Lecture notes
Cardiovascular diseases lecture 2
- Institution
- De Montfort University (DMU)
Lecture notes of 9 pages for the course MSCI3015 Pharmacology and Therapeutics at DMU
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Cardiovascular diseases II (CVD II) – Hypertension, AtherosclerosisLearning objectives
At the end of the session you should be able to discuss pathophysiology, causes and clinical
manifestation in relation to treatments of the following conditions:
• Hypertension
• Atherosclerosis
• Dyslipidaemia
Hypertension (HTN)
• Hypertension (HTN): presence of persistently elevated blood pressure ->
morphological/functional changes in the heart and blood vessels.
- The increased afterload (pressure on the heart), results in left ventricle hypertrophy
- Increased pressure in arterioles results in thickening of arterial wall.
• Blood pressure value: systolic pressure (mmHg)/ diastolic pressure (mmHg)
• Blood pressure is considered normal when the values are below 120/80 mmHg
• The two main guidelines which are commonly used in hypertension diagnosis are AHA and
NICE:
HTN can be classified into diff stages and each stage will have diff bp values.
Hypertension (HTN)
Type of HTN: 95% primary and 5% secondary HTN
• 95% of HTN cases - classified as primary hypertension in which there is no apparent
underlying cause or other diseases
• 5% cases - secondary HTN- underlying cause and diseases are found
Contributing factors:
• Sedentary lifestyle
• Genetics • Excessive alcohol intake
• Ageing • Stress and anxiety
• Low birth weight
• Diet and obesity
, Mechanisms behind HTN:
• Increased sympathetic drive -> ↑ vasomotor tone <- chronic stress + abnormal
baroreceptor
- The output from sympathetic system is involved in vasomotor tone & BP regulation.
- Increased sympathetic output would result in increased vasomotor tone hence
elevated BP.
- Increased sympathetic output could be due to chronic stress or abnormal baroreceptor
• Activation of the renin-angiotensin-aldosterone system:
• Angiotensin: ↑ vasoconstriction
• Aldosterone: sodium and water retention
- Renin-angiotensin-aldosterone system plays significant role in regulating BP.
- Once activated, angiotensin will cause vasoconstriction while aldosterone causes
an increase in salt and water retention.
• Increased blood volume
- As a result of the increased sodium and water retention, the blood volume also
increases.
Secondary HTN:
The diseases and conditions which underly secondary HTN include CKD, Renovascular condition and
Endocrine condition. Secondary HTN also results from medication and pregnancy.
Chronic Kidney Disease (CKD): the most common cause of 2nd HTN
• Mechanism of HTN in CKD: impaired sodium excretion -> ↑ blood volume and CO
• The most frequent complication of HTN -> renal function test
- Patients with CKD usually have defective sodium excretion which results in water retention
hence increased blood volume and cardiac output.
- CKD is also the most frequent complication in patients w/ HTN, so the patient should have
renal function test carried out regularly.
Renovascular HTN
• Mechanism of HTN in renovascular HTN: atherosclerosis -> renal artery stenosis -> ↑renin
- Renovascular condition causing HTN is caused by blockage of the renal artery, blockage
means there will be less blood reaching kidney. When there's less blood reaching kidney,
renin angiotensin system is activated therefore it increases salt and water retention
Endocrine HTN include:
• Cushing syndrome: excess of adrenocortical hormone such as cortisol. Cortisol activates
renin-angiotensin-aldosterone system -> increase the salt and water retention.
• Acromegaly: over production of growth hormone -> anti-natriuretic. Acromegaly – there’s
an excessive amount of GH -> GH has an anti-natriuretic effect which means it stops sodium
from being excreted in urine -> increases salt and water retention.
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