cardiovascular pathology II Flashcards

1
Q

what is the rough amount for BP to be hypertension?

A

140/90

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2
Q

what chronic renal disease s can cause secondary hypertension?

A
  • diabetic nephropathy, obstructive nephropathy
  • renal vessel disease: renal artery stenosis
  • adult polycystic kidney disease
  • vasculitis
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3
Q

what are other causes of seconday hypertensoin?

A

coarctation of the aorta
endocrine disease
drugs
pregnancy

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4
Q

how does hypertension affect atherosclerosis?

A

accelerates atherosclerosis

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5
Q

what is arteriosclerosis?

A

hardening of the artery

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6
Q

what are two types of arteriosclerosis?

A

Hyaline and hyperplastic

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7
Q

what is the change seen in hyaline arteriosclerosis?

A

collagen replaced smooth muscle cells in the media

deposition of plasma proteins

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8
Q

what accelerates hyaline arteriosclerosis?

A

hypertension
D.M
age

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9
Q

what is the effect of hyaline arteriosclerosis?

A

increased rigidity causing lower complience

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10
Q

why are people susceptible to hypotension if they have hyaline arteriosclerosis?

A

the hyaline arteriosclerosis leads to decreased complience.

the auto regulation curve shifts to the right meaning the BP needs to be higher before it’s corrected

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11
Q

what is the difference between arteriosclerosis and atherosclerosis?

A

arteriosclerosis has no lipid deposition and no chronic inflammation

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12
Q

what is hyperplastic arteriosclerosis?

A

The BP causes fibrinoid necrosis in the vessel wall. there is then proliferation of the intimal cells

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13
Q

how does hypertension affect the heart?

A

Coronary artery atherosclerosis

left ventricular hypertrophy

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14
Q

what retinal changes are caused by hypertension?

A

flame haemorrhages
hard exudates
cotton wool spots
papilloedema

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15
Q

what is malignant/accelerated hypertension?

A

Raised diastolic pressure and end organ damage

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16
Q

what is the characteristic histology responsible for malignant/ accelerated hypertension?

A

hyperplastic arteriosclerosis

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17
Q

what is aortic dissection?

A

A tear in the intima causes the formation of a false lumen.

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18
Q

what is the clinical presentation of an aortic dissection?

A

A tearing pain down the shoulder blades
hypertension
asymmetrical pulses

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19
Q

what are the major risk factors for aortic dissection?

A

hypertension
abnormal media
pregnancy

20
Q

what is a type A aortic dissection?

A

involving the ascending aorta

21
Q

what is a type B aortic dissection?

A

not involving the ascending aorta

22
Q

what aortic dissection is more serious?

A

Type A so management is normally immediate surgical repair

23
Q

what is stenosis?

A

Failure of a valve to close completely meaning there can be reverse flow

24
Q

what is the most common valve disease?

A

Aortic stenosis

25
Q

what are common causes of aortic stenosis?

A
  • cusp calcification of a bicuspid valve
  • age related calcification of a tricuspid valve
  • post rheumatic fever valve disease
26
Q

why can aortic stenosis lead to left ventricular hypertrophy?

A

more left ventricular pressure is needed to drive blood into the aorta –> LV compensation

27
Q

what is the presentation for aortic stenosis?

A

angina
syncope on exertion
congestive cardiac failure

28
Q

what murmur is associated with aortic stenosis?

A

Ejection systolic murmur

29
Q

what are common causes of mitral regurgitation?

A
mitral annulus
mitral valve prolapse
infective endocarditis
post rheumatic fever
rupture of papillary muscles after MI
30
Q

what are the normal causes of acute mitral regurgitation?

A

infective endocarditis

MI causing papillary muscle rupture

31
Q

what are the consequences of acute mitral regurgitation?

A

No time to compensate so blood will flow back into the LA causing the pressure to rise. the pressure is transmitted towards the pulmonary circulation causing pulmonary oedema

32
Q

what are causes of chronic mitral regurgitation?

A

dilatation of a mitral valve ring
mitral valve prolapse
post rheumatic fever
papillary muscle ischaemia

33
Q

what is the most common cause of mitral valve regurgitation?

A

Mitral valve prolapse

34
Q

what happens in mitral valve prolapse?

A

the normal dense collagen/elastin matric of the valve is replaces with loos myxomatous connective tissue

35
Q

what bacteria can cause infective endocarditis?

A

Streptococci, S.viridans

S.aureus in IV drug users

36
Q

In infective endocarditis a vegetation forms on the valve, what is a vegetations?

A

A thrombus containing microorganisms

37
Q

what are the complications of infective endocarditis?

A

disturbance of valve function
embolism which can present as stroke
formation of antigen=antibod immune complexes

38
Q

what are the investigations for infective endocarditis?

A

Blood cultures: 3 sets from different sites taken an hour apart before antibiotics
- transoesophageal echocardiography

39
Q

what is dukes major criteria for diagnosing infective endocarditis?

A

Major criteria:
- positive blood cultures with typical microrganisms in 2 seperate cultures. persistant positive blood cultures taken over 12 hours apart
three or more cultures taken over more than 1 hour apart
evidence of endocardial involvement on echocardiography such as new valve regurg, abscess or vegetations

40
Q

what is dukes minor criteria for diagnosing infective endocarditis?

A
  • predisposing valve or cardiac abnormality
  • temperature above 38
  • vasculitic phenomena
  • embolic phenomena
  • positive blood cultures but not meeting major critera
41
Q

what is needed to diagnose infective endocarditis?

A

two major criteria
one major and 3 minor
5 minor

42
Q

what is heart failure?

A

when the pumping action of the heart doesn’t meet the needs of the body

43
Q

what is systolic failure?

A

failure of the pumping action when the ventricle is in systole. the ventricle is normally dilated and fails to contract normally so the ejection fraction is reduced

44
Q

what is diastolic failure?

A

failure of the ventricle to fill due to increased stiffness of the wall.

45
Q

what is BNP?

A

A Hormone secreted by ventricular myocytes in response to volume or pressure overload of the LV.