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Cardiology finals KTB > Carditis and cardiomyopathy > Flashcards

Carditis and cardiomyopathy Flashcards

1
Q

Define pericarditis. What are the types?

A

Inflammation of the lining of the heart

  • Acute: <4-6 weeks vs constrictive (typically chronic)
  • Fibrinous (dry) vs effusive (fluid-purulent, haemorrhagic or serous)
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2
Q

Describe the epidemiology of pericarditis

A

Common in adults

M > F

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3
Q

Describe the aetiology of pericarditis

A

90% are idiopathic/infectious
Idiopathic
Infection: viral (coxsackie, echovirus, mumps)
Systemic inflammatory disease: SLE, RA, SS, vasculitis
Post-MI (Dressler’s syndrome)
Metabolic: uraemia
Toxins/drugs

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4
Q

Describe the presentation of acute pericarditis

A

Diagnosis is clinical, with 2 of 4:

  1. Sharp pleuritic chest pain, radiates to the back, improved by leaning forward
  2. Pericardial friction rub
  3. Widespread concave ST elevation/PR depression
  4. New pericardial effusion
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5
Q

Describe the signs of pericarditis

A

Pericardial friction rub (heard best over LSE)
Signs of systemic illness
Fever
Tachycardia

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6
Q

What are the complications of pericarditis?

A 
Cardiac tamponade (in effusive disease)
Constrictive pericarditis (occurs months later)
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7
Q

Describe the signs of cardiac tamponade

A

Beck’s triad:

  • Distended neck veins/raised JVP
  • Muffled heart sounds
  • Hypotension
Pulsus paradoxus
Electrical alternans (ECG)
Heart failure
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8
Q

Describe the investigations in suspected pericarditis

A
  • ECG: widespread saddle ST elevation/PR depression
  • Bloods: FBC, CRP, ESR, troponin, U+Es, LFTs
  • CXR
  • Echo
  • Pericardiocentesis (diagnostic and therapeutic)
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9
Q

Describe the management of pericarditis

A

Conservative:

  • For mild cases with likely viral/idiopathic origin and no worrying features
  • Rest and avoid exercise

Medical:

  • NSAIDs and colchicine as first line + PPI. Continue NSAID for 1-2 weeks and taper, continue colchicine for 3 months (6 months if recurrent)
  • Consider corticosteroids
  • Purulent: antibiotics

Surgical/interventional:

  • Pericardiocentesis: for tamponade/purulent/neoplastic
  • Pericardectomy in recurrent/TB/constrictive
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10
Q

When would you consider admission for patients with pericarditis?

A
  • Any underlying cause that requires admission

- Severe features: high fever, effusion, tamponade, failure to respond to NSAIDs, immunosuppression, etc

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11
Q

Describe the follow-up for pericarditis

A
  • Monitor response to treatment after 1-2 weeks

- Monitor CRP

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12
Q

What is amyloidosis?

A

A group of conditions that are characterised by the deposition of abnormal proteins that are resistant to degradation.

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13
Q

Describe the aetiology of amyloidosis

A

Can be either AL amyloid as a result of conditions associated with light chains (MM, MGUS)
Or AA amyloid, associated w chronic inflammation
Several types of familial amyloidosis

Most commonly affects kidneys, GI tract, thyroid, heart

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14
Q

Describe the presentation of amyloidosis

A 
May present in a variety of ways eg. 
-Cardiomyopathy
-Nephrotic syndrome
-Neuropathy
Specific to cardiac:
-HF symptoms: dyspnoea, fatigue, oedema, weight loss
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15
Q

Describe the signs of amyloidosis

A

Peripheral oedema
Raised JVP
Hepatomegaly
Various skin changes

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16
Q

Describe the investigations of amyloidosis (cardiac)

A

ECG: hypertrophy
Bloods: serum light chains, general screen, trop, BNP
Echo: HFpEF
Cardiac MRI: helps distinguish from hypertrophic cardiomyopathy
Biopsy: essential for diagnosis

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17
Q

Describe the management of amyloidosis (cardiac)

A

MDT approach
AL: suppress light chain production- SCT, chemo
AA: treat inflammatory disease- immunosuppressants

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18
Q

What type of cardiomyopathy is caused by amyloidosis?

A

Restrictive- this is the most common cause of death in amyloidosis

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19
Q

What is cardiomyopathy?

A

A group of various conditions in which the heart muscle is structurally and functionally abnormal, in the absence of CAD, HTN, CHD and valve disease sufficient to cause the observed pathology

20
Q

Describe the aetiology of cardiomyopathy

A

5 types of cardiomyopathy:
-Hypertrophic: genetic
-Restrictive: idiopathic, familial, sarcoid, amyloid, etc
-Dilated: post-myocarditis, alcohol, chemo, haemochromatosis, AI disease, metabolic/endo diseases (thyroid, phaeo, DM), nutrition (thiamine, etc)
-Arrhythmogenic: genetic
-Unclassified: channelopathies, peripartum
May be primary or secondary (systemic disease)
Can be familial or acquired

21
Q

Describe the epidemiology of cardiomyopathy

A
  • HCM: 1/500 affected

- DCM: 1/250

22
Q

Describe the presentation of cardiomyopathy

A 
Commonest symptoms:
-Dyspnoea
-Palpitations
-Syncope
History of cause eg. family history of SCD, PMH, DHx
23
Q

Describe the investigations for cardiomyopathy

A

ECG: may show hypertrophy
Bloods: FBC, U+Es, LFTs, TFTs, BNP, B12, iron studies
CXR
Echo
Cardiac MRI is sensitive for cardiomyopathy
Catheterisation

24
Q

Describe the management of cardiomyopathy

A

Medical:
-Symptomatic treatment: diuresis if needed, beta-block/CCBs (HCM)

