1. HTN & RENOVASCULAR HTN By : Dr WAQAR MBBS, MRCP ( London)
ASSISTANT PROFESSOR
MAAREFA MEDICAL COLLEGE

2. DEFINITION 1) HTN is defined as : * Systolic BP > 140mmHg on 2
* Diastolic BP > 90mmHg separate days
2) Normal BP : Systolic :<120, Diastolic <80
3) Pre HTN : b/w / b/w 80-90
(usually no Rx, just lifestyle changes)

3. Beware of “ White Coat Hypertension”( high BP in doctor’s office).
Sometimes, you may need 24 hrs continuous BP monitoring at home ( ambulatory BP monitoring) to diagnose HTN.

4. 24 hrs BP monitoring

5. EPIDEMIOLOGY * In K.S.A, more than ¼ of the adult population
has HTN ( saudi medical journal, 2007)
* In the U.S., 29% of the adults have HTN
* Incidence is rising throughout the world
( ? Due to lifestyle)

6. WHY IS HTN HARMFUL ?

8. STAGES OF HTN Stage 1 : 140 to 159 (systolic) 90 to 99 ( diastolic)
Stage 2 : 160 and above ( systolic)
100 and above ( diast)
Hypertensive Crisis
Urgency Emergency

9. Hypertensive Urgency:
* Very high BP. DBP usually >120, but NO acute
end organ damage (encephalopathy, angina,
papilloedema etc)
Hypertensive Emergency :
* Very high BP ( SBP > 210, and DBP> 130) +
end organ damage begins.

10. TYPES OF HTN PRIMARY SECONDARY ( no known cause) ( secondary to an
Also called essential underlying disease)
HTN
( most cases are prim.)

11. Primary HTN Also called Essential HTN. Etiology not known
Most cases are primary HTN( >90%)
Not due to any underlying disease, but the following may contribute to it :
genetics, obesity, high salt intake, alcohol,
smoking.

12. Secondary HTN Secondary to some other disease
Accounts for less than 10% of HTN cases
Renal causes: Most cases of sec. HTN are due to renal diseases
* Chronic renal failure ( due to any cause)
* Renal artery stenosis
* DM nephropathy
* Polycystic kidney disease

13. Contd.
2) Endocrine Causes : * Cushing’s disease, * Hyperaldosteronism, * Pheochromocytoma, * Acromegaly 3) Drugs & Meds. : * NSAIDs, * Steroids, * Estrogens, * Flu & cold meds ( will worsen HTN), * Cocaine 4) Coarctation of Aorta 5) Pre-eclampsia

14. 1) Young age ( less than 30 yrs) 2) HTN not responding to max. therapy
WHEN TO SUSPECT SEC. HTN?
1) Young age ( less than 30 yrs)
2) HTN not responding to max. therapy
3) Clinical features of the secondary causes
( acromegaly, Cushing’s etc)
4) HTN wth low K suspect Hyperaldosteronism

15. S/S of HTN Very non-specific Asymptomatic
Headache, dizziness, body pain
Sec. HTN: features of the underlying disease
Severe rise in BP can present as angina/MI, CHF, stroke/TIA, altered mental status (encephalopathy)

16. Physical Exam Look for features of secondary causes, like
abdominal bruit in Renal artery stenosis,
Cushingoid features, radiofemoral delay in
coarctation of aorta
Look for end organ damage : retinopathy, CHF, neuro deficits

17. HYPERTENSIVE RETINOPATHY
Divided into 4 grades , based on severity Grade 1: Retinal vessels become less clear Grade 2: A-V nipping Grade 3: Edema, hemorrhages, Copper wiring Grade 4: Optic disc edema, silver wiring

18. Routine investigations
CBC, urea, creatinine, electrolytes, lipid profile, ECG, blood sugar, urinalysis
If secondary HTN is suspected order further tests accordingly
ECG may show left ventricular hypertrophy
High creatinine suspect renal pathology
REMEMBER : HTN can cause renal disease OR renal disease can cause HTN !

19. TREATMENT Aim of BP : * < 140/90
* In DM and CRF, aim is < 130/80

20. Rx contd.
1) First, a trial of non pharmacologic steps for about 2 months ( depending on the BP) * low salt diet * wt. reduction * exercise * eat more fruits & vegetables * stop smoking 2) Add medicine if the above fails. 3) Start with 1 medicine and gradually go to the max. dose 4) Give at least 2-3 wks for a medicine to work fully. Then add another medicine if needed.

