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Year 3 - CR > Cardio-Vascular Pathology > Flashcards

Cardio-Vascular Pathology Flashcards

1
Q

Define heart failure

A

Inability of the heart to pump blood at a rate commensurate with the requirements of the metabolising tissues

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2
Q

How does heart failure develop

A

Slowly
- cardiac hypertrophy

actue

  • MI
  • acute valve dysfunction
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3
Q

How common is heart failure

A

5 million in US

  • commonest discharge diagnosis in under 65
  • under 1 million hospitalised
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4
Q

What are the two types of heart failure

A
  • Systolic dysfunction

- Diastolic dysfunction

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5
Q

Name the causes of systolic dysfunction

A
  • Ischaemic heart disease
  • pressure or volume overload such as systemic hypertension or aortic stenosis (AS)
  • Cardiomyopathy
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6
Q

Name the causes of diastolic dysfunction

A
  • Inability to reflex/fill
  • amyloid deposition
  • myocardial fibrosis
  • constrictive pericarditis - after radiotherapy particularly for breast, TB, connective tissue disorders
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7
Q

How does amyloid deposition interfere with tissues function

A
  • a collection of protein that are undigestible by the proteases therefore the protein when deposited in tissues interferes with the tissues function
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8
Q

What are the two consequences of heart failure

A

Forward

Backward

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9
Q

describe the forward and backward problem (consequence of heart failure)

A

Forward

  • deliver the oxygen to the organs.
  • The heart is not pumping out enough blood to satisfy the needs of the cells of the body. Thus, excess fluid retention and edema increase

backward

  • hypoxic blood in the venous system
  • One of the ventricles fails to pump out all of its blood that comes into it. Thus, the ventricular filling pressure and systemic or pulmonary edema increase.
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10
Q

Name mechanisms that are used to cope with heart failure

A
  • frank-starling
  • hypertrophy +/- chamber dilation
  • activation of neurohormonal systems such as noradrenaline, RAAS and atrial natriuretic peptide
  • may eventually be exceeded
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11
Q

What is the frank starling law

A
  • this is the idea that increase in stretching of the heart causes an increase in contraction
  • relation to EDV - as EDV increases this causes the heart muscle to stretch and increase in contraction to pump the EDV out
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12
Q

What are the consequences of heart failure

A
  • Heart size/weight increase
  • hypertrophy
  • pressure overload - concentric hypertrophy
  • volume overload - cavitary dilation maybe without thickening
  • hypertrophy - can cause capillary decrease - increase in fibrous tissue - increase metabolic needs - vicious circle that leads to failure
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13
Q

Anything that does cause hypertrophy in the left ventricle is associated with…

A

Sudden death

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14
Q

Why do people who have left sided heart failure present the way they do

A

Main features are due to decreased peripheral pressure and damming of blood in the pulmonary circulation

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15
Q

What is the presentation of someone with left sided heart failure

A
  • Lung congestion
  • oedema
  • accumulation of haemosiderin laden macros - leads to dyspneoa due to fluid build up on lungs, orthopnoea - fluid getting worse when you lie down, PND
  • heart depends on cause - IDH, HT, Valves
  • Brain and kidneys if severe suffer hypoxia (hypoxia - peripheral blood becomes hypoxic)
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16
Q

Describe what causes the symptoms of right sided heart failure

A
  • Usually secondary to LVF

- primary association with severe pulmonary hypertension

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17
Q

What are the symptoms of right sided heart failure

A

Liver

  • pure liver congested - nutmeg
  • centrilobular necrossi and firbosis
  • portal vein pressure increase - splenomegaly, ascities, kidneys and brain hypoxia, peripheral oedema
  • biventricular - plus LVF
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18
Q

What is hypertension defined as

A
  • systolic greater than 140mmHg

- diastolic greater than 90mmHg

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19
Q

What is hypertension as risk factor for

A
  • IDH
  • Cerebrovascular disease
  • aortic dissection
  • cardiac failure
  • renal failure
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20
Q

Name the types of hypertension

A
  • Primary/essential (95%)
  • secondary
  • benign or malignant/accelerated (5%)(has severe end organ damage)
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21
Q

Name the causes of secondary hypertension

A

Renal

  • Chronic renal disease
  • glomerulonephritis
  • renal artery stenosis

Neurological

  • stress including surgery
  • psychogenic
  • raised intracranial pressure

Cardiovascular

  • coarctation of the aorta
  • systemic vasculitis
  • increased intravascular volume

Endocrine

  • cushings
  • conns
  • exogenous hormones
  • pheochromocytoma
  • acromegaly
  • thyroid disease
  • pregnancy
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22
Q

How do you measure blood pressure

A

Cardiac output x peripheral resistance

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23
Q

What influences cardiac output

A

Blood volume

  • sodium
  • mineralocorticoids

cardiac factors

  • heart rate
  • contractility
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24
Q

