CVS 2 Flashcards

1
Q

Explain the concept of systemic hypertension

A

Hypertension refers to raised blood pressure in the systemic vascular bed.

Therefore, hypertension is usually defined as a systolic BP > 140mmHg or diastolic BP > 90mmHg.

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2
Q

Describe the effects of systemic hypertension on blood vessels

A

Hypertension accelerates atherosclerosis (remember, hypertension is one of the major modifiable risk factors for developing atherosclerosis).

Hypertension also accelerates arteriosclerosis- hardening of the arteries

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3
Q

Describe the causes of aortic dissection.

A

hypertension
abnormal media
pregnancy

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4
Q

Describe how valve stenosis and regurgitation may cause disease

A

As stenosis progresses, blood flow through the aortic valve becomes more and more impeded during systole. ie. there is development of left ventricle (LV) outflow obstruction. In order to maintain cardiac output, the LV must produce more force to drive blood through the aortic valve and into the aorta.
Since aortic stenosis develops over a chronic course, the LV is able to do this by undergoing compensatory hypertrophy.

Regurgitation: blood flows back into the left atrium, causing the pressure in the LA to rise.
The high pressure in the LA is transmitted backwards into the pulmonary circulation and the high pressure in the pulmonary circulation causes transudation of fluid from the circulation into the lung interstitium and alveoli (pulmonary oedema) ie. acute left heart failure.

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5
Q

Describe the causes of infective endocarditis

A

• usually bacterial: Streptococci, usually S. viridans (40-50%) – weakly pathogenic. Usually originating in the mouth.
- Staphylococci eg. S. aureus (20-30%) – highly pathogenic.
S. aureus is the most common cause in iv drug users; usually affecting the tricuspid valve.
• other bacteria eg. gram negative bacteria such as E. coli.
• less commonly fungi eg. Candida, Aspergillus.
- typically immunocompromised, iv drug users and patients with indwelling venous lines.

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6
Q

Important causes of secondary hypertension.

A
  • chronic renal disease (the most important cause overall):
  • chronic kidney disease of any cause:
  • eg. diabetic nephropathy, obstructive nephropathy, chronic glomerulonephritis etc
  • renal vessel disease (renal artery stenosis, most commonly due to atherosclerosis)
  • adult polycystic kidney disease
  • acute glomerulonephritis (hypertension is one of the presenting features of nephritic syndrome, seen in IgA nephropathy, post-infectious GN, lupus nephritis)
  • autoimmune disease - vasculitis (particularly polyarteritis nodosa), systemic sclerosis
  • Coarctation of aorta (mainly due to renal underperfusion and excess renal secretion)
  • Endocrine disease
  • Cushing’s syndrome, Conn’s syndrome, Phaeochromocytoma, Acromegaly
  • Drugs
  • eg. steroids, oral contraceptive pill, NSAIDs
  • Pregnancy (pre-eclampsia)
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7
Q

Describe the effects of systemic hypertension on the heart

A

accelerates coronary artery atherosclerosis

left ventricular hypertrophy- the LV has to push harder against the increased pressure in the systemic circulation in order to eject blood into the aorta

myocardial ischaemia

arrhythmia

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8
Q

Describe the effects of systemic hypertension on kidney

A
renal ischaemia 
tubular atrophy
interstitial fibrosis 
progressive glomerular sclerosis 
progressive CKD
atrophy of kidneys
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9
Q

Describe the effects of systemic hypertension on brain.

A

intracerebral haemorrhage
berry aneurysms
hypertensive encephalopathy

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10
Q

Describe the pathophysiology of acute and chronic heart failure.

A

as the left ventricular hypertrophy progresses there is increasing metabolic demands of myocardium. However, the heart becomes progressively less able to meet these demands because: the myocardial capillary bed does not expand in tandem with the increased myocardial O2 demand, thus increasing distance across which O2/nutrients must diffuse.

accelerated atherosclerosis (due to hypertension).

eventually the hypertrophied LV will decompensate and fail (left heart failure).

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11
Q

What are the two types of arteriosclerosis?

A

Hyaline- There is a gradual change in the artery/arteriole: smooth muscle cells in the media are replaced by collagen and there is also deposition of plasma proteins, together resulting in hyaline change

Hyperplastic- The very high systolic blood pressure pressure causes fibrinoid necrosis in the vessel wall. The body’s healing response results in proliferation of the intimal cells

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12
Q

what is aortic dissection

A

Aortic dissection occurs when there is a tear in the intima. A split forms in the media and blood tracks in the newly formed ‘false lumen’.

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13
Q

two types of aortic dissection?

A
  • type A dissection involves the ascending aorta.

* type B dissection does not involve the ascending aorta

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14
Q

How do aortic dissections cause disease?

A
  • the false lumen reduces the blood flow through the ‘true’ lumen. The dissection may extend into other arteries and cause ischaemia/infarction of the organ supplied by that artery.
  • the dissection may rupture externally into the pleural cavity, pericardial space or abdominal space.
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15
Q

Pathogenesis of infective endocarditis

A

Bacteria are delivered to the heart during an episode of bacteraemia. This may be due to an event as trivial as tooth brushing or associated with a more invasive procedure such as surgery. As a consequence of the bacteraemia, the organisms adhere to and invade the valve.

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16
Q

complications of infective endocarditis

A

disturbance of valve function

embolism- part of vegetation may break away from valve

formation of antigen-antibody immune complexes- immune complexes may be deposited in the glomeruli which results in the activation of complement and recruitment of inflammatory cells.

17
Q

2 ways to diagnose infective endocarditis

A

blood cultures

echocardiography

18
Q

describe the vicious cycle of left ventricular hypertrophy

A

Chronic LVF is a progressive disorder in which a vicious cycle becomes established which escalates cardiac workload and worsens the degree of LVF.
Because poor cardiac output reduces tissue perfusion, the body responds by increasing the sympathetic drive and activating the renin-angiotensin-aldosterone system.

The end result is retention of sodium and water by the kidneys, which leads to increase myocardial stress and declining cardiac function.

19
Q

How is chronic heart failure divided into groups?

A

systolic failure

diastolic failure

20
Q

Describe systolic failure in chronic heart failure

A

Systolic failure
• the underlying problem is failure of the pumping action of the ventricle during systole.
• usually a consequence of ischaemic heart disease or hypertension.
• the ventricle is usually dilated and fails to contract normally such that the proportion of blood ejected in each beat (normally 50-70%), the ejection fraction, is reduced.

21
Q

Describe diastolic failure in chronic heart failure

A

Diastolic failure (= Heart Failure Normal Ejection Fraction (HFNEF)
• systolic function is not impaired.
• there is failure of the ventricle to fill adequately due to increased stiffness of the wall.
• it may be a consequence of massive LV hypertrophy, myocardial fibrosis or other conditions eg. amyloidosis.
• diastolic LVF is increasingly recognised in older patients.
• diastolic HF accounts for 50% of cases of HF. The prognosis in diastolic HF is the same as for systolic HF.

22
Q

how to diagnose LVF

A
hx 
exam
CXR
echocardiography
BNP levels