Cardiomyopathy, Myocarditis and Pericarditis Flashcards Preview

The Cardiovascular System > Cardiomyopathy, Myocarditis and Pericarditis > Flashcards

Flashcards in Cardiomyopathy, Myocarditis and Pericarditis Deck (59)
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1
Q

What is cardiomyopathy?

A

Chronic disease of the heart muscle

2
Q

What are the three main types of cardiomyopathy?

A
  1. Dilated
  2. Restrictive
  3. Hypertrophic
3
Q

Describe dilated cardiomyopathy

A

The heart can be up to 2-3 times normal size

Contractile muscle fibres are not in optimal directions

Contractile force is often less than required

4
Q

What are causes of dilated cardiomyopathy?

A
  1. Genetics - any gene involved in heart muscle protein
  2. Toxins including alcohol
  3. Chemotherapy agents - doxorubicin
  4. Complications in pregancy
5
Q

How may dilated cardiomyopathy present clinically?

A
  • Heart failure
  • Breathlessness
  • Poor exercise tolerance
  • Low cardiac output
6
Q

Describe hypertrophic cardiomyopathy

A
  • The heart becomes big (thick walled) and solid
  • A strong contractile force is mainatined
  • Outflow obstruction and filling problems may occur due to the heart shape
7
Q

What are the cause(s) of hypertrophic myopathy?

A

Genetics

The heart muscle is still relatively functional, just less efficient as heart muscle fibres are less ordered

8
Q

Describe restrictive cardiomyopathy

A

There is a lack of compliancy

Filling of ventricles is restricted

Contractile strength and wall thickness is normal - just not relaxation and filling

9
Q

What are the causes of restrictive cardiomyopathy?

A

Deposition

Metabolic by products such as:

  • Amyloid
  • Sarcoid - causes bilateral lymphadenopathy in lungs (granulomatous)
  • Tumours (from elsewhere)
  • Radiation fibrosis
10
Q

What is arrhythmogenic right ventricular dysplasia?

A
  • Genetic disease affecting desmosomes
  • Right ventricle becomes replaced with large amounts of fat causing inefficiency
11
Q

What are some symptoms of arrhythmogenic cardiac dysplasia?

A
  • Syncope (funny turns due to low BP)
  • Arrhythmia
  • Sudden death
12
Q

What is myocarditis?

A

Inflammation of the heart

13
Q

What can cause myocarditis?

A

Infection due to:

  • Viruses
  • Bacteria
  • Fungi
  • Protozoa
  • Helminths

Non infectious causes:

  • Hypersensitivity reaction to drugs
  • Poststreptococcal and rheumatic fever
  • Microscopic - Aschoff bodies - granulomatous body in heart
  • Systeic lupus erythematosus (SLE)
14
Q

What is amyloid and why is it bad?

A

It is abnormal protein deposition which tend to form beta sheets.

Its deposition can obstruct the fucntion of tissues

15
Q

What is senile cardiac amyloidosis?

A

A type of restrictive cardiomyopathy

  • Passage of electrical impulses can be disrupted causeing ECG abnormalities
  • Amyloid deposits can replace normal heart muscle
16
Q

What is abnormal atrial natriuretic protein?

A
  • Released by atrial cells (localised to atria)
  • The protein is a potent vasodilator
  • Can stimulate sodium loss and can reduce BP (opposite to aldosterone)
  • Accumulation can lead to isolated atrial amyloidosis potentially leading to arrythmias
17
Q

How can amyloid be identified?

A

It tests postive for congo red stain and when combined with plane polarised lihgt, it exhibits apple green birefringence (looks green)

18
Q

What is pericarditis?

A

Inflammation of the pericardium as a result of infection or other factors

19
Q

When may pericarditis be present?

A
  • Post MI inflammation
  • Uraemia - kidney failure
  • Connective tissue diseases (rheumatoid, lupus)
  • Friction rub (bread and butter pericarditis)
20
Q

What is Dressler’s syndrome?

A

Occurs several weeks after MI

Immune mediated response due to unencountered material being released from damaged heart muscle

21
Q

What is endocarditis?

A

Inflammation of endocardium

22
Q

Infectious endocarditis vegetations. What are these and why are they bad?

A

Vegetations - aggregates of colonies on valves (composed of bacteria, occasionally fungi)

Can cause emboli by coming lose

23
Q

Which gram negative bacteria may cause endocarditis?

A

HACEK

  • Haemophilus
  • Aggregatibacter
  • Cardiobacterium
  • Eikenella
  • Kingella

Lupus (not gram negative bacteria) can also cause the condition

24
Q

How does endocarditis usually present?

A

Right sides murmur

Typically IV drug user - infcetion reaches right side first due to venous injections

25
Q

During a physical examination, which signs may be indicative of endocarditis?

A
  1. Osler’s nodes
  2. Janeway legions
  3. Roth spots
  4. Splinter haemorrhages
  5. Systemic emboli (brain, lungs and kidneys)
26
Q

What is marantic endocarditis?

A

This is a non-bacterial thrombotic endocarditis

27
Q

How does lupus cause endocarditis?

A

This condition is called Libman-sacks endocarditis

Small sterile emboli present on the under surfaces of valves or on heart chords.

This can cause lesions (immune complexes/mononuclear cells) to appear

28
Q

What is carcinoid heart disease?

A

Involves neoplasms of neuroendocrine cells seen in mucosa (common in GI tract and lung)

Hormones can be released affecting the right heart valves and eventually causing right sided heart failure

Hormones include serotonin, histamine and bradykinin

29
Q

What are the symptoms of carcinoid heart disease?

