153 - Hypertension Flashcards
Proportion of Australians over 18 who are hypertensive
~30%
Arbitrary definition of hypertension
Systolic over 140mmHg and diastolic over 90mmHg
Primary/essential hypertension
No specific identifiable cause.
Responsible for 90-95% of hypertension
Secondary hypertension
Identifiable pathology that is causing hypertension
5-10% of hypertension
Benign hypertension
Blood pressure rises gradually, over a long period.
Majority of cases.
Malignant hypertension
Blood pressure rises rapidly, over a short period.
Minority of cases.
Two forces that leads to blood pressure
Cardiac output (stroke volume, heart rate, blood volume) and resistance in arteiroles.
Aortic changes from age
1
2
3
Aorta: loss of elasticity, hardening i.e. ‘arteriosclerosis’
Media: fragmentation of elastin, increased collagen
Intima: increased collagen
What effect does hypertension have on blood vessels?
Exacerbates age-related changes.
Aorta: loss of elasticity, hardening i.e. ‘arteriosclerosis’
Media: fragmentation of elastin, increased collagen
Intima: increased collagen
Age-related arterial changes in small and medium arteries
1
2
– Media: fragmentation of elastin, increased collagen, sometimes calcification
– Intima: increased collagen -> thickening
Age-related arteriolar changes 1 2 3 4
Arteriolar hyalinosis/hyaline arteriolosclerosis
– Deposition of plasma proteins in wall
– Increased collagen
– Smooth muscle atrophy
–Arteriole wall becomes thickened by homogenous eosinophilic glassy material (‘hyaline’) and the lumen narrowed
Arteriolar change in hypertension, or with age
Arteriolar hyalinosis/hyaline arteriosclerosis
What can hyaline arteirolosclerosis lead to?
Can slightly increase diastolic blood pressure with age.
Genetic predispositions to primary hypertension 1 2 3 4 5 6
– Polygenic genetic influences. Genetic polymorphisms may influence for example
• Sympathetic responses
• Transport of ions across cell membranes in vessels or kidney
• Arteriolar responses to local regulatory factors
• Activity of components of the renin-angiotensin-aldosterone system and secretion of renin
• Genetic determinants may also influence target organ damage
Lifestyle factors contributing to primary hypertension 1 2 3 4
- Amount of salt in diet
- Alcohol intake
- Levels of physical activity
- Abdominal obesity and metabolic syndrome (can influence e.g. renal sodium retention, increased sympathetic activity, ion transport across cell membranes)
Age, gener, race predispositions to primary hypertension
1
2
- Prevalence lower in premenopausal females than in age-matched males and in postmenopausal women
- Higher in those of African descent
Broad divisions of primary hypertension
High plasma renin and low plasma renin.
Possibly correlate with vasoconstrictor and volume-dependent forms of hypertension.
Systolic hypertension with wide pulse pressure
1
2
Several groups:
• Decreased compliance of aorta (arteriosclerosis).
Age related changes –> loss of elasticity -> elevation of the systolic pressure and widening of the pulse pressure. If excessive -> isolated systolic hypertension
• Increased stroke volume e.g. aortic regurgitation, hyperthyroidism, fever (can treat some of these causes)
Most common pathology leading to secondary hypertension
Renal disease
EG: diabetic glomerulosclerosis, certain glomerulonephritides, polycystic renal disease, chronic renal diseas
Examples of non-renal causes of secondary hypertension 1 2 3 4
– Endocrine e.g. adrenocortical adenoma producing cortisol or aldosterone, phaeochromocytoma, pituitary adenoma producing ACTH
– Vascular e.g. coarctation of aorta, renal artery stenosis
– Medications e.g. corticosteroids, oestrogen
– Other e.g. neurogenic/cerebral, hypercalcemia, toxaemia of pregnancy, obstructive sleep apnoea, cocaine use