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Concepts Of Disease > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

What are risk factors of CVD?

A

Risk factors in CVD
* hypertension
* Smoking
* Alcohol misuse
* Unhealthy diet
* Physical inactivity
* Psychosocial factors
* Aging
* Gender
* Race/ ethnicity
* Genetic predisposition
* Obesity
* Diabetes
* Dyslipdaemia

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2
Q

What is atherosclerosis?

A

• Major underlying cause of CVD
• Build up of fatty material in arterial walls causing narrowing and stiffening
• Peripheral arteries
• Coronary arteries
• Cerebral atherosclerosis
• Restricted blood flow
-In heart= angina
-limb ischaemia
-stroke

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3
Q

What is a myocardial infarction?

A

Plaque rupture or blood clot occludes one or more arteries supplying the myocardium
Deprives regions of o2 and nutrients
Reduced activate area of contacting tissue during systole

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4
Q

What happens during circulatory collapse? How can circulation be maintained

A

Decreased contraction causes fall in BP and cardiac output. Immediate cardiopulmonary resuscitation (CPR) helps maintain circulation.

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5
Q

What are reperusion strategies?

A

• Clot busting drugs- thrombolytics break down fibrin
• Angioplasty- balloon catheter to restore blood flow to blocked artery
• Coronary artery bypass graft - take blood vessel from somewhere else in body usually leg and attach to heat- so bypass the heart

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6
Q

What are the acute effects of MI

A

Myocardial necrosis downstream of blockage- the cells begin to die - the longer a ligature is attached from more cellls have died

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7
Q

What is the immediate inflammatory response in infarct?

A

Pro-inflammatory response to clear necrotic cells
Release of cytokines triggers accumulation of neutrophils monocytes, macrophages

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8
Q

What happen during scar formation?

A

Reduction in pro-inflammatory signals transitions to a reparative phase
Fibroblasts differentiate into myofibroblasts speculating in producing large amounts of extra cellular matrix
Scar tissue non contractile and stiff

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9
Q

What’s the equations for wall stress?

A

Pressure X radius divided by 2 x wall thickness

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10
Q

What are the immediate effects of MI on the heart?

A
  • Tissue hypoxia
    Reduced rhythmic contraction
    Reduced bp
    Reduced cardiac output
    Tissue necrosis
    Inflammation in infarct region
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11
Q

What are the chronic effects of MI on the heart?

A

Widespread inflammation
Increased fibrosis
Increase ventricle stiffness
Increase hypertrophy
Increase ventricle dilation
Decrease systolic pressure
Deceased cardiac output Tissue necrosis

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12
Q

What is systemic hypertension?

A

A leading cause of CVD
Constriction of vascular smooth muscle cells
Increase cardiac output and systemic vascular resistance

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13
Q

How do you calculate mean arterial pressure?

A

Cardiac output X total peripheral resistance (TPR)

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14
Q

Does adding sacromeres in Paralell or series increase force generation?

A

In parallel

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15
Q

What are the hypertrophic signalling pathways?

A

Neuohumoral activation - insulin like growth factor-1 (IGF-1) AKt/ mTOR
Associated with physiological hypertrophy in response to exercise

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16
Q

Advantages and disadvantages of ECG

A

Advantages:
• information on electrical properties, conduction
• Low cost
• Simple
• Non-invasive- just electrodes
Limitations
• no info on contractile function or by
• Requires specialist to interpret

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17
Q

Advantages and disadvantages of BP monitor

A

Advantages
• info on systolic/ diastolic by
• Low cost
• Simple and easy to interpret
• Non invasive
Limitations
• dependent on vascular function
• Limited to systemic circulation- not pulmonary/RV function, atria - limbs
• No Ino on diastolic pressure in the heart

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18
Q

Ultrasound advantages and Disadavantages

A

Ultrasound
Advantages
• 2D/3D quantification of heart structure and contraction (stroke volume, ejection fraction, hypertrophy
• Indirect systolic pressure measurement using Doppler
• Moderate cost
• Also assess vascular function
• Fast
Disadavantages
• contraction measurements dependent on preload (ventricular filling) and afterload (vascular resistance
• No information on diastolic pressures or other phases of cardiac cycle
• Limited spatial resolution
• Image quality can be limiting- e.g obesity

