Brainscape's Knowledge GenomeTM

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


See full index

!!!!! BRS YR2 !!!!! > Cardio - Structural Heart Diseases > Flashcards

Cardio - Structural Heart Diseases Flashcards

1
Q

What are structural heart diseases?

A

defects that affect the valves + chambers of the heart + aorta

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

What are the 2 main types of structural heart diseases?

A

→ congenital heart defects

→ ones formed later in life

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

What are some examples of congenital structural heart diseases?

A 
→ atrial septal defect (ASD)
→ ventricular septal defect (VSD)
→ coarctation of aorta
→ patent foramen ovale (PFO)
→ Patent ductus arteriosus (PDA)
→ Tetralogy of Fallot (TOF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some examples of structural heart diseases developed later in life?

A

→ valvular dysfunctions (Atrial stenosis /regurgitation)

→ muscular (cardiomyopathies)

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

What is ventricular septal defect (VSD)?

A

→ ventricular wall between two ventricles doesn’t develop properly
→ leads to hole in wall

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

What are pathophysiological consequences of VSD?

A

mix of oxygenated + deoxygenated blood in the ventricles

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

How does a child present with VSD?

A

→ poor weight gain
→ poor feeding
→ heart palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is VSD treated?

A

→ sometimes if hole small enough, it closes as the child develops
→ if not, open heart surgery needs to be done to put a patch on the hole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is tetralogy of fallot (TOF)?

A

→ combination of 4 defects
→ ventricular septal defect
→ pulmonary stenosis (narrow pulmonary trunk)
→ widening of aortic valve (allows mixing of right ventricular + aortic blood)
→ right ventricle hypertrophy (thickening of right ventricular wall)

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

What is atrial septal defect (ASD)?

A

hole in the wall between the 2 atria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the coarctation of the aorta?

A

narrowing of the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the consequences of coarctation of the aorta?

A

→ ventricle has to work harder to pump blood through the aorta
→ causes thickening of ventricular muscle

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

What is cardiomyopathy?

A

→ disease of the heart muscle that makes it harder for heart to pump blood to the rest of the body
→ can lead to heart failure

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

What are the 3 types of cardiomyopathy?

A

→ dilated
→ hypertrophic
→ restrictive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is dilated cardiomyopathy?

A

characterised by left ventricular chamber enlargement + systolic dysfunction with normal left ventricular wall thickness

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

When does dilated cardiomyopathy most commonly occur?

A

third or fourth decade of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the causes of dilated cardiomyopathy?

A 
→ familial
→ idiopathic
→ heart valve disease
→ after child birth
→ thyroid disease
→ myocarditis
→ alcoholism
→ autoimmune disorders
→ ingestion of drugs
→ mitochondrial disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the hallmark gross finding of dilated cardiomyopathy?

A

left ventricular dilation, more than 4cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is familial DCM?

A

→ genetic predisposition to dilated cardiomyopathy
→ rare autosomal dominant inheritance pattern
→ first degree relative have a 50 % chance of getting DCM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the abnormal physiology of DCM?

A

→ Enlargement of the left ventricle
→ lower ejection fraction and increase in the ventricular wall stress and end systolic volumes
→ Early compensatory mechanisms include an increase in heart rate and tone of the peripheral vascular system.
→ neurohumoral activation of the renin-angiotensin aldosterone system and an increase in circulating levels of catecholamines.
→ levels of natriuretic peptides are also increased.
→ Eventually these compensatory mechanisms become overwhelmed + heart fails.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the common history + presentation of DCM?

A 
→ dyspnoea
→ murmur
→ fatigue
→ angina
→ pulmonary congestion
→ low cardiac output
→ displaced apex beat (S3 or systolic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the investigations that can be done for DCM?

A 
→ genetic testing
→ viral serology
→ ECG
→ chest X-ray
→ cardiac catheterisation
→ cardiac MRI / CT scan
→ exercise stress test
→ echocardiography (ECG)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is DCM managed ?

