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6. CP - Diseases of the Cardiovascular System > (3) Cardiovascular diseases 3 > Flashcards

(3) Cardiovascular diseases 3 Flashcards

1
Q

What is endocarditis?

A

Inflammation of the endocardium of the heart (thin, smooth membrane which lines the inside of the chambers of the heart and forms the surface of the valves)

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2
Q

What is the prototypical lesion in endocarditis?

A

Vegetations on the valves

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3
Q

What are the 2 main forms of endocarditis?

A
  • infective endocarditis (clinically important)

- non-infective endocarditis

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4
Q

Name 2 types of non-infective endocarditis

A
  • nonbacterial thrombotic endocarditis (NBTE)

- endocarditis of SLE (Libman-Sacks Disease)

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5
Q

What is infective endocarditis?

A

Colonisation/invasion of heart valves or heart chamber endocardium by a microbe - clinically serious infection

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6
Q

Describe the vegetations in infective endocarditis

A
  • mixture of thrombotic debris and organisms
  • destroy underlying cardiac tissue
  • aorta, aneurysmal sacs, blood vessels, prosthetic valves can also be infected
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7
Q

What causes infective endocarditis?

A

Most cases are caused by bacterial infection

Fungi/other classes can also cause IE

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8
Q

Name 2 classifications of infective endocarditis

A
  • acute infective endocarditis

- sub-acute infective endocarditis

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9
Q

Which type of infective endocarditis is the worst? (acute or sub-acute)

A

Acute infective endocarditis

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10
Q

What type of organism causes acute infective endocarditis vs. sub-acute infective endocarditis?

A

actue infective endocarditis = highly virulent organisms

sub-acute infective endocarditis = organisms of lower virulence

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11
Q

What type of lesions are there in acute infective endocarditis vs. sub-acute infective endocarditis?

A

acute infective endocarditis = necrotising, ulcerative, destructive lesions

sub-acute infective endocarditis = less destructive

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12
Q

How are acute infective endocarditis and sub-acute infective endocarditis cured?

A

acute infective endocarditis = difficult to cure with antibiotics and usually require surgery

sub-acute infective endocarditis = cured with antibiotics

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13
Q

What are the main features of acute infective endocarditis? (nasty)

A
  • can occur with infection of a previously normal heart valve
  • caused by highly virulent organisms
  • necrotising, ulcerative, destructive lesions
  • difficult to cure with antibiotics and usually require surgery
  • death frequent days to weeks despite treatment
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14
Q

What are the main features of sub-acute infective endocarditis? (less nasty than acute)

A
  • organisms of lower virulence
  • insidious infections of deformed valves
  • less destructive
  • protracted “wax and wane” course of weeks to months
  • cured with antibiotics
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15
Q

Infective endocarditis can occur in normal hearts but what are the risk factors?

A
  • cardiac/valvular abnormalities
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16
Q

What used to be a major cause/risk factor of infective endocarditis?

A

Rheumatic heart disease

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17
Q

Cardiac/valvular abnormalities are risk factors for infective endocarditis. Give examples

A
  • MV prolapse
  • valvular stenosis
  • artificial valves
  • unprepared and repaired congenital defects
  • bicuspid AV
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18
Q

How does an infection get into the heart?

A

Any route of bacteria into the blood stream eg.

  • dental abnormalities
  • IVDU
  • wounds
  • bowel cancer
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19
Q

Give 3 examples of bacteria that cause infection in the heart

A
  • streptococcus viridans
  • S. aureus
  • coagulase-negative staphylococci
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20
Q

Which is the most common bacterial cause of infective endocarditis?

A

Streptococcus viridans (50-60% of cases)

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21
Q

Streptococcus viridans can cause infective endocarditis. Where does it come from and what does it infect?

A
  • from the mouth

- causes endocarditis in native but damaged/abnormal valves

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22
Q

What proportion of infective endocarditis cases are caused by S. aureus?

