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*Medicine: Cellular Pathology > Cardiovascular pathology (2) > Flashcards

Cardiovascular pathology (2) Flashcards

1
Q

What is hypertension?

A
  • refers to raised BP in systemic vascular bed
  • we know incidence of complications is proportional to blood pressure
  • clinical trials have shown tx if oten beneficial (good > harm) with sustained BPs >140/90mmHg
  • therefore hypertension usually defined as systolic BP >140mmHg or diastolic BP >90mmHg
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2
Q

Hypertension may be either essential (primary) or secondary.

What is the aetiology of essential/primary HT?

A
  • approx 95% cases
  • diagnosed in absence of an identifiable secondary cause
  • due to an interplay of genetic + env factors:
    • BP has polygenic inheritance - candidate genes include thos encoding angiotensinogen, renin and ANP receptor genes
    • most important env factors = stress, diet (inc salt + alcohol) and the intrauterine env (babies w/ low birthweight have an increased incidence of HT and other cardiovascular disorders in adult life)
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3
Q

In secondary hypertension an identifiable (and sometimes treatable) underlying cause is found. What are some causes of secondary hypertension?

A
  • chronic renal disease (most important cause overall)
    • CKD: diabetic nephropathy, obstructive nephropathy, chronic glomerulonephritis
    • renal vessel disease (renal artery stenosis, most commonly due to atherosclerosis)
    • adult polycystic kidney disease
    • acute glomerulonephritis
    • autoimmune disease - vasculitis, systemic sclerosis
  • coarctation of aorta (narrowing)
  • endocrine - Cushing’s, Conn’s, phaeochromocytoma, acromegaly
  • drugs - steroids, OCP, NSAIDs
  • pregnancy (pre-eclampsia)
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4
Q

What are clinical features of hypertension?

A

clinically silent until a complication occurs

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5
Q

Hypertension accelerates atherosclerosis (remember, it’s one of the major modifiable risk factors for deveoping atherosclerosis).

Hypertension also accelerates arteriosclerosis - what is arteriosclerosis?

A
  • arteriosclerosis is literally hardening of an artery or arteriole
  • can be divided into two histological forms:
    1. hyaline arteriosclerosis
    2. hyperplastic arteriosclerosis
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6
Q

What is hyaline arteriosclerosis?

A
  • gradual change in artery/arteriole
  • sm muscle cells in media are replaced by collagen
    • deposition of plasma proteins -> hyaline change
  • process accelerated by HT, DM + age
  • arteriosclerosis increases rigidity of arteries
  • so lowers compliance of arterial tree
  • contributes to age-related increase in systolic BP + alters tissue autoregulation by shifting autoregulatory curve to right
  • -> inc susceptibility to hypotension + inc mortality of shock in elderly
    • narrowing of lumina -> decreased BF
  • end result = progressive chronic ischaemia of tissue supplied by artery/arteriole
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7
Q

What is the key difference between atherosclerosis and arteriosclerosis?

A

arteriosclerosis differs from atherosclerosis in that there is no intimal lipid deposition w/ resultant inflammation

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8
Q

What is hyperplastic arteriosclerosis?

A
  • characteristic of but not limited to malignant/accelerated hypertension
  • the v high systolic BP -> fibrinoid necrosis in vessel wall
  • body’s healing response -> proliferation of intimal cells
  • imparts an “onion-skin” appearance + causes significant narrowing of vessel lumen
  • -> significant reduction in BF through vessel + consequent ischaemia of supplied tissue
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9
Q

Hypertension has a number of adverse effects on the heart eg. it accelerates coronary artery atherosclerosis worsening IHD.

Hypertension also causes left ventricular hypertrophy, how does this happen and what can it lead to?

A
  • LV has to push harder against inc pressure in systemic circulation in order to eject blood to aorta
  • LV undergoes compensatory left ventricular hypertrophy
  • pt may be asymptomatic during this period of compensation
  • as LVH progresses, there is inc metabolic demands of myocardium
  • however, heart becomes progressively less able to meet demands bc:
    • hypertrophy renders myocardium stiff
    • inc distance across which O2/nutrients must diffuse
    • accelerated atherosclerosis (due to hypertension)
  • eventually the hypertrophied LV will decompensate + fail -> LEFT HEART FAILURE
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10
Q

What is hypertension the commonest cause of?

