John, a smoker, had controlled HT for five years, and it has recently been uncontrolled ( 155/95 mmHg ) when you checked his blood pressure twice in the clinic with a two-week gap. He is on ramipril 5mg once daily. He is taking his medications regularly.
1.what are the possible causes ( list 5 )
1. stress at work
2. possible weight gain  
3. lack of exercise
4. Diet change with increased salt
5. wrong Blood Pressure reading due to wrong cuff size
6. Smoking
7. Undiagnosed secondary cause developing Eg – developing CKD
So in a case of BP becoming uncontrolled in a previously controlled patient – think of
1. stress –
2. weight gain ( can lead to OSA )
3. S – Heavy smoking
4. N – poor nutrition – with high salt
5. A – increased alcohol intake
6. P – lack of physical activity
7. Lack of compliance  
2. What would be your next step in management ( single answer )
1. organize home blood pressure monitoring
3. You do his blood tests, and the following results are available –
HBA1C 5.5%
His eGFR is 40  per 1.73 sq M  – which has been stable for the past four years.
urine ACR is 3.7 mg/mol ( Male < 2 )
T.C – 4 mmol/l  
LDL – 2
HDL – 1
What are the Medication changes you would do now? ( write 2 )
1. start amlodipine 5 mg daily oral
2. start rosuvastatin 5mg daily oral
Increasing ACEI to the maximum tolerable is also indicated here. The idea is to look at the 3rd question and think of the 2nd questions answer. You would have questions like this at the exam. Some would tend to write add amlodipine as an answer to the 2nd question. However, when you go to the 3rd question, you would realize that’s not what they were expecting. Some read the full questions- but I did not do so, because such questions are very rear – max 1-2/26.
Treatment targets – 
  • CKD, CVD risk high- and normal pop – 140/90 or less if tolerable 
  • secondary prevention of coronary heart disease – 130/80  – < 120 if possible 
  • DM – regardless of Proteinurea – the target is 130/80 
1) ACEI / ARBS  
Clinical use –
1) HT
2) HT and metabolic syndrome or  HT and DM
3) LVH
4) CKD – to prevent insufficiency
5) Diabetic nephropathy and non-Diabetic nephropathy
6) proteinuric kidney disease
7) endothelial dysfunction
8) Post MI (especially after LV failure)
9) Heart failure
10) in people with high risk of IHD
ACEI does not cause hypotension in healthy people. It reduces blood pressure in patients where the Renin-Angiotensin – aldosterone ( R-A-A ) system is highly active.
It causes profound fist dose hypotension in patients with HF, especially in those with frusemide, as they have a highly active RAA system.
(As long as the K is less than 5.5, this is the first line in <55 patients who are not blacks )
ARBS/ACE should be started at low dose and increased gradually every two weeks, after checking K+, kidney functions (S.Cr) and anemia/HB
if the S.Cr is raised over > 25% of base, or if K above 6, – stop ACEI/ARBS
if the S.Cr rise is less than <25%, continue the same dose and repeat the renal functions in 2 weeks
In Heart Failuer  patients’, – start frusemide and ACEI together
If the patient is already on frusemide –  the frusemide should be stopped the previous day ( for 24 hours), and ACE started as a night dose – with 1/2 the minimum dose ( low dose)
Then try to reach the maximum tolerable dose increasing it every two weeks.
Check cardiovascular states –
in B/L Renal artery stenosis
Taste disturbance is transient
Cough – will happen with ACEI – transient in most – 15% will have it in the long term – change them to ARBS
Hypotension – fist dose
Pemphigus vulgaris
ACEI is renal excreted
ARBS are metabolized in the liver
NSAID acts against ACEI/ARBS action –
2) Calcium Chanel blockers – CCB – 
2 types – dihydropyridinic and nondihydropyridinic
Dihydropyridinic –
eg – nifedipine and amlodipine
   acts on peripheral vascular smooth muscles only
   ADR –
*        flushing, headaches
*        gum hypertrophy
*        nocturia
  this can be used with Beta-blockers ( unlike nondihydropyridine)
  recommended to be used in HT + Asthma
          also for DM and HT  
nondihydropyridinic –
nondihydropyridinic –
eg – verapamil and diltiazam
       verapamil – action heart mainly –
                blocks AV nod – reduce the rate of contraction
                acts on muscle – mitigate the force of contraction
             Hence,  Contraindicated (CI)  – in Heart failure and CI in Heart blocks
             thus should do an ECG before starting
*       Constipation –
*       heart block
Diltiazem – acts on both smooth muscles in the periphery and heart equally.
                   hence CI for verapamil applied for this too 
3) Thiazide Diuretics – 
acts on Na+/K+ co-transporter
Indications –
HT – mainly in elderly ( no prostate enlargement / urinary symptoms ) – with Kidney functions of eGFR > 50, or S.Cr below 150 – ( if not this won’t work ) 
If renal functions very low – loop diuretics are needed instead to reduce blood pressure –  
( eg – if the eGFR goes below 30, stop thiazides and do loop diuretics ) 
Four weeks after starting the medication ( thiazide diuretic ) – check for Ca, Mg , Na and K
thiazide diuretics reduce all these electrolytes  – so when starting thiazides, ask the patient to eat foods with all these elements – eg – lentils, fiber  nuts 
if K+ becomes low – add amiloride 
          or can change to ACEI – 
ADR – 
  • DM + hypelipidaemia ( indepamide does not cause this) 
  • Gout 
  • Impotence 
  • Carmps  + muscle weekness
  • Liver failure in cirrhosis +
  • pancreatitis 
  • might aggravate BPH symptoms 
4) LOOP Diuretics – 
Acts on Na+/K+ ATPase 
causes profound diuresis and vasodilatation 
used in 
1) Acute Heart Failure
2) CKD – in renal failure 
3) Cirrhosis 
4) Nephrotic Syndrome 
ADR – 
  • Deafness – ototoxicity 
  • reduces Na, K, Ca, Mg and H 
  • causes metabolic alkalosis 
  • Gout 
5) Spironolactone – ( also called Aldosterone Antagonist or  K+ spearing diuretic )
indications –
2nd line for HT  – as add on therapy
Conns syndrome
Heart failure
A rapid normalization or reduction of BP in response to spironolactone therapy may indicate underlying primary hyperaldosteronism.
This converts testosterone to estrogen
testicular atrophy and gynecomastia in males
in females – menstruation abnormality
increases H and K  (consequently causes gastric ulcers )
6) Amiloride –  is also a K spearing Diuretic 
increases K+ and H+ – just like spironolactone 
reduces uric acid – 
7) Alpha Blockers –
Alpha blockers are not recommended for first-line therapy of elevated BP because they may increase the rate of cardiovascular events (especially heart failure) compared to other BP-lowering drugs.
They may be useful in men with both elevated blood pressure and benign prostatic hypertrophy, as they improve urine stream in benign prostatic hypertrophy.
May cause postural hypotension – especially the first dose. warn about this to patients
Content Under Copyright. Unable To Copy