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IHS > Heart > Flashcards

Heart Flashcards

0
Q

When does one use anti microbial prophylaxis?

A

In situations where infection is common and predictable

In situations where the effect of infection would be very detrimental

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1
Q

What are the 4 chambers of the foetal heart called?

A

Sinus venosus
Atrium
Ventricle
Bulbus cordis

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2
Q

What is an anti microbial prophylaxis

A

An agent that has activity against most of the expected organisms

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3
Q

What factors determine the efficacy of antimicrobial prophylaxis

A

The antibiotic sensitivity of the likely pathogens

Adequate levels of the medication needs to be given at the time of risk

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4
Q

What are the disadvantages of antimicrobial prophylaxis?

A

Cost
Adverse effects
Antibiotic resistance
Insufficient attention to other preventative measures

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5
Q

When is prophylaxis used in HIV?

A
  • Post-exposure antiretrovirals - mother to child, rape survivors, occupational exposure
  • With advanced AIDS - prevent initial/recurrent infections (cotrimoxazole to prevent PCP, flu console to prevent cryptococcal infection)
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6
Q

What is the preferred antibiotic for surgical prophylaxis?

A

Cefazolin (1st generation cephalosporin mainly active against staph)

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7
Q

If operating on the GIT, what antibiotic would you prescribe and why?

A
  • co-amoxiclav
  • cefazolin and metronidazole

They cover S. aureus and other organisms found in the colon (anaerobes and gram-neg bacilli)

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8
Q

When must prophylaxis be given for surgery?

A

At the time of the anesthesia to ensure food levels are present at the time of risk of infection

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9
Q

Why is antimicrobial prophylaxis necessary in patients with rheumatic fever and not with glomerulonephritis?

A

There are multiple rheumatogenic strains of strep pyogenes and only a few nephrotogenic strains

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10
Q

What is the aim of antimicrobial prophylaxis in rheumatic fever patients?

A

To prevent repeat infections with strep pyogenes

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11
Q

What are the recommended antibiotics prescribed as prophylaxis for rheumatic fever?

A
  • benzathine penicillin (IM monthly)
  • penicillin (12 hourly)
  • erythromycin (12hourly)
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12
Q

How long should a rheumatic fever patient be on antimicrobial prophylaxis?

A
  • without proven carditis : 5 years after last attack/ until 18
  • with mild carditis : 10 years after last attack/ until 25
  • with severe valvular disease : lifelong
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13
Q

Why does penicillin still work as an effective prophylaxis for rheumatic fever?

A
  • s. pyogenes has never developed resistance to it

- it has relatively little effect on other commensal bacteria

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14
Q

What is endocarditis?

A

An infection of the endocardium of the heart or valves, usually relating to turbulence or abnormal flow of blood resulting in damage to endocardium and development of vegetations (infected clumps of platelets and protein)

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15
Q

What commonly causes endocarditis?

A

Viridans streptococci (low virulence organism present as normal flora in mouth and upper airway)

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16
Q

According to new research, who should be given prophylaxis for infective endocarditis?

A
  • had previous endocarditis
  • had valve replacements
  • have surgically constructed shunts
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17
Q

What is autoimmunity?

A

An influx of auto reactive immune cells and/or antibodies in body tissues that initiate inflammation and represent failure of tolerance induction

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18
Q

What can cause a loss of self-tolerance?

A
  • a loss immunological privileged status (infection)
  • viral/drug induced altered self-antigens (haemolytic anaemic)
  • regulatory T-cell dysfunction
  • molecular mimicry (shared common antigens)
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19
Q

Describe the pathogenesis of rheumatic fever

A
  • pharyngeal infection by group A strep 2-6 weeks before clinical manifestation
  • antibodies made against group A strep cross-react with human tissue
  • molecular mimicry (heart valve and brain share common antigenic sequences with GAS bacteria)
  • host immune responses may play a role in determining who gets ARF following infection
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20
Q

What is the relationship between hypersensitivity reactions and ARF?

A

Type 2 - carditis
Type 3 - synovitis/ arthritis and s. chorea
Type 4 - subcutaneous nodules and carditis

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21
Q

What are Aschoff nodules?