A

10-20% of cases overall, especially in IVDU

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23
Q

S. aureus can cause infective endocarditis. Where does it come from?

A

The skin

causes cases when there is IVDU

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24
Q

Give an example of a coagulase-negtive staphylococci (can cause infective endocarditis)

A

S. epidermidis

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25
Q

Coagulae-negative staphylococci can cause infective endocarditis. What does it commonly infect?

A

Prosthetic heart valves

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26
Q

What should infective endocarditis caused by Strep. bovis prompt?

A

Investigation for bowel cancer

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27
Q

What makes up 10-15% of cases of infective endocarditis?

A

Culture negative endocarditis

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28
Q

What is culture negative endocarditis? (10-15% of cases)

A

No endocarditis-causing bacteria can be found on a blood culture eg. because the certain bacteria do not grow well on culture

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29
Q

Describe the vegetations in acute infective endocarditis

A
  • friable, bulky and potentially destructive

- single, multiple and often more than one valve

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30
Q

Where do you get vegetations in acute infective endocarditis?

A
  • aortic valve
  • mitral valve
  • right heart ( especially in IVDUs)
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31
Q

What can occur with vegetations in acute IE?

A

Can erode into the myocardium and cause ring abscesses

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32
Q

What happens when bits of the vegetations break off? (in acute IE)

A

Can cause septic emboli which contain large number of virulent organisms

  • get abscesses at sites where the emboli lodge in distant vessels
  • this can cause septic infarcts or mycotic aneurysms
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33
Q

What is the difference in the vegetations in sub-acute IE compared to acute IE?

A

Less destruction

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34
Q

State the clinical features of infective endocarditis

A
  • fever
  • non-specific symptoms
  • murmurs
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35
Q

Fever is a clinical sign of infective endocarditis. Explain in more detail

A
  • most consistent sign
  • rapidly developing fever, chills, weakness
  • can be slight or absent, particularly in the elderly
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36
Q

In infective endocarditis, there are non-specific signs as well as fever and murmurs etc. Give examples

A
  • weight loss

- flu-like syndrome

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37
Q

Murmurs are a clinical sign in infective endocarditis. Give more detail

A
  • 90% of patients with left-sided IE

- new valvular defect or represent a pre-existing abnormality

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38
Q

Give an example of complications associated with infective endocarditis

A
  • immunologically mediated conditions eg. glomerulonephritis
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39
Q

What are the clinical manifestations of infective endocarditis? (micro-thromboemboli)

A
  • splinter/subungual haemorrhages
  • Janeway lesions
  • Osler’s nodes
  • Roth spots
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40
Q

Janeway lesions are a clinical manifestation of infective endocarditis. What are they?

A

Erythematous or haemorrhagic non-tender lesions on the palms or soles

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41
Q

Osler’s nodes are a clinical manifestation of infective endocarditis. What are they?

A

Subcutaneous nodules in the pulp of the digits

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42
Q

Roth spots are a clinical manifestation of infective endocarditis. What are they?

A

Retinal haemorrhages in the eyes

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43
Q

How can you remember the clinic signs/manifestations of infective endocarditis?

A

FROM JANE

F - fever
R - Roth spots
O - Osler’s nodes
M - murmurs

J - Janeway lesions
A - anaemia
N - nail (splinter) haemorrhages
E - emboli (septic)

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44
Q

What is non-bacterial thrombotic endocarditis (NBTE) also known as?

A

Marantic endocarditis

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45
Q

Who does non-bacterial thrombotic endocarditis occur in?

A

Debilitated patients eg. cancer or sepsis

Those who are chronically ill

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46
Q

What is non-bacterial thrombotic endocarditis associated with?

A

Hypercoagulable state

(hence DVT, PE, and mutinous adenocarcinomas)

(pro-coaguant effects of tumour-derived mucin or tissue factor)

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47
Q

Non-bacterial thrombotic endocarditis (NBTE) is a part of what?