A 
→ diet modification (fluid + sodium restrictions)
→ treatment of the underlying cause
→ treat the symptoms of heart failure
→ treat thrombo-embolic events
→ treat arrhythmias, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What dietary modifications can be made for DCM?

A

fluid + sodium restrictions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do you treat DCM if the underlying cause is sarcoidosis or myocarditis?

A

immunosuppressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How do you treat DCM if the underlying cause is haemochromatosis?

A

phlebotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How do you treat the symptoms of heart failure for DCM?

A

→ ACE inhibitors
→ beta blockers
→ addition of angiotensin II receptor antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

When should the dose of ACEi be reduced in patients of DCM?

A

if patient develops:
→ a cough
→ hypotension
→ and/or renal dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is given to surgical candidates of DCM when heart failure treatment is ineffective?

A

→ LVAD

→ orthotropic heart transplantation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is given to non-surgical candidates of DCM when heart failure treatment is ineffective?

A

→ LVAD

→ optimise medical management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How are arrhythmias treated in patients with DCM?

A

→ amiodarone
→ dofetilide
→ ICD or CRT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How are thromboembolic events in patients with DCM treated?

A

anticoagulants e.g. warfarin after assessing previous TE, severe systolic dysfunction or ventricular dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is hypertrophic cardiomyopathy?

A

→ defined by increase in LV wall thickness

→ not solely explained by abnormal loading conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How is HCM contracted?

A

→ genetic cardiovascular disease

→ familial HCM = autosomal dominant Mendelian-inherited disease in approx 50 % of cases

35
Q

What is HCM the leading cause of?

A

sudden cardiac death (in preadolescent + adolescent children)

36
Q

What are the symptoms of HCM?

A

→ most patients are asymptomatic

→ first clinical manifestation can range from atrial fibrillation, tachycardia or sudden cardiac death

37
Q

What is the hallmark of HCM?

A

myocardial hypertrophy that is inappropriate, often asymmetrical, occurs in absence of obvious hypertrophy stimulus

38
Q

Where does HCM frequently present in the left ventricle?

A

→ can be anywhere

→ frequently involves inter ventricular septum

39
Q

What does hypertrophy of the inter ventricular septum result in?

A

obstruction of flow through the LF outflow tract

40
Q

What is the abnormal physiology of HCM?

A

→ abnormal diastolic function = impaired ventricular filling + increased filling pressure despite small or normal ventricular cavity
→ abnormal calcium kinetics
→ sub-endocardial ischemia
→ related to profound hypertrophy + myopathic process

41
Q

What are some of the signs and symptoms of symptomatic HCM?

A 
→ double carotid artery impulse
→ S3 gallop
→ syncope
→ presyncope
→ ejection systolic murmur
→ congestive heart failure
→ dizziness
→ palpitations
→ angina
→ sudden cardiac death
42
Q

What are the investigations that can be done to confirm HCM?

A 
→ haemoglobin level 
→ brain natriuretic peptide (BNP)
→ troponin T levels
→ ECG
→ CXR
→ cardiac MRI
43
Q

Why does Hb level need to be checked in HCM?

A

anaemia exacerbates chest pain + dyspnea

44
Q

Why do BNP and troponin T levels need to be check in HCM?

A

high levels of both are associated with higher risk of CVD events, heart failure + death

45
Q

How are the symptoms of HCM managed? What are the medications and order of prescription?

A 
→ beta blockers
→ verapamil
→ disopyramide
→ mechanical therapy
→ PM with short AV delay
→ septal myectomy or ablation
46
Q

When is verapamil given to a patient with HCM instead of or after beta blockers?

A

→ after side effects from beta blockers

→ instead of beta blockers if there is non-cardiac contraindication to beta blockers

47
Q

When is disopyramide given to a patient with HCM?