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19
Q

Cardiac MRI advantages and disadvantages

A

Cardiac MRI
Advantages
* detailed 3D quantification of structure contraction and blood flow in all chambers
* Contrast techniques to measure fibrosis
Limitations
* dependent on preload (ventricular filling) and afterload (vascular resistance)
* No direct pressure measurment
* Expensive - 3k per scan
* Slow 1-2H - not real time

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20
Q

Pressure volume catheterisation advantages and disadvantages

A

Advantages
• direct systolic and diastolic pressures in all heart chambers and vessels
• Accurate volumes
• Real time throughout entire cardiac cycle Limited spatial
• Load independence measurement of heart function

Limitations
* invasive
* No info on heart structure
* No info on heart structure electrical function

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21
Q

What does an increase in slope of ESPV indicate?

A

Increased contractility- indicates how easily the hear expands as it fills
Steeper ESPVR indicates resistant to filing

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22
Q

What are the passive determinants of relaxation?

A

Fibrosis, microtubules and titin

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23
Q

What is fibrosis?

A

Fibrosis
* Interstital collagen normally present at low amounts (2-4%) in myocardium
* Mostly type 1 and 111 fibrillar collagen - structured
* Increased collagen deposition by myofibroblasts
* Diffuse or localised fibrosis impairs diastolic function
* Fibres covalently cross linked by glycosylation increases stiffness

24
Q

Describe microtubules

A

Microtubules
-cytoskeleton proteins formed by polymerisation of alpha and beta Tubulin
Dynamic structures that assemble and disassemble in minutes/ hours
Stability influenced by pot-translational modification, such as detyrosination of alpha tubulin

25
Q

Describe titin

A

Titin
* largest known protein (3.5MDa) spans rom Z-disk to M-line of sarcomere- 1um
* Bidirectional spring- resits strength, restores length during shortening
* Two isoforms N2B and N2BA (more compliant)
* Many post-translational modifications (Phosphorylation, oxidation splice variants) after compliance

26
Q

What happens during the beta adrenergic signaling cascade?

A

Noradrenaline and adrenaline bind to g-protein coupled beta1AR in sarcolemma
• Initiates singalling cascade leading to prodcution of cAMP by adenylyl cyclase
• CAMP activates protein kinase A (PKA) (serine specific kinases)
• Phosphate group reversible added to serine residues on target proteins modifying their function

27
Q

What happens during beta1- adrenoreceptor desensitisation?

A

Beta1-adrenoceptor desensitisation
• heart becomes reliant on catecholamines to maintain heart function e.g following MI
• B1-AR itself becomes phosphorylated and signals it for internalisation and degradation (negative feedback)

Reduced expression of proteins in the B1-AR singalling pathway in heart failure Increases
Chronic receptor activation leads to desensitisation and reduced B-adrenergic responsiveness
Less able to increase heart rate, contraction, relaxation

28
Q

What are the active determinants of relaxation?

A

Cystolic calcium
Myofilaments
Repolarisation

29
Q

What happens during excitation contraction coupling in the hear

A

• action potential initiates calcium release from Intracellular store (sarcoplasmic reticulum)
• Binding to myofilaments initiates contraction
• Calcium pumped back into SR and dissociates from myofilaments

30
Q

What is SERCA activity determined by?

A

SERCA Expression
Phospholamban expression
PLB phosphorylation

31
Q

What is the major calcium removal pathway in humans?

A

Ca repuptake in SR

32
Q

What happens to ca uptake in heart failure

A

Slower calcium uptake
As reduced SERCA activity
Calcium handling worsens at faster rates e.g exercise
Deceased SERCA expression in en stage heart failure

33
Q

How is calcium pump regulated?

A

Phospholamban;a ban acts as a brake on sarco(endo)plasmic reticulum ca ATPase (SERCA), PHOHSPHORYLATION of PLB relieves SERCA inhibitions and speeds calcium uptake

34
Q

What happens to phospholamban in heart failure?

A

No change in PLB expression
Hypophosphoylation of PLB in heart failure

35
Q

What does PLB hypophosphorylation do?

A

• reduces Ionotrophic (contraction) and lusitropic (relaxation) response
• Mutant non-phosphorylatable PLB diminished response to beta- AR stimulation

36
Q

How can family screening be used for CVD?

A

Families may have a history of sudden death, can then identify a pathological gene variant in the patient, and do genetic screening of family member that turn up asymptomatic but are carriers of the mutant alleles

37
Q

What are cardiomyopathies?