A

Trousseau syndrome of migratory thrombophlebitis

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48
Q

What is the Trousseau syndrome of malignancy? (NBTE is part of it)

A

Medical sign involving episodes of vessel inflammation due to blood clot (thrombophlebitis) which are recurrent or appearing in different locations over time (migratory thrombophlebitis).

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49
Q

What predisposes you to non-bacterial thrombotic endocarditis (NBTE)?

A
  • endocardial trauma/indwelling catheter eg. central line
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50
Q

Describe the vegetations in non-bacterial thrombotic endocarditis (NBTE)

A
  • small (1-5mm) sterile thrombi on valve leaflets
  • single or multiple on line of closure of leaflets or crisps
  • not invasive/no inflammatory reaction = minimal local effect
  • systemic emboli (infarcts into the brain, heart etc)
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51
Q

Another type of non-infective endocarditis is Libman-Sacks endocarditis. What is it associated with?

A

Systemic lupus erythematosis (SLE)

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52
Q

What are the symptoms of Libman-Sacks endocarditis?

A
  • usually asymptomatic (other than features of SLE)

- rarely cardiac failure or systemic emboli

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53
Q

Which valves are affected in Libman-Sacks endocarditis?

A
  • mitral valve

- tricuspid valve

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54
Q

Describe the vegetations in Libman-Sacks endocarditis?

A
  • small (1-4mm) sterile pink warty vegetations
  • single or multiple
  • AV valves (often under-surfaces), on the chordae, valvular endocardium or mural endocardium of atria or ventricles
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55
Q

What is rheumatic fever?

A

Acute, immunologically-mediated, multi-system inflammatory disease following group A streptococcal pharyngitis

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56
Q

Why is rheumatic fever now rare?

A

Because of improved diagnosis/treatment

- 15 million in developing countries/poor Western populations

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57
Q

What are Aschoff bodies?

A
  • distinctive cardiac lesions in rheumatic fever
  • foci of T cells, plasma cells and macrophages
  • can be found in all 3 cardiac layers
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58
Q

What are the vegetations called in rheumatic fever?

A

Veruccae

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59
Q

Changes to which valve are classical in rheumatic fever?

A

Mitral valve changes

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60
Q

What is the virtually the only cause of mitral stenosis?

A

Rheumatic fever

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61
Q

What kind of mitral valve changes do you get in rheumatic fever?

A

Leaflet thickening

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62
Q

In rheumatic fever you get mitral valve changes only is most cases (virtually always involved in chronic disease). What other valve may be affected?

A

Aortic valve in 25% of cases

Tricuspid valve and pulmonary valves - uncommon

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63
Q

What kind of mitral stenosis do you get in rheumatic fever?

A

Fibrous bridging of valvular commissures and calcification

“fish mouth” or “buttonhole” stenoses

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64
Q

Describe the aetiology of rheumatic fever

A
  • hypersensitivity reactions (combined antibody and T-cell mediated response
  • immune responses to group A strep (pharyngitis)
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65
Q

Explain how the immune response to group A strep causes rheumatic heart disease

A
  • antibodies directed against the M proteins of streptococci = cross-react with self antigens in the heart
  • CD4+ T cells specific for streptococcal peptides = react with self proteins in the heart, produce cytokines that activate macrophages eg. Aschoff bodies
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66
Q

Which criteria is used for diagnosis of rheumatic heart disease?

A

Jones criteria

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67
Q

What is the required criteria in Jones criteria for diagnosis of rheumatic fever?

A

Evidence of streptococcal infection

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68
Q

What is the major diagnostic criteria in Jones criteria for diagnosis of rheumatic fever?

A
  • carditis
  • polyarthritis
  • chorea
  • erythema marginatum
  • subcutaneous nodules
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69
Q

What is the major diagnostic criteria in Jones criteria for diagnosis of rheumatic fever?

A
  • fever
  • arthralgia
  • previous RHD
  • acute phase reactions (ESR/CRP/leukocytosis)
  • prolonged PR interval
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70
Q

How is diagnosis made in Jones criteria?

