Hypertension is defined as persistent blood pressure readings of 140/90 mmHg or higher. It is a major risk factor for cardiovascular disease and premature death. While usually asymptomatic, regular screening is important for detection. Treatment involves lifestyle modifications and medication to lower blood pressure to under 140/90 mmHg to reduce health risks. Malignant hypertension is a medical emergency characterized by severely high blood pressure that requires urgent treatment and hospitalization.

1. Hypertension
1
Prepared & Presented by
AbdirazaaqAliYusuf
Internship doctor
Internal medicine department
Mogadishu- Somali Turkey Recep Tayip Erdogan

2. Hypertension
Definition: Hypertension is defined as a persistent elevation in office systolic BP
≥140 and/or diastolic BP ≥90 mmHg, which is equivalent to a 24-hr ABPM
average of ≥130/80 mmHg or an HBPM average of ≥135/85 mmHg.(AHA
Definition)
hypertension is diagnosed if, when it is measured on two different days, the
systolic blood pressure readings on both days is ≥140 mmHg and/or the diastolic
blood pressure readings on both days is ≥90 mmHg.(WHO)
European guidelines, hypertension is defined as a BP ≥140/90 mm Hg while
the Americans choose a lower threshold of BP ≥130/80 mm Hg. American
guidelines classify Stage 1 hypertension as SBP ≥130‐139 mm Hg or DBP
≥80‐89 mm Hg while the Europeans define this as high normal BP (130-
139/85-89 mm Hg).

3. Hypertension
Hypertension is the most important risk factor for premature death and
CVD; causing ~50% of all vascular deaths (8≈106/yr).
Usually asymptomatic, so regular screening (eg 3-yrly) is a vital task—
most preventable deaths are in areas without universal screening.
If a BP reading is >= 140 / 90 mmHg patients should be offered ABPM
to confirm the diagnosis.
Confirm with 24hr ambulatory BP monitoring (ABPM); or a week of
home readings.
NB: the diagnostic threshold is lower ~135/85mmHg.
Patients with a BP reading of >= 180/110 mmHg should be considered
for immediate treatment.
3

4. Hypertension
• 90-95% Essential HTN
• 05-10% Secondary

5. Essential Hypertension
• MultifactorialAetiology.
– Genetic factors
– Fetal factors
• Environmental factors
– Obesity
– Alcohol intake
– Sodium intake
– Stress
– Smoking
• Insulin resistance
– (Metabolic syndrome)
The majority (80–90%) of patients with hypertension have primary elevation of blood
pressure, i.e. essential hypertension of unknown cause.

6. Secondary Hypertension
• Identifiable cause
• Suspected in ;
– Early onset
– First episode over age 50 years
– Those previously well controlled become refractory to treatment

7. Primary or ‘essential’ hypertension: (Cause unknown.) ~95% of cases.
Secondary hypertension: ~5% of cases. Causes include:
1. Renal disease: the most common secondary cause. 75% are from
intrinsic renal disease: glomerulonephritis, polyarteritis nodosa (PAN),
systemic sclerosis, chronic pyelonephritis, or polycystic kidneys. 25% are
due to renovascular disease, most frequently atheromatous (elderly Male
cigarette smokers, eg with peripheral vascular disease) or rarely
fibromuscular dysplasia (young female).
2. Endocrine disease: Cushing’s and Conn’s syndromes,
phaeochromocytoma, acromegaly, hyperparathyroidism, Liddle's syndrome
& Congenital adrenal hyperplasia (11-beta hydroxylase deficiency).
3. Others: coarctation, pregnancy, liquorice, drugs: steroids, MAOI, oral
contraceptive pill, cocaine, amphetamines.
7

8. Secondary causes of Hypertension
Endocrine Adrenal Renal Cardiovascular Drugs
• Cushing's • Conn's • Diabetic • Aortic • NSAIDs
syndrome syndrome nephropathy coarctation • Oral
contraceptives
• Acromegaly • Adrenal • Chronic • Steroids
hyperplasia glomeruloneph • Carbenoxalone
• Thyroid ritis • Liquorice
disease • Phaeochromoc • Sympathomim
ytoma • Adult etics
• Hyperparathyr polycystic • Vasopressin
oid disease disease • Monoamine
oxidase
• Chronic inhibitors (with
tubulointerstiti tyramine)
al nephritis
• Renovascular
disease