Interventional/surgical:

  • Septostomy (HCM)
  • ICD, pacemaker
25
Describe the management of cardiomyopathy
Medical: -Symptomatic treatment: diuresis if needed, beta-block/CCBs (HCM) Interventional/surgical: - Septostomy (HCM) - ICD, pacemaker
26
Define myocarditis
Inflammation of the heart muscle in the absence of acute/chronic ischaemia
27
Describe the aetiology of myocarditis
Commonly caused by: - Infection: viral (coxsackie, echo, mumps, flu, etc), bacterial (Strep, TB), Chagas, Lyme, etc - Immune/inflammatory: connective tissue disease, vasculitis, thyrotoxicosis - Toxins/drugs (may be hypersensitivity rxn): CO, alcohol, cocaine, antibiotics, thiazides, lithium, etc
28
Describe the presentation of myocarditis
- Fulminant: presents with acute HF symptoms, SCD with viral illness (7-10 previous on average) - Acute: days-weeks of HF symptoms, chest pain - Chronic
29
Describe the investigations for myocarditis
History and examination ECG Bloods: FBC, CRP, ESR, U+Es, BNP, trop CXR Echo *Endomyocardial biopsy is diagnostic but rarely performed -Further testing as indicated: serology, metabolic screen, cardiac MRI etc
30
Describe the management of myocarditis
Conservative: -Rest, fluids, paracetamol Medical: - HF symptomatic Mx: diuretics, BBs, etc * ICU, inotropes etc as needed in severe cases
31
Describe the epidemiology of infective endocarditis
Occurs in patients w previous valve surgery, nosocomial infection, IVDU
32
Describe the pathogens involved in infective endocarditis
``` Native valves: Strep viridans Prosthetic valves: Coagulase negative Staph, Staph epidermidis (early replacement) IVDU: S aureus, gram negatives *Colorectal Ca: Strep bovis HACEK bacteria also ```
33
Which pathogens are more common in acute IE?
Staph aureus
34
Which pathogens are more common in subacute IE?
Strep species
35
Describe the presentation of IE
Acute: fever, chills, fatigue, tachycardia, HF Subacute (more vague than acute): fever, haematuria, fatigue Septic emboli features: stroke, septic joint, splenic infarct ALWAYS suspect if fever + emboli/HF/risk factors
36
Describe the signs of IE
Systemic: tachycardia, fever Chest: new murmur Splenomegaly Vascular lesions: Janeway lesions, splinter haemorrhages, petechiae Immune phenomena: Osler's nodes, Roth's spots
37
Name risk factors for IE
- Prosthetic valve - Cardiac surgery/intervention - IVDU - Immunosuppression - Structural congenital heart disease - Recent vascular access eg picc line
38
Describe the investigations for IE
As soon as you suspect: - Urine dip (haematuria) - Bloods: FBC, CRP, U+Es, CULTURES!!! (3 sets, 30mins apart, different locations) - ECG - CXR - Echo (TTE or TOE- more sensitive)
39
Describe the diagnostic criteria for IE
Duke criteria: 2 major OR 1 major + 3 minor OR 5 minor Major: -Positive blood cultures (typical from 2) -Evidence of endocardial involvement (echo) -Single positive culture for Coxiella Minor: - Predisposing cardiac condition or IVDU - Fever >38 - Vascular phenomena - Immune phenomena - Micro evidence (does not meet major criteria)
40
Describe the management of IE
Depends on causative organism and valves MDT approach: cardio, micro, surgeons ABC approach, sepsis 6 as needed Medical: - Start empirical BS antibiotics while awaiting cultures - Switch to specific depending on sensitivities - Continue for 4-6 weeks, usually use PICC line Surgical/interventional: - Most pts require surgery eg. valve replacement - Offer emergency if acute HF Monitoring: - Monitor cultures during treatment - Repeat echo after treatment
41
Describe the epidemiology of rheumatic fever
More common in developing countries | RHD may be present in older populations in developed countries
42
Describe the pathophysiology of rheumatic fever
Grp A Streptococcal infection (tonsillitis) -> molecular mimicry -> acute rheumatic fever -> rheumatic heart disease after several years
43
Describe the presentation of acute rheumatic fever
Classically presents weeks after Grp A strep tonsillitis - Fever - Erythema marginatum - Arthritis/arthralgia - Carditis: chest pain, dyspnoea, palpitations, murmur - SC nodules - Chorea: can be up to 6 mos after, F > M
44
Describe the diagnostic criteria for acute rheumatic fever
``` Modified Jones criteria: Need evidence of recent Grp A strep infection + 2 major OR 1 major + 2 minor Major: -Arthritis -Erythema marginatum -SC nodules -Carditis -Chorea ``` Minor: - Fever - Arthralgia (w/o arthritis) - PR prolongation (w/o carditis) - Raised ESR or CRP
45
Describe the investigations for suspected acute rheumatic fever
History and exam suggestive - ECG (PR prolongation) - Throat swab - Bloods: FBC, CRP, ESR, ASOT, cultures (exclude) - CXR - Echo
46
Describe the management of acute rheumatic fever
Acute: - Rest and NSAIDs (paracetamol until Dx confirmed) - Antibiotic treatment (phenoxymethylpenicillin/benzathine benzylpen) acutely (erythromycin if pen allergic) - Mx of HF if present Prophylaxis: -Penicillin prophylaxis (IM injection monthly 10 years) Surgical/interventional: -As needed for RHD Monitoring: - ESR/CRP weekly until normalised - Repeat echo after Dx. If RHD -> yearly echo
47
Describe the prognosis of acute rheumatic fever (in terms of RHD)
50-70% of individuals will develop RHD | Treatment is not of prognostic benefit

Cardiology finals KTB (4 decks)

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