A
  • 1 required criteria + 2 major criteria + 0 minor criteria
    OR
  • 1 required criteria + 1 major criteria + 2 minor criteria
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71
Q

What is pericarditis?

A

Inflammation of the pericardial sac

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72
Q

What are the 3 main causes of pericarditis?

A
  • infections
  • immunologically mediated processes
  • miscellaneous conditions
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73
Q

Give examples of infections that can cause pericarditis

A
  • viruses (coxsackie B)
  • bacteria
  • TB
  • fungi
  • parasites
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74
Q

Give examples of immunologically mediated processes that can cause pericarditis

A
  • rheumatic fever
  • SLE
  • scleroderma
  • post-cardiotomy
  • late post-MI (Dressler’s)
  • drug hypersensitivity
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75
Q

What is Dressler’s syndrome?

A

Form of pericarditis that occurs in injury to the heart or pericardium

Also known as postmyocardial infarction syndrome

Believed to be an immune system response after damage to heart tissue or to the pericardium, from events such as a heart attack

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76
Q

Give examples of miscellaneous conditions that can cause pericarditis

A
  • post-MI (early)
  • uraemia
  • cardiac surgery
  • neoplasia
  • trauma
  • radiation
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77
Q

What are the 2 main different forms of pericarditis?

A
  • acute pericarditis (inflamed)

- chronic pericarditis (stuck down)

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78
Q

What are the different forms of acute pericarditis?

A
  • serous
  • serofibrinous/fibrinous
  • purulent/suppurative
  • haemorrhagic
  • caseous
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79
Q

What are the different forms of chronic pericarditis?

A
  • adhesive
  • adhesive mediastinopericarditis
  • constrictive pericarditis
80
Q

What happens in serous pericarditis?

A

Inflammation cause clear serous fluid accumulation

81
Q

What causes serous pericarditis?

A

Non-infectious aetiologies generally

  • inflammation in adjacent structures can cause pericardial reaction
  • rarely by viral pericarditis (coxsackie B/echovirus)
  • immunologically mediated processes (RF, SLE, scleroderma)
  • miscellaneous conditions (uraemia, neoplasia, radiation)
82
Q

What is the clinical triad in Dressler’s syndrome?

A
  • fever
  • pleuritic chest pain
  • pericardial effusion
83
Q

What is the aetiology of Dressler’s syndrome?

A

Autoimmune reaction to antigens released following myocardial infarction

84
Q

Is Dressler’s syndrome the same as acute pericarditis that occurs immediately after large MI?

A

No - In Dressler’s syndrome there is a delay of weeks post the MI

85
Q

What causes purulent/suppurative pericarditis?

A

Infections

86
Q

What are the features of purulent/suppurative pericarditis?

A

Red, granular exudate ie. pus (can be up to 500mls)

87
Q

What other condition can occur in purulent/suppurative pericarditis?

A

Inflammation can extend causing mediastino-pericarditis

88
Q

What is the usual outcome in purulent/suppurative pericarditis?

A

Complete resolution is rare

Organisation by scarring - restrictive pericarditis = serious

89
Q

What do you get in haemorrhagic pericarditis?

A

Blood mixed with serous (watery) or suppurative (pus) effusion

90
Q

What are the common causes of haemorrhagic pericarditis?

A
  • neoplasia (malignant cells in effusion)
  • infections (inc. TB)
  • following cardiac surgery leading to cardiac tamponade
91
Q

What is cardiac tamponade?

A

Compression of the heart by an accumulation of fluid in the pericardial sac

92
Q

What causes caseous (cheesy) pericarditis?

A
  • TB

- fungal

93
Q

What often comes after acute pericarditis?

A

Chronic pericarditis!

94
Q

What happens in adhesive pericarditis?

A

Fibrosis/stringy adhesions obliterates the pericardial cavity

95
Q

What does adhesive mediatinopericarditis follow?