9. Blood pressure classification:
9

10. PATHOPHYSIOLOGY
 The normal blood pressure is maintained by four
mechanisms
Sympathetic nervous system activities
Activities of vascular endothelium
Activities of renal system
Activities of endocrine system

11. SYMPATHETIC NERVOUS SYSTEM ACTIVITIES
 When the BP is decreasing the activation of SNS will occur.The
increased SNS activity increases the heart rate and cardiac contraction.
 The increased the heart rate and cardiac contraction produce
vasoconstriction in the peripheral arterioles and promotes the release
of renin from kidney.
 The net effect of SNS activation is to increase the arterial blood pressure
by increasing cardiac output and systemic vascular resistance.
BP=CO X SVR

12. ACTIVITIES OF VASCULAR ENDOTHELIUM
 The vascular endothelium is a single cell layer that lines the
blood vessal.
 It will produce vasoactive substances and growth factors like
nitric acid, endothelin etc..
 These substances are potent vasoconstrictors and causes
increases blood pressure level.

13. ACTIVITIES OF RENAL SYSTEM

14. ACTIVITIES OF ENDOCRINE SYSTEM
 When the angiotensin-II is stimulated in the adrenal cortex, it
will secrete aldosterone.
 The aldosterone will stimulate the kidneys to retain sodium and water.
Thus the BP and cardiac output will get increased.

15. Signs and symptoms
Some times the high blood pressure does not causes any
symptoms, so that it is known as silent killer disease eg: Dm and
old Age patients.
In some patients the symptoms will develop like:
Severe head ache Blurred vision Dizziness
Nausea Vomiting Fatigue Confusion epistaxis
Chest pain Shortness of breath Irregular heart beat
papilledema

16. Signs and symptoms
16
Usually asymptomatic (except MALIGNANT HYPERTENSION).
Headache is no more common than in the general population.
Always examine the CVS fully and check for retinopathy.
Are there features of an underlying cause (phaeochromocytoma), signs of renal disease,
radiofemoral delay, or weak femoral pulses (coarctation), renal bruits, palpable kidneys, or
Cushing’s syndrome?
Look for end-organ damage: LVH, retinopathy and proteinuria—indicates severity and
duration of hypertension and associated with a poorer prognosis.
Examples of target (end-organ) damage:
1. LVH
2. PMH of MI or angina
3. PMH of stroke/TIA
4. Peripheral vascular disease
5. Renal failure.

17. Whom to treat: All with BP ≥160/100mmHg (or ABPM ≥150/95mmHg).
For those ≥140/90, the decision depends on the risk of coronary events,
presence of diabetes, or end-organ damage.
White-coat hypertension Refers to an elevated clinic pressure, but normal
ABPM (day average <135/85). NICE says don’t treat; but more likely to
develop hypertension in future, and may have ↑risk of CVD.
Masked hypertension is the opposite.
Malignant’ or accelerated phase hypertension: A rapid rise in BP leading to
vascular damage (pathological hallmark is fibrinoid necrosis). Usually there
is severe hypertension (eg systolic >200, diastolic>130mmHg) + bilateral
retinal haemorrhages and exudates; papilloedema may or may not be present.
Symptoms are common, eg headache +/- visual disturbance. It requires urgent
treatment, and may also precipitate acute kidney injury, heart failure, or
encephalopathy, which are hypertensive emergencies. Untreated, 90% die in
1yr; treated, 70% survive 5yrs. It is more common in younger and in black
subjects. Look hard for any underlying cause.
17

18. Grading hypertensive retinopathy
1. Grade 1: Tortuous arteries with thick shiny walls (silver or copper
wiring).
2. Grade 2: AVnipping (narrowing where arteries cross veins).
3. Grade 3: Flame haemorrhages and cotton-wool spots.
4. Grade 4: Papilloedema.

19. Diagnosis & Tests
19
1. Tests To confirm diagnosis: ABPM or home BP monitoring.
2. To help quantify overall risk: Fasting glucose; cholesterol.
3. To look for end-organ damage: ECG or echo (any LVhypertrophy? past
MI?); urine analysis (protein, blood).
4. To ‘exclude’ secondary causes: U&E (eg K+↓ in Conn’s); Ca2+ (↑ in
hyperparathyroidism).
5. Special tests: Renal ultrasound/arteriography (renal artery stenosis); 24h
urinary meta-adrenaline; urinary free cortisol; renin; aldosterone; MR aorta
(coarctation).

