Hypertension

Question 1

Atherosclerosis 5 steps

Answer 1

Endothelial wall damage
Uptake + modification of LDL
Infiltration of macrophages in subendothelial space
Formation of fatty streaks
Smooth muscle proliferation and fibrous cap formation

Question 2

Atherosclerosis- Endothelial wall damage

Answer 2

Shear stress- hypertension
Toxic damage- e.g. cigarette smoke
Exposure to high levels of LDL

Question 3

Atherosclerosis- uptake and modification of LDL

Answer 3

Following endothelial damage, LDL and monocytes infiltrate subendothelial space
Once taken up, LDL is modified:
- oxidation- in presence of reactive O2 species (e.g. smoking)
- glycation- in presence of glucose

Question 4

Atherosclerosis- infiltration of macrophages into subendothelial space

Answer 4

Oxidised LDL stimulates endothelial cells to produce inflammatory mediators required for uptake of monocytes
Monocytes taken up + transform into macrophages

Question 5

Atherosclerosis- formation of fatty streaks

Answer 5

Macrophages take up excess LDL via scavenger receptors (unlimited) + transform into foam cells)

Question 6

Atherosclerosis- Smooth muscle proliferation + fibrous cap formation

Answer 6

Endothelial cells + macrophages release growth factors, including smooth muscle proliferation + collagen deposition (can form fibrous cap)
Ca2+ deposits onto plaque, hardening it
Smooth muscle cells can also take up LDL + become foam cells
Fibrous cap is v fragile + can break off- collagen exposed to blood –> thrombus formation

Question 7

How many vascular deaths does hypertension cause

Answer 7

Around 50%

Question 8

Hypertension Stage 1

Answer 8

140-59 SBP, 90-99 DBP

ABPM 135/85

Question 9

Hypertension Stage 2

Answer 9

160-79 SBP, 100-109 DBP

ABPM 150/95

Question 10

Hypertension Stage 3

Answer 10

Systolic >180 or Diastolic >110

Question 11

Postural Hypertension

Answer 11

Measure BP seated or supine
Stand the patient for 1 minute
Systolic drops by more than 20mm

Question 12

Malignant/Accelerated Phase HTN

Answer 12

Rapid rise in BP leading to vascular damage (pathology:fibrinoid necrosis)

Question 13

Malignant HTN signs

Answer 13

Severe HT (SBP>200, DBP>130) + bilateral retinal haemorrhages and exudates + papilloedema and exudates+- papilloedema

Question 14

Malignant HTN symptoms

Answer 14

Headache +- visual disturbance

Question 15

Malignant HTN treatment

Answer 15

Urgent treatment required

May precipitate AKI, HF, encephalopathy (hypertensive emergencies)

Question 16

Isolated Systolic HTN

Answer 16

Most common form in UK

Question 17

Secondary Hypertension- Renal disease

Answer 17

Intrinsic renal disease (75%)- glomerulonephritis, polyarteritis nodose (PAN), systemic sclerosis, chronic pyelonephritis, polycystic kidneys
Renal vascular disease (25%)- commonly atheromatous (elderly, male, smokers), rarely fibromuscular dysplasia (young, female)

Question 18

Secondary HTN- endocrine disease

Answer 18

Cushing's and Conn's syndromes
Phaeochromocytoma
Acromegaly
Hyperparathyroidism
Congenital adrenal hyperplasia

Question 19

Secondary HTN- other causes

Answer 19

Coarctation
Pregnancy
Liquorice
Drugs (steroids, MAOI, COCP, cocaine, amphetamines)

Question 20

BHS classification hypertension

Answer 20

Optimal= <120 SBP, <80 DBP
Normal= <130 SBP, <85 DBP
High Normal= 130-9 SBP, 85-9 DBP
Grade 1 (Mild)= 140-59 SBP, 90-99 DBP
Grade 2 (moderate)= 160-79 SBP, 100-109 DBP
Grade 3 (severe)= >180 SBP, >110 DBP