A

Follows pericarditis caused by infections, surgery or radiation

96
Q

What happens in adhesive mediastinopericarditis?

A
  • obliterated pericardial cavity with adherence to surrounding structures
97
Q

What does adhesive mediastinopericarditis cause?

A

Cardiac hypertrophy/cardiac dilation

98
Q

What do you get in constrictive pericarditis?

A

Heart encased in fibrous scar - limits cardiac function

99
Q

How is constrictive pericarditis treated?

A

Treated by surgery to remove ‘shell’ around heart

100
Q

What are the clinical symptoms of pericarditis?

A
  • sharp central chest pain
  • pericardial friction rub
  • fever, leucocytosis, lymphocytosis, pericardial effusion
101
Q

Sharp central chest pain is a big clinical feature of pericarditis. Describe in more detail

A
  • exacerbated by movement, respiration, lying flat
  • relieved by sitting forwards
  • radiates into the shoulders and neck
  • differentials = angina, pleurisy
102
Q

Pericardial friction rub is a clinical feature of pericarditis. Describe in more detail

A

Loudest with diaphragm, left sternal edge

103
Q

What is leucocytosis? (a clinical feature in pericarditis)

A

An increase in the number of white cells in the blood, especially during an infection

104
Q

What are the potential complications associated with pericarditis?

A
  • pericardial effusion

- cardiac tamponade

105
Q

What does cardiomyopathy mean?

A

“heart muscle disease”

Disorder of the myocardium

106
Q

What are the 4 main types of cardiomyopathy?

A
  • dilated
  • hypertrophic
  • restrictive
  • arrythmogenic right ventricular cardiomyopathy
107
Q

What do you get in dilated cardiomyopathy?

A
  • progressive dilation leading to contractile (systolic) dysfunction
  • heart enlarged, heavy, flabby (dilation of chambers)
  • myocyte hypertrophy with fibrosis
108
Q

What are the 3 categories of causes of dilated cardiomyopathy?

A
  • genetic
  • alcohol and other toxins
  • others
109
Q

What causes 20-50% of cases of dilated cardiomyopathy?

A

Genetics

  • autosomal dominant (mainly)
  • cytoskeletal proteins gene mutation
110
Q

What causes 10-20% of cases of dilated cardiomyopathy?

A

Alcohol and other toxins eg. chemotherapy

111
Q

Other than genetics and alcohol and other toxins, what are some other causes of dilated cardiomyopathy?

A
  • SLE
  • scleroderma
  • thiamine deficiency
  • acromegaly
  • thyrotoxicosis
  • diabetes
112
Q

At what age does dilated cardiomyopathy occur?

A

Any age but commonly 20-50

113
Q

What are the clinical symptoms of dilated cardiomyopathy?

A

Slow progressive signs/symptoms of congestive cardiac failure

  • shortness of breath
  • fatigue
  • poor exertional capacity
114
Q

What is the 5 year survival rate in dilated cardiomyopathy?

A

25%

Death due to CCF, arrhythmia/embolism (inta-cardiac thrombus)

115
Q

What is the treatment for dilated cardiomyopathy?

A
  • cardiac transplantation

- long-term ventricular assist (can induce regression)

116
Q

What is hypertrophic cardiomyopathy defined by?

A

Myocardial hypertrophy in absence of obvious cause e.g. hypertension

Thick-walled, heavy, and hyper-contracting

117
Q

What kind of dysfunction do you get in hypertrophic cardiomyopathy?

A
  • poorly compliant (stiff) left ventricular myocardium
  • diastolic dysfunction with preserved systolic function
  • intermittent ventricular outflow obstruction (3rd of cases)
118
Q

What is the cause of hypertrophic cardiomyopathy?

A

100% genetic

  • mutation sarcomeric proteins
  • can be sporadic
119
Q

What do you see on histology in hypertrophic cardiomyopathy?