A
  • atrial fibrilation (+ other arrhythmias)
  • dangerous bc thrombi may form in atria as a consequence of stasis -> the thrombi may embolise
  • cardiac output may fall bc loss of normal atrial contraction can significantly reduce LV filling + stroke vol

HT can also manifest as MI and progressive left heart failure

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11
Q

How does hypertensive renal disease come about and what imaging finding will show?

A
  • progressive hyaline arteriosclerosis in renal arterioles
  • causes chronic + progressive renal ischaemia
  • results in tubular atrophy, interstitial fibrosis + progressive glomerular sclerosis
  • in turn -> leads to development of progressive chronic kidney disease (CKD)
  • vicious cycle established: hypertension causes CKD which in turn worsens hypertension
  • ultrasound will show small kidneys -> small bc of atrophy + fibrosis
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12
Q

What are the retinal changes that occur in hypertension?

A
  • flame haemorrhage
  • papilloedema
  • cotton wool spot
  • hard exudates
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13
Q

What kind of strokes can hypertension result in? Why is this?

A
  • intracerebral haemorrhagic stroke
  • HT commonest cause of intracerebral haemorrhage
  • due to rupture of tiny charcot-bouchard aneurysm
    • they form in arterioles weakened by long-standing HT
  • most strokes (80%) are ischaemic strokes due to atherosclerosis
  • hypertension accelerates atherosclerosis + so increases risk of developing an ischaemic stroke as well as haemorrhagic stroke
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14
Q

What kind of aneurysms are subarachnoid haemorrhages due to?

A
  • berry aneurysm
  • thought to develop under influence of hypertension + atherosclerosis
  • in ppl with congenital weakness in media of cerebral vessels
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15
Q

What is malignant/accelerated hypertension?

A
  • clinicopathological syndrome characterised by markedly raised diastolic BP (usually >130-140mmHg) + end organ damage
  • occurs in <1% pts w/ 1o hypertension
  • more commonly in cases of 2o HT (esp when due to renovascular disease)
  • usually affects younger ppl w/ HT; new cases present at 30-40yrs
  • underlying pathogenesis is poorly understood
  • characteristic histological lesion is hyperplastic arteriosclerosis - also fibrinoid necrosis of small arteries + arterioles
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16
Q

What are the clinical consequences of malignant hypertension?

A
  • acute left ventricular failure
  • stroke (cerebral haemorrhage)
  • acute renal failure
  • blurred vision (due to retinal haemorrhages/exudates and papilloedema)
  • hypertensive encephalopathy (headache, irritability, alteration in consciousness)
  • microangiographic haemolytic anaemia + disseminated intravsacular coagulation (DIC)
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17
Q

Why does renal damage and encephalopathy occur in malignant hypertension? What age group is this common in?

A
  • due to failure to protect microcirculation from increased pressure
  • there is a breakdown of normal autoregulation mechanism
    • rare in elderly bc cerebral autoreg curve is shifted to right, thus arteriosclerosis protects against development of renal damage + encephalopathy
    • more common in young people whose arteries are unprotected by arteriosclerosis
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18
Q

What does failure of autoregulation in the kidney result in?

A
  • increased pressure to glomeruli
  • fibrinoid necrosis + microaneurysms of glomerular capillaries
  • pressure also causes fibroid necrosis of afferent glomerular arterioles -> may rupture or be associated w/ luminal thrombosis -> small infarcts
  • thrombosis damages RBCs - microangiopathic haemolytic anaemia
  • ischaemia of juxtaglomerular apparatus leads to inc secretion of renin -> further inc in BP (vicious cycle)
  • together, these effects give rise to proteinuria and haematuria
  • similar changes occur in brain in hypertensive encephalopathy
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19
Q

What is aortic dissection?

A
  • occurs when there is a tear in the intima
  • a split forms in the media
  • blood tracks in the newly formed ‘false lumen’
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20
Q

What is the clinical presentation of aortic dissection?

A
  • classically a tearing pain between shoulder blades w/ hypertension and asymmetrical pulses
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21
Q

What are the major risk factors for aortic dissection?

A
  • hypertension
  • abnormal media eg. Marfan’s, ehler-danlos syndrome
  • pregnancy
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22
Q

Aortic dissection are classified into type A and type B - what do these mean?

