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Y5 Cardiovascular System > List II - Less Common 'Know of' Conditions > Flashcards

List II - Less Common 'Know of' Conditions Flashcards

1
Q

What is a pericardial effusion?

A
  • Occurs when there is excess fluid in the pericardial sac

* Normal pericardial sac contains around 30-50mL of fluid

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2
Q

What are the signs/symptoms of pericardial effusion?

A
  • Will relate to the speed at which the pericardial fluid has accumulated
  • Acute onset will not allow the pericardium to stretch - therefore more problems
  • Symptoms are related to cardiac function and intrapericardial pressure leading to an impaired filling of low pressure chambers, particularly the right atrium
  • Dyspnoea and reduced exercise tolerance will be early signs, progressing to severe impaired cardiac output and death in severe cases e.g. cardiac tamponade
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3
Q

What are the causes of pericardial effusion?

A
  • Idiopathic (presumed viral, post-viral or immune related)
  • Inflammatory
  • SLE
  • RA
  • Scleroderma
  • Sjogren syndrome
  • Vasculitis
  • Post MI - Dressler syndrome
  • Infectious
  • Viral
  • Bacterial
  • Tuberculosis
  • Post surgical or traumatic
  • Pulmonary arterial hypertension
  • Radiotherapy
  • Malignancy
  • Pericardial mesothelioma
  • Metastatic
  • Paraneoplastic
  • Endocrine
  • Hypothyroidism
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4
Q

What are the radiological signs of pericardial effusion?

A

X-ray

* Global enlargement - water bottle sign

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5
Q

What is the treatment of pericardial effusion?

A
  • Small - conservative treatment

* Large - pericardiocentesis to drain the fluid

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6
Q

What is the most common cardiomyopathy?

A
  • Dilated cardiomyopathy - 90% of cases of myopathy
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7
Q

What are the causes of dilated cardiomyopathy?

A
  • Idiopathic - most common
  • Myocarditis - coxsackie B, HIV, diptheria, Chagas disease
  • Ischaemic heart disease
  • Peripartum
  • Hypertension
  • Iatrogenic e.g. doxorubicin
  • Substance abuse e.g. alcohol, cocaine
  • Inherited: familial to DCM or specific to a syndrome e.g. Duchenne muscular dystrophy
  • 1/3 genetic
  • Majority of genetic are autosomal dominant
  • Infiltrative e.g. haemochromatosis, sarcoidosis

(+ these causes may also lead to restrictive cardiomyopathy)
- nutritional e.g. wet beriberi (thiamine deficiency)

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8
Q

What is the pathophysiology of DCM?

A
  • Dilated heart leading to predominately systolic dysfunction
  • All 4 chambers are dilated, but the left ventricle more so than right ventricle
  • Eccentric hypertrophy (sarcomeres added in series) is seen
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9
Q

What are the clinical features of DCM?

A
  • Classic findings of heart failure
  • Systolic murmur: stretching of valves may result in mitral and tricuspid regurgitation
  • S3
  • Balloon appearance of heart on the chest x-ray
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10
Q

What is takotsubo cardiomyopathy?

A
  • Type of non-ischaemic cardiomyopathy associated with a transient, apical ballooning of the myocardium
  • May be triggered by stress
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11
Q

What is the pathophysiology of takotsubo cardiomyopathy?

A
  • Japanese word for octopus trap
  • Apical ballooning appearance occurs due to severe hypokinesis of the mid and apical segments with preservation of activity of the basal segments
  • Simple terms
  • Bottom of the heart (apex) does not contract therefore appears to balloon out
  • Top (base) continues to contract creating the neck of the octopus trap
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12
Q

What are the clinical features of takotsubo cardiomyopathy?

A
  • Chest pain
  • Features of heart failure
  • ECG: ST elevation
  • Normal coronary angiogram
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13
Q

What is the management of patients with Takotsubo cardiomyopathy?