A
  • Skin flushing
  • Nausea, diarrhoea
  • Right side valve disease
  • Tricuspid and pulmonary insufficiency
30
Q

What are deep tumours of the myocardium called?

A

Rhabdomyomas

(benign)

31
Q

What is the most common form of heart cancer?

A

Myxoma

32
Q

Where are myomas normaly found and why do they cause problems?

A

Atria

Can cause ball/valve obstruction and also myxoid emboli

Similar presentation to endocarditis (systemic fever, malaise, IL-6 secretion)

33
Q

What is Carney’s syndrome?

A

AD condition

Myxomas present in both heart and skin

Usually associated with left atrium

Spotty skin pigmentation may be present

34
Q

What is the term given to a blood clot within a vessel?

A

Thrombosis

35
Q

What is Virchow’s triad and what does it describe?

A
  1. Endothelial injury
  2. Hypercoaguable blood
  3. Turbuent blood flow (circulatory stasis)

It describes the areas, or conditions, required for thrombosis formation

36
Q

What is produced at the end point of platelet activation?

A

Fibrin

37
Q

GP IIb/IIIa on platelets will bind to what?

A

Collagen via von Willebrand factor

38
Q

What are the two pathways for coagulation?

A
  1. Intrinsic
  2. Extrinsic
39
Q

Describe the intrinsic pathway to coagulation

A

Begins with Hageman factor (XII) and kallikrein (a protease)

  • XII → XIIa
  • XI → XIa (also activated by thrombin)
  • IX → IXa
  • VIII → VIIIa (activated by thrombin, not IXa)
  • X → Xa (by VIIIa and IXa)
  • V → Va (by thrombin)
  • II → IIa (by Va and Xa)
  • Fibrin → fibrinogen (by thrombin (factor IIa)
40
Q

Describe the steps in the extrinsic coagulation pathway

A

Begins with a tissue injury and the release of tissue factor

  • VII → VIIa (by TF - tissue factor)
  • X → Xa
  • V → Va (activated by thrombin)
  • II → IIa (activated by Xa and Va)
  • Fibrinogen to fibrin
41
Q

What is the time taken for the common pathway to occur termed?

A

Prothrombin time (PT time)

It is used to measure how long blood takes to clot

42
Q

What is the activated partial thromboplastin time?

A

This measures how long blood taken to coagulate via the extrinsic pathway

It is used to monitor treatment effects such as heparin

43
Q

Why is vitamin K essential for coagulation?

A

It is required to form factors:

  • II
  • VII
  • IX
  • X
44
Q

Which factors may be affected if there is liver disease?

A

Vitamin K is stored in the liver and is used to make factors II, VII, IX and X

These factors will therefore be produced less

45
Q

What effect does warfarin have on clotting factors?

A

It stops production of clotting factors II, VII, IX and X

46
Q

What may cause endothelial injury in vessels?

A
  • Hypertension
  • Toxins (smoking)
  • Infectious agents
  • Autoimmune disease (primary vasculitis)
  • Previous DVT
47
Q

In which areas of the arterial system is turbulent blood flow more likey and what is the consequence?

A

Branching regions

This can cause endothelial damage

48
Q

How is the normal laminar blood flow affected by circulatory stasis?

A

It is not maintained and blood components move to vessel walls

49
Q

Why does circulatory stasis increase chances for clotting to occur?

A

Platelets have increased contact with vessel walls (loss of laminar blood flow)

This increases the likelihood of coagulation

50
Q

Where does circulatory stasis most often occur?

A

Deep venous system

(Faulty valves can increase stasis)

51
Q

Name three anti-clotting proteins and the clotting factors they degrade

A
  1. Protein C - degrade factors V and VIII
  2. Protein S - degrade factors V and VIII
  3. Antithrombin III - degrade factors II, IX and X
52
Q

What can plasmin do?

A

It is an enzyme that can degrade fibrin clots

53
Q

What may cause hypercoagubility?

A
  1. Protein C/S deficiency
  2. Factor V Leiden (name of specific gene mutation that results in thrombophilia - an increased tendency to form abnormal blood clots occulding vessels)
  3. Antithrombin III deficiency
54
Q

What are some secondary causes for hypercoagubility?

A
  • Atrial fibrillation
  • MI
  • Cancer - tumour can produce TF
  • Marantic endocarditis
  • Chemotherapeutic agents
  • The birth control pill
  • Cardiomyopathy
  • Smoking
55
Q

What can an embolism be?

A
  • Air
  • Septic
  • Amniotic fluid
  • Tumour
  • Fat
  • Thrombus
56
Q

What is the difference between ischaemia and infarction?

A

Ischaemia - lack of blood flow and oxygen

Infarction - death of tssue as a result of ischaemia

57
Q

Why can increased calcium levels in blood lead to tissue damage?

A

Calcium can stimulate:

  • ATPase - aids calcium efflux from cells
  • Phospholipase - membrane damage
  • Proteases - membrane and cytoskeleton damage
  • Endonuclease - DNA damage and breakdown
  • Mitochondrial permeability - release of pro-death factors e.g. cytochrome C
58
Q

Where is thrombosis most likely to occur?

A
  • Sites of turbulence (branching vessels)
  • Atherosclerotic areas
59
Q

Give some sites of branching vessels in the body where thrombosis is likely to occur

A
  • Carotid bifurcation
  • Aortic bifuration
  • Renal arteries
  • Cornonary vessles
  • Superior mesenteric artery