A

Myocyte hypertrophy and disarray

120
Q

What are the main clinical features of hypertrophic cardiomyopathy?

A
  • decreased stoke volume
  • obstruction to the left ventricular outflow
  • exertional dyspnoea due to above
  • systolic ejection murmur
121
Q

Why do you get a decreased stroke volume in hypertrophic cardiomyopathy?

A
  • impaired diastolic filling
  • reduced chamber size
  • reduced compliance of hypertrophied left ventricle
122
Q

In how many hypertrophic cardiomyopathy patients does obstruction to left ventricular outflow occur?

A

25% of patients

123
Q

What kind of murmur do you get in hypertrophic cardiomyopathy?

A

Systolic ejection murmur

  • ventricular outflow obstruction
  • anterior mitral leaflet moves towards the ventricular septum during systole
124
Q

What are the potential complications associated with hypertrophic cardiomyopathy?

A
  • atrial fibrillation
  • mural thrombus formation leading to embolisation/stroke
  • cardiac failure
  • ventricular arrhythmias
  • sudden death, especially in some affected families (most common cause of sudden death in athletes)
125
Q

What is the treatment for hypertrophic cardiomyopathy?

A
  • decreased heart rate and contractility (B-adrenergic blockers)
  • reduction of the mass of the septum, which relives the outflow tract obstruction
126
Q

What is restrictive cardiomyopathy?

A

Decrease in ventricular compliance

- impaired ventricular filling during diastole

127
Q

What are the causes of secondary restrictive cardiomyopathy? (infiltration)

A
  • fibrosis
  • amyloidosis
  • sarcoidosis
  • metastatic tumours
  • deposition of metabolites (inborn errors of metabolism)
128
Q

Describe the morphology in restrictive cardiomyopathy

A
  • ventricles normal size or slightly enlarged
  • chambers normal
  • myocardium is firm and noncompliant
129
Q

What is arrhythmogenic right ventricular cardiomyopathy also known as?

A

Arrhythmogenic right ventricular dysplasia

130
Q

What is arrhythmogenic right ventricular dysplasia?

A

Caused by genetic defects of the desmosomes on the surface of myocytes which link the cells together

The desmosomes are composed of several proteins, and many of those proteins can have harmful mutations.

Primarily in the right ventricle.

131
Q

Why type of genetic disease in arrhythmogenic right ventricular cardiomyopathy?

A

Autosomal dominant

Around 1 in 5000

132
Q

What features do you get in arhythomogenic right ventricular dysplasia?

A

Right ventricular dilation and myocardial thinning

Fibrofatty replacement of the right ventricle

133
Q

What is arrhythmogenic right ventricular dysplasia a disorder of specifically?

A

Cell-cell desmosomes in the right ventricle

134
Q

What happens with exercise in arrhythmogenic right ventricular cardiomyopathy?

A

Cells detach and die

135
Q

What symptoms/complications do you get in arrhythmogenic right ventricular cardiomyopathy?

A

Silent, syncope, chest pain, palpitations

Sudden cardiac death - young/exercise

136
Q

What is myocarditis?

A

Infective (or inflammatory) process leading to myocardial injury

Inflammation of the heart muscle

137
Q

What infections may cause myocarditis?

A
  • coxsackie A&B viruses (most common cause in the West)

- Chagas disease (trypanosoma cruzi) protozoa (important non-viral cause, endemic in South America, 10% die acutely)

138
Q

What are the broad clinical features of myocarditis?

A
  • asymptomatic
  • heart failure, arrhythmias, sudden death
  • non-specific symptoms eg. fatigue, dyspnoea, palpitations, precordial discomfort, fever
  • can mimic acute MI
  • DCM can develop
139
Q

What are the immune mediated causes of myocarditis?

A
  • post-viral
  • post-streptococcal (RF)
  • SLE
  • drugs eg. methyldopa, sulphonamides
  • transplant rejection
140
Q

What are the ‘other ‘ causes of myocarditis? (not infectious or immune mediated)

A
  • sarcoidosis

- giant cell myocarditis

141
Q

What is vasculitis?

