Hypertension – modified DIASG

BP >140/90, has three grades

Grade 1: (mild) 140–159 and/or 90–99

Grade 2: (moderate) 160–179 and/or 100–109

Grade 3: (severe) ≥180 ≥110

Isolated systolic has a particularly bad prognosis and is associated with a 3 fold increase in mortality.



Isolated systolic hypertension:

Grade 1 140–149 <90

Grade 2 >160 <90

BP increases with age in developed countries.

In world adult population there is 20-30% of pop with HTN

Higher incidence in black Africans (40-45% of adults)

80-90% of patients have ‘PRIMARY’ HTN, which means essential HTN of unknown cause.


Essential HTN has a multifactorial aetiology:

  • Genetic: (unidentified genes)
  • Fetal factors: (low birth weight is associated with HTN – may be associated with fetal adaption to interuterine under nutrition)
  • Environmental factors:
    • Obesity
    • ETOH intake
    • High sodium intake
    • Stress
  • Humeral mechanics:
    • Autonomic NS
    • RAAS
    • Natriuretic peptide system
  • Metabolic syndrome:
    • Major risk factor for CVD


Secondary HTN, is HTN due to a specific and potentially treatable cause.

Secondary causes:


  • Cushing’s syndrome
  • Acromegaly
  • Thyroid disease
  • Hyperparathyroidism disease


  • Conn’s syndrome
  • Adrenal hyperplasia
  • Phaeochromocytoma


  • Diabetic nephropathy
  • Chronic glomerulonephritis
  • Adult polycystic disease
  • Chronic tubulointerstitial
  • nephritis
  • Renovascular disease


  • Aortic coarctation


  • NSAIDs
  • Oral contraceptives
  • Steroids
  • Carbenoxalone
  • Liquorice
  • Sympathomimetics
  • Vasopressin
  • Monoamine oxidase
  • inhibitors (with
  • tyramine


Male = worse in terms of risk factors and prognosis
Genetics and geography
Black Africans, Hispanic and Native Americans = higher incidence
Increases with age
Predisposing factors
See above
Blood pressure measurement (HTN is usually only abnormal finding)


  • Usually pt is asymptomatic
  • Can present with headaches
  • Palpitations
  • Headaches
  • Epistaxis
  • Nocturia
  • Breathlessness due to LVH/failure
    • Malignant HTN may present with severe headaches, visual disturbance, fits, transient LOConciousness or symptoms of heart failure.



  • BP
  • Signs of an underlying cause should be sort:
    • Renal artery bruits in renovascular HTN
    • Radio-femoral delay in coarctation of the aorta
  • Features of LVH
  • If cardiac failure is present there may be sinus tachycardia and/or a 3rd heart sound.


  • Urine dip-stick for protein and blood
  • Fasting blood tests for lipids (total and HDL cholesterol) and glucose
  • Serum urea, creatinine and electrolytes
  • ECG

Consider ambulatory blood pressure monitoring.



Made after 3 BP measurements on different occasions that are all above baseline. (caution for white coat syndrome).
For essential HTN it remains unclear.
Macroscopic pathology
Microscopic histopathology
Clinical Features/S+S/complications
      • Cardiac changes:

Resistance vessels (the small arteries and arterioles)

show structural changes in hypertension with an

increase in wall thickness and a reduction in the

vessel lumen diameter. It is an increased peripheral

resistance that maintains the elevated blood pressure.

The cardiac output is normal. These mechanisms would result in an increased overall peripheral vascular resistance.


Large vessel changes occur: there is thickening of

the media, an increase in collagen and the secondary

deposition of calcium. These changes result in a loss

of arterial compliance, which in turn leads to a more

pronounced arterial pressure wave.


Pulse wave velocity:  A measure of arterial stiffness

and is inversely related to distensibility. With each

systolic contraction, a pulse wave travels down the

arterial wall before the flow of blood. Thus, the more

rigid the arterial wall, the faster the wave travels. It

can be measured but is not in routine use. Atheroma

develops in the large arteries owing to the interaction

of these mechanical stresses and low growth factors.


Left ventricular hypertrophy:  which results from

increased peripheral vascular resistance and

increased left ventricular load, is a significant

prognostic indicator of future cardiovascular events.


      • Renal changes: Eventually, changes in the renal

vasculature lead to a reduced renal perfusion, reduced

glomerular filtration rate and, finally, a reduction in

sodium and water excretion. The decreased renal

perfusion may lead to activation of the renin-angiotensin

system with increased secretion of aldosterone and further sodium and water retention.



      • CVA (There is a 6 fold increase in rates – both hemorrhagic and thrombogenic)
      • Coronary artery disease
      • Renal failure
      • Peripheral vascular disease

note: there is a 3 fold increase in the rates of cardiac death due to coronary events or cardiac failure.


Malignant HTN:

Also ‘accelerated’ HTN. It is associated with the rapid onset of the above complications with the addition of rapid renal failure, heart failure, aortic dissection cerebral oedema in a risk, papilloedema and haemorrhages in the eyes. Without treatment Malignant HTN has <20% survival rate.



      • ACE inhibitors
      • Diuretics (thiazide)
      • Calcium channel blocker
      • Beta Blocker



ARBs (f there is ace-i intolerance)

Alpha blockers

Vasodilators (hydralazine)



      • Diet
      • Exercise
      • Low sodium
      • ETOH decrease
      • Smoking cessation
      • Weight loss


Prognosis (with and without treatment)
Depends on a number of variables:

  • Level of BP
  • Presence of target organ changes
  • Co-existing risk factors for CVD such as hyperlipidemia, diabetes, smoking,  obesity, male sex
  • Age at presentation


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