21. DRUGS FOR HTN Diuretics ACE inhibitors
ARBs (angiotensin receptor blockers)
Beta blockers
Ca. channel blockers
Others

22. WEAKNESS, HYPOKALEMIA, HYPERGLYCEMIA, HIGH CHOLESTEROL, HIGH URIC ACID
DRUG CLASS
EXAMPLES
COMMON SIDE
EFFECTS
AVOID IN
DIURETICS
THIAZIDES
WEAKNESS, HYPOKALEMIA, HYPERGLYCEMIA, HIGH CHOLESTEROL, HIGH URIC ACID
DM, GOUT, HIGH CHOLESTEROL
ACE INHIBITORS
CAPTOPRIL, ENALAPRIL, LISINOPRIL, RAMIPRIL
DRY COUGH, RASH, ANGIOEDEMA,HYPERKALEMIA, HIGH CREATININE
PREGNANCY, RENAL ARTERY STENOSIS
ARBs
(angiotensin receptor blockers)
VALSARTAN, CANDESARTAN etc
ALLERGIC REACTIONS
( DON’T CAUSE COUGH)
SAME
BETA BLOCKERS
PROPRANOLOL, BISOPROLOL, ATENOLOL, METOPROLOL
BRADYCARDIA, BRONCHOSPASM, WEAKNESS, IMPOTENCE, VASOSPASM
ASTHMA/COPD, PVD, DM, HEART BLOCK, ACUTE CHF
CALCIUM CHANNEL BLOCKERS
AMLODIPINE, VERAPAMIL, DILTIAZEM
CONSTIPATION , BRADYCARDIA & HEART BLOCK (VERAPAMIL), PEDAL EDEMA, HEADACHE,
CHF, HEART BLOCK & BRADYCARDIA
OTHERS
METHYLDOPA, ALPHA BLOCKERS, HYDRALAZINE, CLONIDINE
VARIOUS

23. GUIDELINES TO START RX Suggested by National Institute of Clinical
Excellence , U.K. ( NICE guidelines)
Age < 55 or white race : ACE or ARB
Age > 55, black race : Calcium channel
blocker or diuretic
Add drugs from other groups if needed

24. SPECIAL SITUATIONS HTN w/ DM : First choice ACE or ARB
HTN w/ IHD : First choice is beta blocker , ACEI
HTN w/ pregnancy: Methyldopa(aldomet), hydralazine, labetolol are safe.
ACEI AND ARBs ABSOLUTELY NO IN PREG.
4) Patient w/ high sympathetic activity (tachycardia, anxious looking, hyperthyroid),
beta blocker

25. MALIGNANT HTN
Malignant or Accelarated HTN is a very rapid rise in BP with severe HTN ( DBP> 120)
It causes fibrinoid necrosis and damage to the renal vessels.
Patients should be admitted and BP should be lowered gradually over few hours, to about Diastolic.
Oral medicines can be given
Some people prefer i.v. medicines(nitroprusside)

26. Malignant HTN (contd.)
Dont “reduce” the BP quickly. Do it over next hrs.
Don’t give sublingual medicines. It will cause sudden drop in BP can cause ischemia to the brain
If not treated timely, malignant HTN can cause permanent end organ damage.

27. RENAL CAUSES OF HTN Renal artery stenosis ( narrowing of renal artery)
Chronic renal parenchymal disease
( glomerulonephritis)

28. RENAL ARTERY STENOSIS

29. RENAL ARTERY STENOSIS
Definition Narrowing or complete stenosis of renal artery. It can affect one or both arteries. What Happens due to stenosis Stenosis of renal artery renal ischemia Release of renin, angiotensin & then aldosterone all these substances cause vasoconstriction & raise the BP

30. ETIOLOGY OF R.A.S. ATHEROSCLEROSIS:
* 85% of RAS cases. Most cases are old age
* Patient usually has atherosclerosis in other
vessels also ( C.A.D. & PVD)
2) FIBROMUSCULAR DYSPLASIA:
* Thickening of the renal artery wall
* 10% -15% of cases. ( females, young ppl)

31. WHEN TO SUSPECT Difficult to control BP
2) Occurrence of “ flash pulmonary edema”
w/out any cardiac disease
3) Abdominal bruit on auscultation
4) One kidney smaller than the other on u/s
( difference >1.5cm)

32. IMAGING FOR R.A.S. Doppler u/s : * Initial test * Non-invasive
2) MRA/CT: (magnetic resonance angiogram)
* More clear images * done if u/s doppler not
clear * MRA is non-invasive also
3) Angiogram:
* Gold standard, but invasive
* Not the first step test
* Done if noninvasive tests are inconclusive.

33. Angiogram showing renal art. stenosis

34. TREATMENT OF R.A.S.
1) Atherosclerotic RAS: * BP control w/ meds. * No ACEI & ARB * Other measures to lower cholesterol 2) Fibromuscular Dysplasia: * Dilation of the stenosis by angioplasty wth. or without stent Angioplasty not usually done in atherosclerotic RAS

35. LAST SLIDE IS VERY IMPORTANT

37. GOOD BYE
AND
ENJOY YOUR DAY