A

if there is:
→ LVOT gradient
→ and persistent symptoms
→ and absence of contraindication to disopyramide

48
Q

When is mechanical therapy given to a patient with HCM?

A

when the patient presents with refractory symptoms

49
Q

When is a PM with an AV delay prescribed to a patient with HCM?

A

when patient has a existing PM or contraindication to more invasive management

50
Q

When is septal myectomy or ablation appropriate for a patient with HCM?

A

when refractory symptoms present to a PM with AV delay AND there’s no contraindication to more invasive management

51
Q

What is restrictive cardiomyopathy?

A

→ increased stiffness of the myocardium
→ diastolic dysfunction with restrictive ventricular physiology
→ atrial enlargement due to impaired ventricular filling during diastole
→ systole function, volume + wall thickness of ventricles is usually normal

52
Q

Why is RCM a less well-defined cardiomyopathy?

A

diagnosis is based on establishing the presence of a restrictive ventricular filling pattern

53
Q

What percent of diagnosed cardiomyopathies does RCM account for?

A

5%

54
Q

What is the aetiology of RCM?

A

→ idiopathic
→ familial (related to troponin I or design mutations to do with skeletal myopathy)
→ various systemic disorders

55
Q

What systemic disorders can cause RCM?

A 
→ haemochromatosis
→ amyloidosis
→ sarcoidosis
→ Fabry's disease
→ carcinoid syndrome
→ scleroderma
→ anthracycline toxicity
→ previous radiation
56
Q

What is the pathophysiology of restrictive cardiomyopathy?

A

→ Infiltrative CMs are characterized by deposition of abnormal substances (ie, amyloid proteins, non-caseating granulomas, iron) within the heart tissue.
→ Infiltration causes the ventricular walls to stiffen, leading to diastolic dysfunction
→ Restrictive physiology predominates in the early stages, causing conduction abnormalities and diastolic heart failure
→ Adverse remodelling may lead to systolic dysfunction and ventricular arrhythmias in advanced cases.

57
Q

What abnormal physiology does RCM present with?

A

→ Increased stiffness of the myocardium causes ventricular pressures to rise precipitously with small increases in volume
→ accentuated filling occurs in early diastole + terminates abruptly at the end of the rapid filling phase
→ reduced compliance due to increased diastolic stiffness = LV doesn’t fill adequately in normal filling pressures
→ reduced LV filling = reduced cardiac output

58
Q

What are the common signs and presentations of RCM?

A

→ more comfy in sitting position because fo fluid in abdomen or lungs
→ frequent ascites + pitting edema of the lower extremities
→ liver enlarged + full of fluid = very painful
→ weight loss + cardiac cachexia common
→ Increased jugular venous pressure
→ pulse volume is decreased, consistent with decreased stroke volume and cardiac output

59
Q

What findings are consistent with amyloidosis causing RCM?

A

→ Easy bruising
→ periorbital purpura
→ macroglossia
→ other systemic findings e.g. carpal tunnel syndrome

60
Q

What investigations can be carried out for RCM?

A 
→ CBC (complete blood count)
→ serology
→ amyloidosis check
→ CXR
→ ECG
→ catheterisation
→ MRI / biopsy
61
Q

How is RCM managed?

A 
→ heart failure medication
→ anti arrhythmic therapy
→ immunosuppression - steroids
→ pacemaker
→ cardiac transplantation
62
Q

What heart failure medication is used to treat RCM?

A 
should be initiated in patients with reduced LV:
→ ACE inhibitors
→ angiotensin receptor II blockers
→ diuretics
→ aldosterone inhibitors
63
Q

What is the equation for cardiac output?

A

cardiac output = heart rate x stroke volume

64
Q

How do you calculate stroke volume?

A

stroke volume = end diastolic volume - end systolic volume

65
Q

How do you calculate ejection fraction?