A
  • Treatment is supportive

* Most patients improve with supportive treatment

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14
Q

What are the primary cardiomyopathies?

A
  • Genetic - both autosomal dominant
  • Mixed
  • Acquired
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15
Q

What are the genetic primary cardiomyopthies?

A
  • Hypertrophic obstructive cardiomyopathy
  • Leading cause of sudden cardiac death in young athletes
  • Usually due to a mutation in the gene encoding B-myosin heavy chain protein
  • Common cause of sudden death
  • Echo findings include MR, systolic anterior motion (SAM) of the mitral valve and asymmetric septal hypertrophy
  • Arrhythmogenic right ventricular dysplasia
  • Right ventricular myocardium is replaced by fibrofatty tissue
  • Around 50% of patients have a mutation of one of the several genes which encode components of desmosome
  • ECG abnormalities in V1-3, typically T wave inversion
  • Epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex
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16
Q

What are the mixed primary cardiomyopthies?

A 
* Dilated cardiomyopathy
Classic causes
- Alcohol
- Coxsackie B virus
- Wet beriberi
- Doxorubicin
* Restrictive cardiomyopathy
Classic causes
- Amyloidosis
- Post-radiotherapy 
- Loeffler's endocarditis
17
Q

What are the acquired primary cardiomyopthies?

A
  • Peripartum cardiomyopathy
  • Typically develops between last month of pregnancy and 5 months post-partum
  • More common in older women, greater parity and multiple gestations
  • Takotsubo cardiomyopathy
  • Stress induced cardio-myopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure
  • Transient, apical ballooning of the myocardium
  • Treatment is supportive
18
Q

What are the secondary causes of cardiomyopathy?

A
  • Infective - coxsackie B virus, Chagas disease
  • Infiltrative - amyloidosis
  • Storage - haemochromatosis
  • Toxicity - doxorubicin, alcoholic
  • Inflammatory - sarcoidosis
  • Endocrine - DBM, thyrotoxicosis, acromegaly
  • Neuromuscular - Friedreich’s ataxia, Duchenne-Becker muscular dystrophy, myotonic dystrophy
  • Nutritional deficincies - Beriberi (thiamine)
  • Autoimmune - SLE
19
Q

What are the 3 main reasons for ischaemia to the lower GI tract/bowel ischaemia?

A
  • Acute mesenteric ischaemia
  • Chronic mesenteric ischaemia
  • Ischaemic colitis
20
Q

What are the common predisposing factors in bowel ischaemia?

A
  • Increasing age
  • Atrial fibrillation - particularly for mesenteric ischaemia
  • Other causes of emboli
  • Endocarditis
  • Malignancy
  • Cardiovascular disease risk factors
  • Smoking
  • Hypertension
  • Diabetes
  • Cocaine use
  • Ischaemic colitis is sometimes seen in young patients following cocaine use
21
Q

What are the common clinical features in bowel ischaemia?

A
  • Abdominal pain - in acute mesenteric ischaemia this is often of sudden onset, severe and out of keeping with physical exam findings
  • Rectal bleeding
  • Diarrhoea
  • Fever
  • Bloods typically show an elevated white blood cell count associated with a lactic acidosis
22
Q

What is the diagnostic imaging of choice for bowel ischaemia?

A
  • CT
23
Q

What are the features of acute mesenteric ischaemia?

A
  • Typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel e.g. superior mesenteric artery
  • Classically a history of atrial fibrillation
  • Abdomen pain is typically severe, of sudden onset and out of keeping with physical exam findings

Management

  • Urgent surgery usually required
  • Poor prognosis, especially if surgery is delayed
24
Q

What are the features of chronic mesenteric ischaemia?

A
  • Relatively rare condition due to its non-specific features and may be thought of as intestinal angina
  • Colicky intermittent abdominal pain occurs
25
Q

What are the features of ischaemic colitis?