A

Inflammation of the vessel walls

142
Q

How many subtypes of vasculitis are there?

A

20

143
Q

Where does vasculitis occur?

A

Any organ and any vessel size

144
Q

What does vasculitis look like on histology?

A

Blue dots in a blood vessel

145
Q

What system is used to name different types of vasculitis?

A

Chapel Hill nomenclature

146
Q

What is classification of different types of vasculitis based on?

A

The size of the affected vessel eg.

  • large vessel vasculitis (aorta)
  • medium vessel vasculitis (arteries)
  • small vessel vasculitis (arterioles, capillaries, venules)
147
Q

Give 2 examples of large vessel vasculitis

A
  • giant cell arteritis
  • Takayasu’s vasculitis

(granulomatous disease)

148
Q

Give 2 types of medium vessel vasculitis

A
  • immune complex mediated eg. polyarteritis nodosa

- anti-endothelial cell antibodies eg. Kawasaki disease

149
Q

What are the 2 categories of small vessel vasculitis?

A
  • ANCA associated

- immune complex mediated

150
Q

What are the immune complex mediated small vessel vasculitis conditions?

A
  • SLE eg. SLE vasculitis
  • IgA eg. Henoch Schonlein purpura
  • cryoglobulin eg. cryoglobulin vasculitis
  • other eg. goodpasture disease
151
Q

What are the ANCA associated small vessel vasculitis conditions?

A
  • vasculitis without asthma or granulomas (microscopic polyangitis)
  • granulomas, no asthma (Wegener granulomatosis)
  • eosinophilia, asthma, and granulomas (Chrug-Strauss syndrome)
152
Q

What is the most common form of vasculitis?

A

Giant cell arteritis (GCA)

153
Q

Who often gets giant cell arteritis (GCA)?

A

Elderly individuals in the West

154
Q

Describe the pathology in giant cell arteritis

A
  • chronic granulomatous inflammation
155
Q

In which vessels do you tend to get giant cell arteritis (GCA)?

A
  • large-medium size arteries
  • especially in the head eg. temporal arteries aka. temporal arteritis
  • also vertebral and ophthalmic arteries
  • also occurs in other vessels eg. the aorta (giant cell aortitis)
156
Q

What happens if you get ophthalmic artery involvement in giant cell arteritis?

A
  • permanent blindness

Giant cell arteritis is a medical emergency requiring prompt recognition and treatment!

157
Q

Describe the morphology in giant cell arteritis (GCA)

A
  • intimal thickening (=reduces the lumenal diameter)
  • med. granulomatous inflammation (elastic lamina fragmentation)
  • multinucleated giant cells (75% of adequately biopsied)
158
Q

What are the clinical signs and symptoms of giant cell arteritis (GCA)?

A
  • rare
159
Q

How is GCA diagnosed?

A

Biopsy and histologic

- segmental disease so 2-3cm length of artery

160
Q

What is the treatment for GCA?

A
  • corticosteroids are generally effective

- anti-TNF therapy in refractory cases

161
Q

What is an aneurysm?

A

Localised, permanent, abnormal dilatation of a blood vessel

162
Q

How can aneurysms be classified?

A
  • shape

- aetiology

163
Q

What are the different types of aneurysm?

A
  • atherosclerotic
  • dissecting
  • berry
  • microaneurysm
  • syphilitic
  • mycotic
  • false
164
Q

Name 2 types of aneurysm named by shape

A
  • saccular

- fusiform

165
Q

What is the most common type of aneurysm?

A

Atherosclerotic aneurysm - often in the elderly

166
Q

Atherosclerotic aneurysms are commonly what?

A

AAA secondary to atherosclerosis

167
Q

How does the chance of rupture of an atherosclerotic aneurysm increase with size?

A

Nil 6cm

168
Q

How are atherosclerotic aneurysms detected?