20. Investigations
Laboratory & ECG
Blood tests: Sodium, potassium, serum creatinine and estimated
glomerular filtration rate (eGFR). If available, lipid profile and fasting
glucose.
Urine test: Dipstick urine test.
12-lead ECG: Detection of atrial fibrillation, left ventricular
hypertrophy (LVH), ischemic heart disease.

21. Imaging Techniques
Echocardiography: LVH, systolic/diastolic dysfunction, atrial
dilation, aortic coarctation.
Carotid ultrasound: Plaques (atherosclerosis), stenosis.
Kidneys/renal artery and adrenal imaging: Ultrasound/renal artery
Duplex; CT-/MR-angiography: renal parenchymal disease, renal
artery stenosis, adrenal lesions, other abdominal pathology.
Fundoscopy: Retinal changes, hemorrhages, papilledema, tortuosity,
nipping.
Brain CT/MRI: Ischemic or hemorrhagic brain injury due to
hypertension.

22. Functional Tests and Additional Laboratory Investigations
Ankle-brachial index: Peripheral (lower extremity) artery disease.
Further testing for secondary hypertension if suspected: Aldosterone-renin
ratio, plasma free metanephrines, late-night salivary cortisol or other screening
tests for cortisol excess.
Urinary albumin/creatinine ratio
Serum uric acid (s-UA) levels
Liver function tests

24. LVH
24

25. Managing suspected
hypertension
25

27. Managing suspected hypertension
27
1. ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension): Treat
if <80 years of age AND any of the following apply: target organ
damage, established cardiovascular disease, renal disease,
diabetes or a 10- year cardiovascular risk equivalent to 20% or
greater.
2. ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension):
Offer drug treatment regardless of age.
3. For patients < 40 years consider referral to exclude secondary
causes.

28. Hypertension—management
28
Look for and treat underlying causes (eg renal disease, ↑alcohol).
Drug therapy reduces the risk of CVD and death.
Almost any adult over 50 would benefit from antihypertensives, whatever their
starting BP.
Treatment is especially important if: BP is persistently ≥160/100mmHg or
cardio vascular risk ↑ (10yr risk of vascular disease ≥20%), or existing
vascular disease or target organ damage (eg brain, kidney, heart, retina)
with BP>140/90mmHg.
Essential hypertension is not ‘curable’ and longterm treatment is needed.

29. Treatment goal <140/90mmHg (<130/80 in diabetes, 150/90 if aged >80
years).
Reduce blood pressure slowly; rapid reduction can be fatal, especially in the
presence of an acute ischemic stroke.
Lifestyle changes ↓Concomitant risk factors: stop smoking; low-fat diet.
Reduce alcohol and salt intake; increase exercise; reduce weight if obese.
Drugs The ALLHAT study suggests that adequate BP reduction is more
important than the specific drug used. However, B-blockers seem to be less
effective than other drugs at reducing major cardiovascular events,
particularly stroke. B-blockers and thiazides may increase the risk of new-
onset diabetes, Ca2+-channel blockers appear neutral, and ACE-i or ARB
may reduce the risk.
29

30. Monotherapy:
A. ≥55yrs, and in black patients of any age, 1st choice is a Ca2+-channel antagonist or
thiazide.
B. If <55 and NonAfro-Caribian Black, 1st choice isACE-i (orARB ifACE-i intolerant,
eg cough).
C. B-blockers are not 1st line for hypertension, but consider in younger people,
particularly if: intolerance or contraindication to ACE-i/ARB, she is a woman ofchild-
bearing potential, or there is ↑sympathetic drive.
Combination Rx:
a. ACE-i + Ca2+-channel antagonist or diuretic is logical, and has been commonly used in
trials.
b. There is little evidence on using 3 drugs but current recommendation is ACE-i, Ca2+-
channel antagonist, and thiazide.
c. If BP still uncontrolled on adequate doses of 3 drugs, add a 4th—consider:
spironolactone 25–50mg/24h or higher-dose thiazide, but monitor U&E.
d. Alternatively, B-blocker, or selective Alpha-blocker and gethelp.
30