A
  • Type A
    • involves the ascending aorta
    • generally more serious than type B
    • requires immediate surgical repair
  • Type B
    • does not involve ascending aorta
    • generally managed medically (rigorous BP control) w/ surgery reserved for if there are complications
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23
Q

What are the 2 main ways aortic dissection can cause disease?

A
  1. false lumen reduces the blood flow through the ‘true’ lumen - dissection may extend into other arteries and cause ischaemia/infarction of the organ supplied by that artery
  2. the dissection may rupture externally into the pleural cavity, pericardial space or abdominal space
24
Q

What are the complications of aortic dissection?

A
  • type A - false lumen may compromise blood flow along branches of aorta as it spreads along its length; eg. carotid dissection -> stroke, coronary dissection -> MI
  • dissection may track back to root of aorta and rupture in pericardium, causing cardiac tamponade
  • also a dissection involving root of aorta may cause stretching of aortic valve -> acute onset aortic regurg
  • dissection may rupture externally into thoracic/abdo cavity causing exsanguination
25
Q

Heart valves ensure one way flow through the heart. Mechanical disturbance of heart valves are an important cause of heart disease.

What are the 2 main types of mechanical defect?

A
  • stenosis
    • failure of valve to open completely -> impede forward flow
    • stenosis is virtually always caused by a chronic process
    • the chronicity of process allows time for compensatory changes in heart, blood vessels, and other organs
  • regurgitation (incompetence)
    • failure of a valve to close completely -> reverse flow occurs
    • regurg may be caused by an acute or chronic process
26
Q

What is the most common valve disease?

A

aortic stenosis

27
Q

What are common causes of aortic stenosis?

A
  • cusp calcification of bicuspid aortic valve - calcification develops approx 30yrs w/ progressive stenosis, thought that years of turbulent flow across abnormal valve disrupt endothelium and collagen matrix of leaflets, resulting in gradual calcium deposition
  • age-related calcification of the normal tricuspid aortic valve - normal aortic valve is tricuspid where about 1-2% of pop have a bicuspid valve, it is thought cumulative wear + tear of valve motion over many years leads to endothelial + fibrous damage, causing calcificiation of an otherwise normal valve
  • post rheumatic fever valve disease (rare in UK)
28
Q

What is the pathophysiology of aortic stenosis?

A
  • blood flow across aortic valve is impeded during systole
  • as a consequence, significantly elevated left ventricular pressure is necessary to drive blood into aorta
  • since AS develops over chronic course, the LV is able to compensate by undergoing hypertrophy in response to the higher systolic pressure it must generate to maintain output
  • ie. gradual development of LV outflow obstruction causes gradual pressure overload of LV + results in compensatory LV hypertrophy
  • however, hypertrophy reduces compliance of ventricle -> resulting elevation of diastolic** pressure -> **LA hypertrophy in order to fill the ‘stiff’ LV

as a consequence of the compensatory changes, there is a long asymptomatic period - eventually, the heart decompensates and there is deterioration in cardiac function leading to development of symptoms.

29
Q

What is the classic clinical presentation of aortic stenosis (triad)?

A
  • angina
  • syncope on exertion
  • development of congestive cardiac failure

AS is also an important cause of unexpected sudden death (due to arrhythmias).

AS is associated with an ejection systolic murmur

30
Q

What is the second most common valve lesion following aortic stenosis?

A
  • mitral regurgitation
31
Q

What are causes of mitral regurgitation?

A
  • mitral annulus
  • cusps
  • papillary muscles
32
Q

What is the pathophysiology of acute mitral regurgitation?

A
  • sudden onset usually due to infective endocarditis or rupture of pap muscle after MI
  • when there is sudden onset, the heart does not have time to undergo compensatory changes
33
Q

What is the pathophysiology of chronic mitral regurgitation?

A
  • gradual onset may be due to dilatation of mitral valve ring, mitral valve prolapse, post-rheumatic fever or pap muscle ischaemia
  • here the heart has time to undergo compensatory changes
    • LA dilates so it can accommodate backflow of blood without a substantial increase in LA pressure
    • the LV undergoes hypertrophy, which mitigates effects of regurg

these compensatory changes maintain cardiac output as near-normal levels + so pt may be asymptomatic for many years

34
Q

What is the most common cause of mitral regurgitation?