A

They broadly affect the structure and function of muscle cells or structure of the myocardium

38
Q

What is hypertrophic cardiomyopathy?

A

Is thickening o the heart

39
Q

What can hypertrophy be mistaken for on ECG?

A

Athletes heart

40
Q

What are thw two genes essential for cross bridging that has predominantly autosomal dominant mutations in causing hypertrophic cardiomyopathy?

A

MYH7
MYBPC3

41
Q

What type of mutuation usually occurs in MYH7?

A

Missense single nucleotide polymorphisms

42
Q

What type of mutation occurs in MYBPC3?

A

Nonsense, resulting in premature stop codon and truncated protein

43
Q

Where do MYH7 mutation occur? What effects does it have on cross-bridge cycling?

A

In head and neck region of B-MHC with ATPase and motor activity.
Lead to increased/ deceased myosin ATPase activity
Altered Ca2+ binding/ release from TnC

44
Q

What does HCM cause and lead to?

A

HCM usually causes hypercontractile cellular phenotype, leading to increased interactive between actin and myosin proteins
Increased force development, but slower relaxation
Increased myofilaments Ca2+ sensitivity

45
Q

What causes the symptoms of dyspnea and heart failure?

A

Septal hypertrophy obstructs the LV outflow tract so reduced cardiac output

46
Q

What is the septal myomectomy technique?

A

Removing a Chunk of the septum so allows blood flow

47
Q

What are the current treatments of cardiomyopathy?

A

 Current treatments include
 beta-blockers or Na channel inhibitor to slow heart rate and make it less
excitable
 implantable cardioverter defibrillator (ICD)
 Septal myectomy for obstructive HCM
 New myofilament desensitising drugs (e.g. Mavacamten) provide
symptomatic relief
 reduce myofilament Ca2+ sensitivity
 Lifestyle interventions may help reduce arrhythmias

48
Q

What are channelopathies?

A

They occur due to mutations in ion channels that regulate the electrical properties of the heart

49
Q

What is long QT syndome and what are symptoms?

A

Prolonged QT interval caused by delayed Repolarisation of the ventricle- develop anting, palpitations and sudden cardiac arrest

50
Q

What are the major genes encoding ion channels that are responsible for over 90% of LTQS

A

KCNQ1
KCNH2
SCN5A

51
Q

What does longer action potential increase the likelihood of? What does this trigger?

A

Early afterdepolarisations - can trigger premature ectopic beats and disrupt normal electrical conduction through the heart

Rapid uncoordinated contraction causes cardiac output to fall

52
Q

What are the treatments and lifestyle alive to treat QT syndrome?

A

 Treatments include
 beta-blockers
 Late sodium current blockers
 implantable cardioverter defibrillator
 left cardiac sympathetic denervation
 Lifestyle advice
 Avoiding strenuous swimming LQT1
 Avoiding loud noises LQT2
 Correcting electrolyte imbalance (e.g.
increasing potassium intake bananas,
vegetables, pulses)

53
Q

What can cause acquired LQTS?

A

Result of drugs e.g antibiotics, antihistamines, antidepressants anti-arrhythmics

Ikr very susceptible to inhibition by different drugs
Ikr block is specifically screened for during new drug development

54
Q

What can people with CPVT experience?

A

Severe arrhythmias during physical or emotional stress bought on by adrenaline

55
Q

What are the majority of cases of CPVT caused by? How does it work?

A

SNPs causing missense mutations in RYR2 gene. RYR2 is a Ca2+ channel located inside muscle cells in the membrane of Intracellular Ca2+ store. During systole, RYR2 channels open allows Ca2+ to pass into cytosol for muscle contraction
RYR2 normally remain closed in diastole- CPVT cases RYR2 to become leaky

56
Q

What are the symptoms of CPVT?

A

Not present at rest but usually provoked by stress, emotional and physical activity

Adrenaline increases Ca2+ loading in hear and overload Ca2+ store - when threshold in exceeded the store empties resulting in Ca2+ waves - Leaky RYR2 have a lower threshold

57
Q

Treatment of CPVT?

A

 beta-blockers to suppress adrenergic stimulation
 flecainide (Na channel inhibitor that may also inhibit
RYR2)
 left cardiac sympathetic denervation
 implantable cardioverter defibrillator

Concepts Of Disease (8 decks)

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