31. 1. Step 1 treatment:
31
A. Patients < 55-years-old: ACE inhibitor (A)
B. Patients > 55-years-old or of Afro-Caribbean origin: CCBs (C)
1. Step 2 treatment: ACE inhibitor + calcium channel blocker (A + C)
2. Step 3 treatment:
Add a thiazide diuretic (D, i.e. A + C + D)
NICE now advocate using either chlorthalidone (12.5-25.0 mg once daily) or indapamide (1.5 mg
modified-release once daily or 2.5 mg once daily) in preference to a conventional thiazide diuretic
such as bendroflumethiazide.
NICE define a clinic BP >= 140/90 mmHg after step 3 treatment with optimal or best tolerated
doses as Resistant Hypertension. They suggest step 4 treatment or seeking expert advice.
1. Step 4 treatment:
a) Consider further diuretic treatment.
b) If potassium < 4.5 mmol/l add spironolactone 25mg OD.
c) If potassium > 4.5 mmol/l add higher-dose thiazide-like diuretic Rx.
d) If further diuretic therapy is not tolerated, or is contraindicated or ineffective,consider
an alpha- or beta-blocker.
e) If BP still not controlled seek specialistadvice.

33. Malignant hypertension
Severe hypertension (e.g. >200/130 mmHg).
Occurs in both essential and secondary types.
Fibrinoid necrosis of blood vessels, leading to retinal
haemorrhages, exudates, and proteinuria, haematuria due to
renal damage (benign nephrosclerosis).
Can lead to cerebral oedema → encephalopathy (Headache,
focal CNS signs, seizures, coma).
33

34. Features of Malignant hypertension :
34
Classically: severe headaches, nausea/vomiting, visual
disturbance
However chest pain and dyspnoea common presenting
symptoms
Papilledema
Severe: encephalopathy (e.g. seizures)

35. Management of Malignant hypertension :
35
Malignant hypertension:
A. In general, use oral therapy, unless there is encephalopathy or CCF.
B. Reduce diastolic but no lower than 100mmHg within 12-24 hrs.
C. Avoid sudden drops in BP as cerebral autoregulation is poor (↑stroke risk).
D. Bed rest; there is no ideal hypotensive, but atenolol or long-acting Ca2+ blockers
may be used PO.
If severe/encephalopathy:
a) Aim to reduce BP to ~110mmHg diastolic over 4h.
b) Admit to monitored area. Insert intra-arterial line for pressure monitoring.
c) Either IV labetalol (eg 50mg IV over 1min, repeated every 5min, max 200mg) or
sodium nitroprusside infusion (0.5mcg/kg/min IVI titrated up to 8mcg/kg/min, eg
50mg in 1L glucose 5%; expect to give 100–200mL/h for a few hours only, to avoid
cyanide risk).

36. Prevention
1. Lose extra pounds and watch your waistline
2. Exercise regularly
3. Eat a healthy diet
4. Reduce sodium in your diet
5. Limit the amount of alcohol you drink
6.stop Quit smoking
7.Cut back on caffeine
8. Reduce your stress
9. Monitor your blood pressure at home and see your doctor regularly
10.Controll your sugar

37. • A 71-year-old woman is reviewed in the clinic. Her blood pressureis 146/ 94 mmHg. This is
confirmed on a second reading. what is the most appropriate next-step?
a) Ask her to come back in 6 months for a blood pressure check
b) Arrange 3 blood pressure checks with the practice nurse over the
next 2 weeks with medical review following
Reassure her this is acceptable for her age
c) Arrange ambulatory blood pressure monitoring
d)
e) Start treatment with a calcium channel blocker

38. • What is the target blood pressure for a patient with type 2 diabetes
(assuming no co-morbidities) ?
a) Less than 120/75mmHg
b) Less than 130/80mmHg
c) Less than 140/80mmHg
d) Less than 150/90mmHg

39. • Taking at least 30 minutes of regular physical exercise is expected to
have what effect on systolic blood pressure ?
a) An increase of 4-7mmHg
b) No effect expected
c) A reduction of 1-2mmHg
d) A reduction of 4-9mmHg

40. The End
40