A
  • mitral valve prolapse (MVP)
  • common w/ incidence of 5%, F>M
  • MVP usually isolated finding but may be found as complication of genetic disorders (eg. Marfan’s, Ehlers-Danlos syndromes)
35
Q

What is the pathophysiology of mitral valve prolapse?

A
  • normal dense collagen + elastic matrix of valve
  • replaced with loose myxomatous connective tissue containing abundant glycosaminoglycans
  • so-called ‘myxomatous degeneration’
  • leaflets become enlarged
  • one of the leaflets ‘prolapses’ back into LA during systole
36
Q

Is mitral valve prolapse always associated with regurgitation?

A

It may or may not be…

  • MVP without MR: generally considered by cardiologists to be asymptomatic (majority)
  • MVP with MR: symptomatic. Only a minority of pts have severe enough MR to warrant surgery.
37
Q

What is infective endocarditis?

A
  • refers to infection of part of the endocardium
  • usually the endocardial surface of a valve
  • atrium and ventricle can also be affected
  • serious disease w/ high mortality
    • untreated -> 100% mortality
    • treated -> 10-30%
38
Q

What are causes of infective endocarditis?

A
  • usually bacterial:
    • streptococci, usually S. viridans (40-50%) - weakly pathogenic
    • staphylococci eg. S. aureus (20-30%) - highly pathogenic, S. aureus is the most common cause in IV drug users; usually affecting tricuspid valve
  • other bacteria eg. gram negative bacteria such as E. Coli
  • less commonly fungi eg. Candida, Aspergillus
    • typically immunocompromised, IV drug users + pts w/ indwelling venous lines
39
Q

What is the pathogenesis of infective endocarditis?

A
  • bacteria delivered to heart during episode of bacteraemia
  • may be due to an event as trivial as tooth brushing
  • or associated with a more invasive procedure eg surgery
  • bacteraemia -> organisms adhere to and invade the valve
  • the endocardium is normally resistant to infection, so for infection to occur:
    • either there must be highly pathogenic organisms (eg. S aureus) colonising a normal valve
    • or weakly pathogenic organisms (eg. S viridans) colonising an abnormal valve eg. prosthetic valve, mitral or aortic regurgitation, mitral valve prolapse

As the organisms replicate they become enmeshed within layers of platelets and fibrin on the valve surface, forming vegetations.

40
Q

What is a vegetation?

A
  • vegetation = thrombus containing microorganisms
  • remember Virchow’s triad:
    • in infective endocarditis, the microorganism causes endothelial injury on the heart valve
    • also if the valve is abnormal there may be turbulent blood flow across valve
41
Q

Complications of endocarditis are due to 3 distinct processes.

What are these 3 processes?

A
  • disturbance of valve function
  • embolism
  • formation of antigen-antibody immune complexes
42
Q

How does disturbance of valve function complicate infective endocarditis?

A
  • over time the underlying structure of the valve is destroyed by infection
  • this results in development of valve regurgitation
43
Q

How does the process of embolism complicate infective endocarditis?

A
  • part of the vegetation may break away from valve + form an embolus
  • the clinical effect will depend on which artery the embolus occluded
  • majority of emboli from vegetations enter the cerebral circulation and so present as a stroke
44
Q

How does formation of antigen-antibody complexes complicate infective endocarditis?

A
  • antigen probs derived from micro-organism and antibody produced by body in response to it
  • immune complexes may be deposited in glomeruli which results in activation of complement and recruitment of inflammatory cells
  • clinical effects depend on where immune complexes are deposited
  • eg. deposition in glomeruli may result in glomerulonephritis ie. the immune complex deposition results in damage to cells in glomerulus with consequent disturbance in normal renal fxn
45
Q

What are the key investigations to confirm the diagnosis of infective endocarditis?

A
  • Blood cultures
    • at least 3 sets of blood cultures from different sites, taken a minimum of 1hour apart before starting Abx
    • these confirm diagnosis + guide appt abx therapy
  • Echocardiography
    • transoesophageal echocardiography to identify vegetations and any complications
46
Q

What diagnostic criteria can be employed to make a diagnosis of infective endocarditis?

A
  • Duke’s criteria
  • place heavy emphasis on blood cultures + echocardiography
47
Q

What is heart failure?

