Hypertension

Question 1

Definition

Answer 1

Sustained elevated high blood pressure (140/90)

There needs to be 3 readings of it to be classed as hypertension or over 3 months

Question 2

Aetiology

Answer 2

3 different types of hypertension

– primary hypertension (95%):
—– several mechanisms seem to be involved
—– most cases atherosclerosis occurs
—- there may be genetic factors or predisposition
—- lifestyle factors:
——– overweight
——– excessiver alcohol intake, tobacco use, insulin resistance
——– low levels of serum nitric oxide- affects the smooth muscles in the blood vessels
——– high cholesterol

– secondary hypertension (5-10% of cases)
—- usually causes a higher blood pressure than primary hypertension

—- result of medical condition:
—— hyperthyroidism
—— hyperparathyroidism
—– kidney disease
—– cushings disease
——- cirrhosis
—— pregnancy

Malignant hypertension (1% of cases)
– very rare
– medical emergency
– rapid increase in blood pressure
– may lead to end organ damage
– diastolic pressure can rise over 130

Question 3

Epidemiology

Answer 3

Estimated 20% of the global adult population have it (50% over the age of 60)

increased incidence with age

Gender: male=female

genetics:
– there are familial predispositions

Question 4

Different stages of hypertension

Answer 4

Optimal 120/80

Pre-hypertension- 120-139/80-99

stage 1- 140-159/90-99

Stage 2- 160+/100+

180/110- 1 week referral instantly

Question 5

Pathophysiology

Answer 5

Cardiac output- how much blood each ventricle is pumping per minute HR x SV

blood pressure can be measured by- CO x Peripheral resistance

Blood pressure can be increased by an increased arterial vasoconstriction:
– caused by an increase in sympathetic activity (adrenaline etc) as it increases the peripheral resistance

If there is increased peripheral resistance:
– it is going to make it harder for blood to flow to the destinations meaning decreased blood flow to organs

RENAL CAUSES (80%):
Decreased blood flow to the kidneys:
– releases renin–>angiotensinogen–> angiotensin 1–> angiotensin 2 (converted by Angiotensin converting enzyme ACE)
—- this leads to constriction, leading to further perisperhal pressure affecting blood pressure even more

Reduced renal sodium excretion may represent a final common pathway in the pathogenesis of hypertension

This leads to an increase in fluid volume, increased cardiac output, and increased peripheral resistance, causing an elevation in blood pressure

ENDOCRINE CAUSES:
- adrenal gland releases aldosterone (CONNS SYNDROME)
– leads to an increase in sodium and H2O reabsorption
– absorbing more blood will lead to increased blood volume, which will then lead to increased cardiac output

– cortisol release (CUSHINGS SYNDROME):
—- increase in norepinephrine and epinephrin receptor sensitivity, they will bind to the beta receptors of the heart, increasing cardiac output– leading to an increased blood pressure

THYROID CAUSES:
– hyperthyroidism:
—- increases levels of T3 and T4— these will then increase HR and increase NE/Epi receptor sensitivity leading to vasoconstriction increasing BP

– hypothyroidism
—- decreased levels of T3 and T4– acting on the kidney increasing sodium retention, this means increase H2O retention. Increasing blood volume increasing BP

– hyperparathyroidism:
—- increase in calcium in blood due to increased PTH leading to vasocconstriction

Aortic:
– coarction of the aorta (narrowing)- increases blood pressure

Medications:
– oral contraceptives:
— increase in eostrogen, leading to an increase in angiotensinogen by kidney–> angiotensin 2–> increased blood pressure

– cushings disease- release of hormones like cortisol known as stress hormones which will increase the blood pressure

Hyperthyroidism increases systolic blood pressure by decreasing systemic vascular resistance, increasing heart rate, and raising cardiac output.

Atherosclerosis pathophysiology

Question 6

Clinical presentation

Answer 6

Hypertension is generally asymptomatic

Secondary hypertension specifically can present with:
– attacks of sweating
– tachycardia

headache

dyspnoea

retinopathy visual changes

chest pain

nose bleeds

Can lead to end organ damage:
– retinal:
—- diplopia
—- blurred vision

– cardiovascular:
—- left ventricular hypertrophy
—- abdominal bruits

– CNS:
—- seizures (coma)
—- disorientation

– renal/kidney:
—- urinary frequency
—- flank pain
—- renal enlargement

Question 7

Treatment

Answer 7

Reduce all cardiovascular risk factors

Lifestyle changes:
– stopping smoking
– reduce alcohol
– weight reduction
– increase exercise
– stress reduction