A

ejection fraction = (stroke volume / end diastolic volume) / 100

66
Q

How can mean arterial pressure (MAP) be calculated using systolic + diastolic pressure?

A

MAP = DP + 1/3(SP-DP)

67
Q

What is infective endocarditis?

A

infection of the endocardium or vascular endothelium of the heart
→ result of bacteria entering the blood stream and forming a “vegetation” in the endocardium
→ vegetation = bacterial infection surrounded by layer o platelets + fibrin

68
Q

What part of the heart does infective endocarditis normally affect?

A

heart valves

69
Q

What are the main bacterial causes? What is the most common?

A

→ STREPTOCOCCI (20 - 40%)
→ strep viridans
→ staph aureus
→ gram negative bacteria

70
Q

What are the signs + symptoms of infective endocarditis?

A 
→ fever
→ malaise
→ sweats
→ unexplained weight loss
→ cardiac decompensation
→ anaemia
→ raised markers of infection
71
Q

What abnormal physiology can be observed in the heart in infective endocarditis?

A

→ vegetation
→ abscess
→ valve perforation and/or new dehiscence of prosthetic valve
→ regurgitation of the affected valve

72
Q

What investigations can be performed for infective endocarditis?

A 
→ ECG
→ CXR
→ blood tests
→ blood cultures
→ transoesophageal echocardiogram
73
Q

Why is a transoesophageal echo better than a trans thoracic?

A

higher sensitivity in the first one

74
Q

What is Duke’s major criteria for infective endocarditis?

A

→ persistently positive blood culture for typical organisms
→ ECHO : vegetation, dehiscence of prosthetic valve, abscess
→ new valvular regurgitation murmur
→ coxiella brunetti infection

75
Q

What is Duke’s minor criteria for infective endocarditis?

A

→ predisposing heart condition or IV drug use
→ fever greater than 38 degrees celsius
→ vascular emboli to organs ro brain
→ immunological signs e.g. glomerulonephritis, Osler snores, Roth spots
→ positive blood cultures that don’t meet the major criteria

76
Q

What part of Duke’s criteria needs to be met to diagnose definite endocarditis?

A

→ 2 major clinical criteria OR
→ 1 major and 3 minor clinical criteria OR
→ 5 minor clinical criteria OR
→ positive gram stain or culture from surgery or autopsy

77
Q

What part of Duke’s criteria needs to be met to diagnose possible endocarditis?

A

→ 1 major and more than 1 minor clinical criteria OR

→ 3 minor criteria

78
Q

What part of Duke’s criteria needs to be met to reject endocarditis?

A

→ resolution after less than 4 days of antibiotic treatment
→ no evidence of infection after surgery
→ definite or possible criteria not met

79
Q

How is infective endocarditis treated?

A

→ first-line medical management = IV antibiotic course

→ surgical management to repair or replace a damaged heart valve or drain away any abscesses

80
Q

What are the signs of cardiac decompensation?

A 
→ shortness of breath
→ frequent coughing
→ swelling of legs + abdomen
→ fatigue
→ raised JVP (jugular venous pressure)
→ lung crackles
→ oedema
81
Q

What valves does infective endocarditis affect the most? The least?

A

→ aortic
→ then mitral
→ then right-sided valves

82
Q

Why are valves most commonly affected by infective endocarditis?

A

→ easier for vegetation to occur on valves that are already damaged
→ damage occurs most to the valves of the heart that experience turbulent blood flow

83
Q

What communities have increased risk of infective endocarditis?

A

→ IV drug users
→ those who undergo dental surgeries
→ immuno-suppressed
→ congenital heart defects that lead to damaged endocardium

84
Q

What genes have been associated with inheritance of DCM?

A 
mutations in genes encoding cardiac cytoskeletal proteins:
→ Titin
→ Lamin
→ Phospholamban
→ Cardiac myosin binding protein C
→ myosin heavy chain

!!!!! BRS YR2 !!!!! (72 decks)

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