A
  • syndrome
  • occurs when pumping action of heart is inadequate for needs of the body
  • ie cardiac output is unable to meet metabolic needs of tissues
  • common: 2-3% prevalence of population; approx 20% in 70-80yr olds
  • serious: mortality 30% in first year and 10% each year after
48
Q

What are ways to classify heart failure?

A
  • acute or chronic (depending on speed of onset)
  • left or right (depending on where dominant site of injury is)
49
Q

Describe acute left heart failure

A
  • sudden major insult to left side of heart
  • no time for compensation
  • cardiac output falls catastrophically
  • sudden failure of LV -> severe congestion in pulm venous system
  • rapid accumulation of fluid in alveolar spaces + interstitium
  • causes pulmonary oedema and presents as severe breathlessness
  • in worst cases, there is underperfusion of organs + development of cardiogenic shock
50
Q

Acute left heart failure is almost always a complication of MI affecting the left ventricle. Examples of how this is true?

A
  • extensive MI renders a large volume of the LV non-functional
  • rupture of a mitral valve papillary muscle
  • development of an arrhythmia
51
Q

Chronic left heart failure is by far the most common form of heart failure.

What is this almost always due to and why?

A
  • almost always due to chronic left ventricular failure
  • left ventricle is damaged slowly over a period of time
  • commonest causes of slow damage to LV are:
    • chronic ischaemic heart disease (due to coronary artery atherosclerosis)
    • systemic hypertension
    • valvular (mitral/aortic) heart disease

Bc damage occurs slowly, there is enough time for compensatory myocardial hypertrophy to occur. This maintains cardiac output + prevents symptoms of HF.

Eventually, myocardium becomes irreversibly damaged + LV decompensates leading to chamber dilatation + falling CO.

52
Q

Chronic LVF is a progressive disorder in which a vicious cycle becomes established which escalates cardiac workload and worsens degree of LVF.

What happens in the body as the poor cardiac output reduces tissue perfusion?

A
  • body responds by increasing sympathetic drive
  • activating renin-angiotensin-aldosterone system
  • end result in retention of sodium + water by kidneys -> inc in myocardial stress + declining cardiac function
53
Q

Discuss decompensation in heart failure

A
  • pts w/ chronic heart failure may decompensate if their heart is stressed
  • pts w/ chronic heart failure freq exp episodes of acute worsening in their symptoms
  • often described as ‘acute decompensation’
  • very commonly seen in routine practice when a concurrent illness (often only a trivial infection) places an additional burden on a critically falling heart + pushes pt into acute failure

Most pts w/ chronic heart failure experience a relapsing and remitting course, with periods of stability interspersed with episodes of decompensation

54
Q

Chronic LVF may be further divided into systolic or diastolic failure.

What is meant by systolic failure?

A
  • underlying prob = failure of pumping action of ventricle during systole
  • ventricle is usually dilated + fails to contract normally
  • such that proportion of blood ejected in each beat (normally 50-70%), the ejection fraction, is reduced
55
Q

What is meant by diastolic failure (=heart failure normal ejection fraction (HFNEF))?

A
  • systolic function not impaired
  • failure of ventricle to fill adequately due to inc stiffness of wall
  • diastolic LVF is increasingly recognised in older pts
  • diastolic HF accounts for 50% of HF
  • prognosis is same as systolic HF
56
Q

Chronic LVF is one of the most common + important problems in clinical medicine. Most patients die within 3 years of diagnosis, making the prognosis of chronic LVF worse than many cancers.

How is the diagnosis of LVF made?

A
  • history + exam
  • ECG (usually abnormal)
  • CXR (cardiomegaly)
  • echocardiography
    • can confirm systolic or diastolic dysfunction
    • it may identify underlying cause -> valve disease
  • BNP plasma levels

Investigations to identify the underlying cause of the heart failure is also important

57
Q

What is the importance of B-type natriuretic peptide (BNP) plasma levels?

A
  • BNP is a hormone secreted by ventricular myocytes in response to volume + pressure overload of LV
  • its normal function is to promote salt + water diuresis by kidney
  • BNP plasma levels are useful bc low levels effectively rule out diagnosis of LVF
  • in contrast, in the correct clinical context, high BNP plasma levels make the diagnosis of LVF very likely

*Medicine: Cellular Pathology (16 decks)

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