A

A form of granulomatous inflammation found in the myocardium around the vessels

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22
Q

What are the major criteria for diagnosing acute rheumatic fever?

A
  • carditis
  • erythema marginatum
  • Sydenham’s chorea
  • subcutaneous nodules
  • arthritis
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23
Q

What are the minor criteria for diagnosing acute rheumatic fever?

A
  • fever
  • high ESR
  • increased CRP
  • long PR interval
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24
Q

What are the symptoms of cardiac failure?

A
  • dyspnoea
  • orthopnea
  • paroxysmal nocturnal dyspnoea
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25
Q

What are the signs of cardiac failure?

A
  • basal crepitations
  • elevated JVP
  • pedal oedema
  • added heart sounds (s3)
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26
Q

What are the principles of cardiac failure management?

A
  • look for reversible, correctable causes
  • sodium restriction
  • fluid restriction
  • pharmacological management
  • avoid drugs that may worsen the failure (NSAIDS, amphetamines, steroids)
27
Q

Describe the action of ACE-inhibitors in cardiac failure

A
  • reduce the after load by causing vasodilation
  • reduce the preload by inhibiting sodium and water retention (anti-aldosterone)
  • reduces remodeling of the heart and vessels
28
Q

When should ACE-inhibitors not be given to a patient with cardiac failure?

A

If they have hyperkalaemia, angioedema or are pregnant

29
Q

What are the adverse effects of ACE-inhibitors?

A
  • angioedema ( rapid swelling of soft tissue)
  • cough
  • hyperkalaemia
30
Q

Describe the action of diuretic in patients with cardiac failure

A

Usually in the loop of Henley Na, K, Cl and water are taken back into the blood stream. Furosemide (high ceiling loop diuretic) blocks these transporters and so the patient looses these things in their urine. It reduces oedema

31
Q

What are the adverse effects of diuretics in cardiac failure?

A
  • hyponatraemia
  • hypokalaemia
  • hypotension
32
Q

Why must NSAIDS not be given to patients with cardiac failure?

A

They inhibit renal prostaglandin synthesis. This may result in sodium retention, reduced renal blood flow and renal failure (patients will already have poor renal perfusion)

33
Q

What is the definition of heart failure?

A

When the heart is unable to pump at a rate to meet metabolic demands

34
Q

Outline the different classifications of heart failure

A
  • right vs left
  • systolic vs diastolic
  • low output vs high output
  • acute vs chronic
35
Q

What are the causes of cardiac failure?

A
  • ischemic heart disease
  • valvular heart disease
  • systemic hypertension
  • pulmonary hypertension
  • myocarditis
  • pericarditis
  • cardiomyopathies
36
Q

What are other less common causes of cardiac failure?

A
  • high output states (pregnancy, anaemia)
  • low output states (hypothyroidism)
  • autoimmune (SLE)
  • endocrine (thyrotoxicosis)
  • inflitrative (amyloid)
  • cardiac tumours (atrial myxoma)
37
Q

What are the 3 mechanisms used to compensate for low cardiac output?

A
  • ventricular dilation
  • blood volume expansion by salt and water retention
  • tachycardia
38
Q

What are the signs and symptoms of left cardiac failure?

A
  • predominantly respiratory
  • cough/ dyspnoea
  • orthopnoea
  • paroxysmal nocturnal dyspnoea
  • pink, blood stained frothy sputum
  • displaced apex beat due to cardiomegaly
  • bibasal crackles in lungs
39
Q

What are the signs and symptoms of right sided cardiac failure?

A
  • pitting oedema in the legs and others dependent areas
  • ascites
  • hepatomegaly
  • splenomegaly
  • raised JVP
  • parasternal heave
40
Q

What are causes of pulmonary hypertension?

A
  • myocardial infarction
  • left ventricular failure
  • atrial / ventricular septal defects
  • pulmonary emboli/ fibrosis
  • emphysema
  • chronic obstructive airways disease ( COAD)
  • idiopathic
41
Q

What is cor pulmonale?

A

When the RV is hypertrophied or dilated due to primary respiratory disease affecting the structure and or function of the lung

42
Q

What is the definition of myocarditis?

A

Inflammation of the myocardium

43
Q

Discuss the aetiology of myocarditis

A
  • usually infectious (viruses)
  • non-infectious (collagen vascular disease)

Usually self-limiting

44
Q

What is the definition of a cardiomyopathy?

A

A myocardial disease of unknown cause

- must exclude HT, ischemia, infection and valvular disease

45
Q

With what are dilated cardiomyopathies associated?

A
  • alcohol
  • toxins
  • malnutrition
  • pregnancy
  • previous viral myocarditis
  • HIV
46
Q

Describe how M-proteins add to strep virulence

A

inhibits the activation of complement and protects the organism from phagocytosis

47
Q

What are the six principal mechanisms of cardiovascular dysfunction?

A
  • failure of the pump
  • obstruction to flow
  • regurgitant flow
  • shunted flow
  • disorders of cardiac conduction
  • rupture of the heart or a major vessel
48
Q

What is cor pulmonale?

A

An increase in the size of the right ventricle in response to an increase in resistance or BP in the lungs (pulmonary HT)

49
Q

What is a shunt?

A

An abnormal communication between cardiac chambers or blood vessels

50
Q

What clinical signs can indicate congenital abmormalities?

A
  • poor feeding
  • failure to thrive
  • impaired growth
  • tachypnoea
  • resp distress
  • cyanosis
  • clubbing
  • polycythemia
  • cardiac failure
  • pulmonary hypertension
  • infective endocarditis
51
Q

What are the 4 components of Tetralogy of Fallot?

A
  • VSD
  • aorta overriding the VSD
  • obstruction to RV outflow
  • RV hypertrophy
52
Q

What is tricuspid atresia?

A

When the tricuspid valve does not develop and is closed. Leads to RV hypoplasia. Often has secondary ASD and VSD allowing for blood to mix

53
Q

Explain three ways in which emphysema leads to pulmonary hypertension

A
  • capillary destruction (obliterative PH)
  • reduced alveolar PO2 (hypoxic vasoconstriction)
  • increased blood viscosity due to polycythemia (increased chances of thrombus formation and obstruction)
54
Q

What is Raynaud’s phenomenon?

A

a vasospastic disorder causing discoloration of the fingers, toes, and occasionally other areas

55
Q

What are 6 complications of atherosclerotic lesions?

A
  • stenosis (leading to ischemic atrophy)
  • plaque rupture, thrombus and embolism (infarction)
  • atheroembolism
  • calcification
  • haemorrhage into plaque
  • weakening of vessel wall
56
Q

What is an aneurism?

A

A localized abnormal dilation of any vessel including the heart

57
Q

What is cardiac tamponade?

A

Pressure on the heart that occurs when blood or fluid builds up in the space between the heart muscle (myocardium) and the outer covering sac of the heart (pericardium).

58
Q

What is a cirsoid aneurysm?

A

A complex of dilated anastomosing arteries and veins (plexiform lesions of pulmonary hypertension)

59
Q

What is a Rasmussen’s aneurysm?

A

An aneurism of an artery inside a TB cavity of lung

60
Q

What is a varicose aneurysm?

A

A false aneurysmal sac liking artery and vein

61
Q

What are the 5 possible complications of aneurysms?

A
  • pressure on adjacent structures
  • rupture with haemorrhage (cardiac tamponade due to rupture of dissecting aneurysm)
  • thrombotic occlusion of branches
  • thromboembolism (vascular dilation + endothelial damage increase chances of thrombosis)
  • ischemia in distal territory (ischemic colitis)
62
Q

What is the role of desmosomes in cardiac muscle?

A

Type of adhering junction that mechanically holds the cells together in response to considerable mechanical stress

63
Q

What is the role of gap junctions in cardiac muscle?

A

Areas of low electrical resistance that allow action potential to spread from cell to cell

64
Q

5 possible causes of arrhythmia

A
  • pace maker dysfunction
  • conduction defects
  • re-entry pathways
  • bundle branch blocks
  • ectopic excitation
65
Q

What are the 4 main determinants of ventricular preload?

A
  • venous return
  • diastolic filling time
  • atrial pressure
  • ventricular compliance (distensibility)

IHS (2 decks)

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