A
  • Ischaemic colitis describes an acute but transient compromise in the blood flow to the large bowel
  • May lead to inflammation, ulceration and haemorrhage
  • More likely to occur in watershed areas such as the splenic flexure that are located at the borders of the territory supplied by the superior and inferior mesenteric arteries

Investigations
* Thumb-printing may be seen on abdominal x-ray due to mucosal oedema/haemorrhage

Management

  • Usually supportive
  • Surgery may be required in a minority of cases if conservative measures fail
  • Indications would include generalised peritonitis, perforation or ongoing haemorrhage
26
Q

What is superior vena cava obstruction?

A
  • Oncological emergency caused by compression of the SVC

* Most commonly associated with lung cancer

27
Q

What are the features of SVCO?

A
  • Dyspnoea is most common symptom
  • Swelling of the face, neck and arms - conjunctival and periorbital oedema may be seen
  • Headache - often worse in the mornings
  • Visual disturbance
  • Pulseless jugular venous distention
28
Q

What are the causes of SVCO?

A
  • Common malignancies
  • Small cell lung cancer, lymphoma
  • Other malignancies
  • Metastatic seminoma
  • Kaposi’s sarcoma
  • Breast cancer
  • Aortic aneurysm
  • Mediastinal fibrosis
  • Goitre
  • SVC thrombosis
29
Q

What is the management of SVCO?

A

If suspected:

  • 16mg dexamethasone (with PPI cover)
  • Depending on the cause:
  • Vascual stent (radiological guidance)
  • Radiotherapy
  • Chemotherapy
  • LMWH (if confirmed thrombus)

More notes in CCC

30
Q

What is raynaud’s phenomenon?

A
  • Characterised by an exaggerated vasoconstriction response of the digital arteries and cutaneous arteriole to the cold or emotional stress
  • Primary - Raynaud’s disease
  • Secondary - Raynaud’s phenomenon
31
Q

Who is affected by Raynaud’s disease?

A
  • Typically presents in young women e.g. 30 years old with bilateral symptoms
32
Q

What are the causes of secondary Raynaud’s phenomenon?

A
  • Connective tissue disorders
  • Slceroderma
  • Rheumatoid arthritis
  • SLE
  • Leukaemia
  • Type I cryoglobulinaemia, cold agglutins
  • Use of vibrating tools
  • Drugs - COCP, ergot
  • Cervical rib
33
Q

What are the factors of Raynaud’s phenomenon suggesting connective tissue disease?

A
  • Onset after 40 years
  • Unilateral symptoms
  • Rashes
  • Presence of autoantibodies
  • Features which may suggest rheumatoid arthritis or SLE for example arthritis or recurrent miscarriages
  • Digital ulcers, calcinosis
  • Very rarely: chilblains
34
Q

What is the management of all patients with suspected secondary Raynaud’s phenomenon?

A
  • Referral to secondary care
  • First line - calcium channel blockers e.g. nifedipine
  • IV prostacyclin (epoprostenol) infusions: effects may last several weeks/months
35
Q

What is lymphoedema?

A
  • Long term swelling that develops due to a fault with the lymphatic drainage system
36
Q

What causes lymphoedema?

A
  • Primary (rare) - failure of development of the lymphatic system
  • Secondary - person with a previously healthy lymphatic system develops a problem or illness that damages it and prevents it from working properly
37
Q

What are the secondary causes of lymphoedema?

A
  • Cancer treatment - node removal
  • Infection - damage to lymph nodes
  • Severe inflammatory problems - acne, genital hidradenitis suppurativa, psoriasis, dermatitis
  • Reduced mobility/paralysis
  • Vein problems
  • Obesity
38
Q

What are the treatments for lymphoedema?

A
  • Management is aimed at controlling swelling through physical treatments designed to stimulate flow through existing or collateral drainage routes
  • Mild/moderate can be treated with exercise plus fitted compression bandaging
  • More severe cases intensive compression bandaging
  • Compression in combination with exercise, weight management and good skin care can be very effective

(British Association of Dermatologists)

Y5 Cardiovascular System (3 decks)

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