What influences peripheral resistance

A

Constrictors

  • angiotensin II
  • catecholamines
  • thromboxane
  • leukotrienes
  • endotheliin
  • alpha adrenergic

Dilators

  • prostaglandins
  • NO
  • Beta adrenergic

local factors

  • autoregulation
  • ionic (pH, hypoxia)
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25
Q

What do you see in the heart when someone has hypertension

A
  • Left ventricular hypertrophy
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26
Q

What do you see in the vessels in someone who has hypertension

A
  • atheroma
  • aortic dissection,
  • cerebrovascular haemorrhages,
  • degenerative changes such as fibrointimal thickening
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27
Q

What do you see in the small vessels in someone who has hypertension

A
  • hyaline arteriolosclerosis esp kidneys,
  • hyperplastic arteriolosclerosis (onion-skinning)
  • fibrinoid necrosis in accelerated
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28
Q

What is cor pulmonale

A

Heart disease as a consequence to lung disease

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29
Q

What is pulmonary hypertension

A

High blood pressure in the pulmonary circulation

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30
Q

What can cause pulmonary hypertension

A
  • diseases of the lung parenchyma such as COPD, cystic fibrosis, diffuse interstitial fibrosis
  • diseases of the pulmonary vessels such as recurrent, PEs, primary PH, severe vasculiits
  • Disorders affecting chest movement such as kyphoscoliosis, neuromuscular disease
  • disorders causing arterial constriction such as hypoxaemia, chronic altitude sickness
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31
Q

What are the two types of cor pulmonale

A

Acute - massive PE can cause this

Chronic - most of the time

32
Q

What changes do you see with cor pulmonale in the heart

A
  • RV hypertrophy
  • RA hypertrophy
  • dilatation in both chambers
  • due to the dilation the tricuspid valve ring may become expansive and this can lead to tricuspid regurgitation
  • see the clinical features for RVF plus the primary disease
33
Q

What is right ventricular hypertrophy defined as

A

Thickened right ventricle above 0.5cm

34
Q

What is vasculitis

A
  • inflammation of the vessel walls

- can be infective or non infectious

35
Q

What can cause non infectious vasculitis

A
  • immune complex
  • ANCA- mediated
  • direct antibody mediated
  • cell mediated
  • paraneoplastic or idiopathic
36
Q

What is classification of vasculitis based on

A
  • pathogenesis

- vessel size

37
Q

Name some examples of

  • Large vessel vasculitis
  • medium vessel vasculitis
  • ANCA - associated small vessel vasculitis
A

Large vessel vasculitis

  • takayasu artertitis
  • giant cell arteritis

Medium vessel vasculitis

  • Polyarteritis Nodosa
  • Kawasaki disease

ANCA - associated small vessel vasculitis

  • Microscopic polyangitis
  • granulomatosis with polyangitis
  • eosinophillic granulomatosis with polyangitis
38
Q

How does vasculitis show

A
  • All show vascular injury with mural necrosis and haemorrhage
  • localised, organ restricted or systemic
  • some are granulomatous
  • secondary ischaemia of down-stream tissue
  • may cause infarction
39
Q

What are granulomas

A

localised collections of epithelial macrophages

40
Q

What is polyarteritis nodosa

A
  • Systemic vasculitis
  • small/medium sized arteries (not veins or smaller arteries)
  • often spares the lungs
41
Q

Describe what you see in polyarteritis nodosa

A
  • Segmental necrotising inflammation of arteries especially renal, cardiac and GI tract
  • branching sites particularly
42
Q

What does polyarteritis nodosa lead to

A
  • Aneurysms, infracts and haemorrhage
  • microscopically transmural inflammation and fibrinoid necrosis
  • possible thrombosis of vessel
  • fibrosis later become nodular
  • lesions of different ages
43
Q

who does polyarteritis nodosa tend to effect

A
  • Young adults

- more common in men than in women

44
Q

How does polyarteritis nodosa present

A

Episodic
acute, subacute, or chronic

  • fever
  • malaise
  • weight loss
  • hypertension
  • abdominal pain
  • malaena
  • muscular pains
  • renal involvement
  • peripheral neuritis
45
Q

What is the treatment of polyarteritis nodosa

A
  • steroids

- cyclophosphamide

46
Q

What antigen presents along with polyarteritis nodosa

A

30% hep B antigen positive

47
Q

What are ANCA related vasculitis

A
  • 85% ANCA antibodies (60-95%)

- group of vasculitis that can be systemic, renal limited or other

48
Q

How does ANCA vasculitis present

A
  • flu like illness
  • fever
  • arthralgia
  • myalgia
  • purpura
  • peripheral neuropathy
  • gastro-intestinal involvement
49
Q