A

Ultra-sound (USS) - elective repair

169
Q

How can atherosclerotic aneurysms be repaired?

A

Repaired endovascularly

Elective repair

170
Q

What are the potential complications of atherosclerotic aneurysms?

A
  • rupture causing retroperitoneal haemorrhage

- embolisation causing limb ischaemia

171
Q

What is a dissecting aneurysm?

A

Tear in then wall, blood tracks between intimal and medial layers

172
Q

What are the classical symptoms of dissecting aneurysm?

A

Tearing pain in chest radiating to upper left shoulder

173
Q

Where do dissecting aneurysms usually occur?

A

Usually thoracic aorta secondary to systemic hypertension

174
Q

What happens in the case of dissecting aneurysm?

A

Progressive vascular occlusion and haemopericardium

175
Q

What is the aim of treatment for dissecting aneurysm?

A

Aim to reduce arterial pressure/surgery

Increase in mortality without treatment

176
Q

What are berry aneurysms?

A

Small, saccular lesions that develop in the circle of Willis

177
Q

Berry aneurysms develop in the circle of Willis but whereabouts?

A

At sites of medial weakness at arterial bifurcations

178
Q

Who are berry aneurysms commonly found in?

A

Young hypertensive patients

179
Q

What would rupture of a berry aneurysm cause?

A

Sub-arachnoid haemorrhage (SAH)

180
Q

What are Charcot-Bouchard aneurysms?

A
  • also known micro aneurysms
  • occur in small blood vessels in the brain
  • associated with chronic hypertension
181
Q

In which vessels do Charcot-Bouchard aneurysms most often occur?

A

In the lenticulostriate vessels of the basal ganglia

182
Q

What do Charcot-Bouchard aneurysms commonly cause?

A

Intracerebral haemorrhage (stroke)

183
Q

What aneurysms can develop in diabetes?

A

Retinal microaneurysms - causing diabetic retinopathy

184
Q

What aneurysms does tertiary syphilis cause?

A

Ascending (thoracic) aorta aneurysms

syphilitic aneurysms/leutic aneurysms

185
Q

What are mycotic aneurysms?

A

Weakening of arterial wall secondary to bacterial/fungal infection (rare)

186
Q

What is the most common underlying infection in mycotic aneurysms?

A

SBE (subacute bacterial endocarditis) is the most common underlying infection

Organisms enter media from vasa vasorum

187
Q

Where do mycotic aneurysms often occur?

A

In the cerebral arteries

188
Q

What is a false aneurysm?

A

Blood filled space around a vessel, usually following traumatic rupture or perforation injury

189
Q

Where is the haematoma in a false aneurysm?

A

In the adventitial fibrous tissue

190
Q

When are false aneurysms commonly seen?

A

Following femoral artery puncture during angiography/angioplasty

191
Q

What are the 3 main general causes of acute arterial occlusion?

A
  • embolus
  • thombosis
  • trauma
192
Q

Where might an embolus come from to cause acute arterial occlusion?

A
  • AF
  • MI
  • endocarditis
  • prosthetic valves
  • aneurysm
  • atherosclerotic plaque
  • paradoxical embolus
193
Q

What might cause thrombosis that leads to acute arterial occlusion?

A
  • vascular grafts
  • atherosclerosis
  • hyper coagulable state
  • low flow state
  • entrapment syndrome
  • thrombosis of aneurysm
194
Q

What are the 6 Ps when checking for acute ischaemia?

A
  • pale/palloro
  • pulseless
  • painful
  • paralysed
  • paraesthetic
  • perishing cold
195
Q

Symptoms of chronic peripheral vascular disease vary depending on severity. Describe this

A

1 = asymptomatic (found during a physical exam (ABI))

2 = intermittent claudication (complaint of pain upon exertion

3 = critical limb ischaemia (rest pain 4 = tissue loss)

6. CP - Diseases of the Cardiovascular System (3 decks)

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