contraction
    • Coronary vessel dilation
  • Ocular
    • Dilates pupils
    • Relaxes ciliary muscles (improves distance vision)
  • Cardiovascular
    • Increased blood flow to skeletal muscles ∴ increased O2 and glucose, enabling muscles to work harder
    • Constricts vessels in skin and GIT
  • Gastrointestinal
    • Inhibits peristalsis
    • Constricts all intestinal sphincters and the urinary sphincter
  • Glycogenolysis (glycogen to glucose)
  • Adrenaline secretion
35
Q

List some effects of the parasympathetic division of the autonomic nervous system

A
  • ‘Rest and digest’
  • Calming
  • Facilitates GIT function
36
Q

What is the effect of atropine?

A

Derived from atropa belladonna, AKA deadly nightshade; blocks the parasympathetic nervous system

Clinical Physiology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions