Cardiovascular Flashcards
Which of the following is a consequence of a myocardial infarction?
A There is loss of contractility within 60 seconds
B Microvascular injury occurs after 2hrs
C ATP reduction of 50% occurs within 20min
D Irreversible cell injury occurs after 60min
A
Explanation
Only severe ischaemia, lasting 20-40min or longer, leads to irreversible cell damage (necrosis). The extent of necrosis is largely complete within 3-6hrs in experimental models. Progression of necrosis in humans follows a more protracted course of 6-12hrs. In these patients coronary arterial collateral system, often stimulated by chronic ischaemia, is better developed and thereby more effective.
This is an old question using a table in the cardiac chapter from older editions.
Note: Approximate time of onset of key events to cardiac myocytes in ischaemia are (as per the table) : Onset of adenosine triphosphate (ATP) depletion occurs in seconds, loss of contractility occurs in <2min, ATP reduced to 50% of normal in 10min and 10% of normal in 40min, irreversible cell injury occurs in 20-40min and microvascular injury occurs >1hr
What is the most common histological change seen within 24 hours following a myocardial infarction?
A Pallor and oedema
B Disintegration of dead myofibres
C Increased collagen deposition
D Liquefactive necrosis
A
Explanation
Myocardial infarcts of less than 24hrs show early coagulation necrosis, pallor, oedema and haemorrhage. There is also pyknosis of nuclei. Disintegration of myofibres occurs from day 3 to 7 and collagen deposition at weeks 2 to 8
There is coagulative necrosis not liquifactive necrosis.
A closer look at the TB:
Early morphologic recognition of acute MI is difficult especially when death occurs within a few hours of the onset of symptoms. Mis<12hrs old are usually not apparent on gross examination. If the infarct preceded death by 2-3hrs, it is possible to highlight the infarcted area using a stain. The gross histochemical stain gives a brick red colour to intact no infarcted myocardium. Dead cells of an infarct appear as an unstained pale zone. By 12-24 hrs after the infarction, an MI can usually be identified grossly as a reddish blue area of discolouration caused by stagnated trapped blood.
Which of the following changes occurs in compensated pressure loaded cardiac hypertrophy?
A Diffuse fibrosis
B Ventricular dilation
C Decreased sarcomeres
D Hyperplasia
A
Explanation
Compensated cardiac hypertrophy results in diffuse fibrosis, a decrease in the capillary myocyte ratio, an increase in the number and mutations of the sarcomeres, synthesis of abnormal and dysfunctional proteins and extreme hypertrophy. Because adult cardiac myocytes cannot divide, augmentation of myocyte number (hyperplasia) cannot occur. In response to pressure loaded cardiac hypertrophy there is the development of a concentric increase in the ventricular wall. In contrast to volume loaded cardiac hypertrophy where there is a dilation of the ventricle
Which of the following is a common cause of fungal endocarditis?
A Actinomyces
B Candida
C Aspergillus
D Cryptococcus
B
Explanation
Candida albicans is the most common cause of fungal endocarditis, causing over half of all cases.
Fungal endocarditis
Candida albicans 24%
Non-albicans sepices of Candida 28%
Aspergillus species 24%
Histoplasma capsulatum 6%
Other 17%
The vegetations caused by fungal organisms tend to be larger than bacterial infections
Question 5
High output failure occurs in all of the following conditions with the exception of?
A Systemic arteriovenous fistulas
B Paget’s disease
C Hypothyroidism
D Morbid obesity
C
Explanation
Causes of high output failure are: anaemia including iron deficiency, vitamin B12, folate deficiency and Sickle cell disease. Renal failure (lack of erythropoietin).Others include: pregnancy, beriberi (vitamin B1/thiamine deficiency), thyrotoxicosis, Paget’s disease, arteriovenous fistulae and arteriovenous malformations, morbid obesity, cor pulmonle, carcinoid syndrome, multiple myeloma, beta-thalassemia intermedia and cirrhosis.
Morbid obesity: appears to be related to vasodilation-mechanism unclear. The effects of obesity on the CVS may be exacerbated by pressure overload states such as hypertension.
Which of the following statements regarding infective endocarditis is correct?
A Cryptococcus is the most common fungal cause
B Is most commonly caused by staphylococcus epidermidis on prosthetic vaves
C Is most commonly caused by streptococcus viridans on healthy valves
D Is most commonly caused by staphylococcus aureus on damaged valves
B
Explanation
According to prescribed texts- the causative organisms differ in the major high risk groups. Endocarditis of native but previously damaged or abnormal valves is caused most commonly by Strep Viridans (50-60% of cases). in contrast, more virulent Staf Aureus organisms commonly found on the skin can infect healthy and deformed valves and are responsible for 10-20% of cases overall. Staf Aureus is the most common offender in IVDU. Prosthetic valves are most commonly caused by S. epidermidis. The remaining organism include enterococci and the HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenellla and Kingella).
Emergency text books of Australia have noted that Staf Aureus entering through a breach in the skin, has surpassed Strep Viridans as the commonest pathogen in both NVE (native valve endocarditis) and prosthetic valve endocarditis. This change reflects better dental care and an increase in nosocomial infections. Proven Staf Aureus bacteraemia the incidence of infective endocarditis is 13-25%
Candida is the most common fungal cause of infective endocarditis. The aortic and mitral valves are the main sites of infection
NOTE: For the primary exam, this may be a contentious question. Apparently this question is featured on the emergency medicine website and the answer is STREP VIRIDANS