What can provoke ANCA vasculitis

A
  • propylthiouracil
  • penicillamine
  • hydralazine
50
Q

What are the two staining patters for somone with ANCA related vasculitis and what antibody do they stain

A
  • Cytoplasmic by IMF - c-ANCA is usually proteinase 3 (PR3)
  • perinuclear by IMF - usually myeloperoxidase (MPO)
  • can have ANCA circulating in patients who do not have vasculitis
51
Q

What is granulomatosis with polyangitis

A
  • effects upper and lower respriatory tract
  • particular the eyes and ear
  • see necrotising grnauloma
  • vasculitis
  • target is proteinase 3 (PR3) - you see c-ANCA usually
52
Q

How do you treat ANCA

A
  • aggressive immunosupression with cyclophosphamide (IV, V oral) and steroids if patient an tolerate
53
Q

what are the prognosis for ANCA with and without treatment

A
  • Untreated 80% 1 year mortality

- Treated 75% 5 year survival (kidney involvement and patient)

54
Q

What is cardiomyopathy

A

cardiac disease that arises from a primary intrinsic myocardial abnormality

55
Q

what are the causes of cardiomyopathy

A
  • Idiopathy
  • Secondary to known cause
  • Primary
56
Q

Name the 4 types of cardiomyopathy

A

• dilated
• hypertrophic
• restrictive
- arrhythomogenic right ventricular cardiomyopathy

57
Q

Describe what dilation cardiomyopathy look like

A

4 chamber dilation

- bigger heart

58
Q

Describe what hypertrophic cardiomyopathy looks like

A
  • septum thickening
59
Q

Describe what restrictive cardiomyopathy look like

A
  • heart looks normal and only able to diagnose it on functional analysis, ECG, biopsy or autopsy
60
Q

describe what happens in dilated cardiomyopathy

A
  • Progressive cardiac dilatation and contractile dysfunction
  • valves/arteries not significantly abnormal
  • may be thrombi
  • micro - myocardial hypertrophy/fibrosis
61
Q

What is the cause of dilated cardiomyopathy

A
  • Idiopathic
  • Genetic (~30%)
  • Post myocarditis
  • Alcohol or other toxicity eg doxorubicin
  • Pregnancy associated
  • Haemochromatosis
  • Sarcoidosis
62
Q

What age does dilated cardiomyopathy occur in

A
  • any age but especially 20-50
63
Q

what are the signs of dilated cardiomyopathy

A
  • progressive CCF
  • signs of LVF+RVF
  • death from failure or sudden death (arrhythmia)
64
Q

What is the treatment of dilated cardiomyopathy

A

Transplantation

65
Q

What happens in hypertrophic cardiomyopathy

A
  • Heart muscle is abnormal
  • fills poorly in diastole
  • often an outflow obstruction due to thickened septum
  • little or no dilatation
  • classically disproportionate thickening of septal myocardium epsically subarotic
  • micro hypertrophy, disarray and fibrosis
66
Q

What is the most common genetic problem associated with hypertrophic cardiomyopathy

A
  • Mutation of muscle protein esp beta-myosin heavy chain
  • most familial
  • many different mutations found
  • leads to poor compliance and reduced LV chamber size +/- outflow obstruction
  • clinically heterogeneous, may need surgery
67
Q

What is the most common genetic problem associated with hypertrophic cardiomyopathy

A

Beta myosin heavy chain

68
Q

Describe restrictive cardiomyopathy

A
  • Primary disease in ventricular compliance
  • idiopathic
  • firm ventricles with normal dilated atria
  • microscopy may reveal cause
69
Q

What can cause secondary restrictive cardiomyopathy

A
  • irradiation fibrosis
  • amyloid
  • sarcoid
  • tumour metastases
70
Q

What is myocarditis

A
  • inflammation causing myocardial injury and not a response to it
71
Q

What infections can cause myocarditis

A
  • viruses such as Coxackieviruses, enteroviruses, other viruses including HIV; chlamydia, rickettsiae, bacteria, fungi, protozoa, Helminths
72
Q

What immunological reactions can cause myocarditis

A

– post-viral, SLE, drug reactions, transplant rej

73
Q

What can also cause myocarditis

A

sarcoidosis, giant cell myocarditis

74
Q

what can cause direct damage to the myocarditis

A

May be direct damage or T cell mediated injury to antigens on myocyte surface
• Inflammation and myocyte necrosis

75
Q

How do the patients present in myocarditis

A
  • fatigue
  • fever
  • chest discomfort
  • heart failure
  • arrhythmias
  • sudden death
76
Q

myocarditis and

A

acute infract can be confused due to similar symptoms

77
Q

What does myocarditis lead onto

A
  • dilated cardiomyopathy

Year 3 - CR (44 decks)

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