8 - Drugs for Hypertension

Question 1

What is Hypertension?

Answer 1

• Hypertension: elevated systemic arterial blood pressure.
• Blood pressure is a measurement of the force against the walls of your arteries as the heart pumps blood through the body.
• Blood pressure is measured with a sphygmomanometer.

Question 2

What 6 Things are Required to accurately measure blood pressure:

Answer 2

1. The patient should be seated for at least 5 minutes.
2. No caffeine or nicotine within 30 minutes of measurement.
3. Feet should be touching the floor (not dangling).
4. Arm should be elevated to heart level.
5. Two measurements in each arm should be taken 5 minutes apart.
6. Before a diagnosis of hypertension, the patient should have this repeated 3 times at least 2 weeks apart.

Question 3

Blood Pressure

Answer 3

• Blood pressure is classified by looking at the systolic and diastolic blood pressure.
• Systole – When the heart contracts.
• Diastole – Period of time when the heart fills after a contraction

ex. systole/diastole

Question 4

Classification of Blood Pressure

Answer 4

Normal: <120 and < 80

Prehypertension: 120-139 OR 80-89

Stage 1 Hypertension 140-159 or 90-99

Stage 2 Hypertension: >160 or >100

Question 5

Primary Vs Secondary Hypertension

Answer 5

Primary Hypertension
- Hypertension of no known cause.
- Approx 92% of all cases of hptn
- 90% of people > 55 have high BP

Secondary Hypertension
- Hypertension with identifiable cause.
- Causes include:
○ 1. Kidney disease
○ 2. Hyperthyroidism
○ 3. Pregnancy
○ 4. Erythropoietin
○ 5. Pheochromocytoma – tumour on the adrenal gland that causes excess epinephrine release.
○ 6. Sleep apnea
○ 7. Contraceptive use

Question 6

Causes of Hyptertention

Answer 6

• Many factors influence BP:
  
  1. Amount of water and salt in the body
  2. The condition of the kidneys, nervous system and blood vessels
  3. The level of certain hormones in the body
• Risk factors for developing hypertension: obesity, stress, smoking, high salt diet, diabetes, African descent
• Meds that are known to cause hypertension: NSAIDs, oral contraceptives, and cold medicines that contain pseudoephedrine

Question 7

Consequences of Hypertension

Answer 7

• Chronic hypertension is associated with increased morbidity and mortality.
• If untreated, hypertension can cause myocardial infarction, kidney failure, stroke or retinal damage.
• Unfortunately, hypertension is a “silent killer” as many patients may have elevated blood pressure for years before they show any symptoms.
• Organ damage due to extreme hypertension
  ○ Brain - swells and has multiple areas of hemorrhage
  ○ Kidney - vasculature of kidney is constricted and urine output is reduced
  ○ Heart - dilated (enlarged) and in cardiac failure

Question 8

Why Lower BP?

Answer 8

• decreasing blood pressure decreases patient morbidity and mortality.
• Lowering blood pressure decreases the incidence of stroke, myocardial infarction and heart failure.
  → decreasing blood pressure by 5 mmHg can reduce the risk of stroke and heart attack by 20 – 35%.

Question 9

What determines Blood Pressure?

Answer 9

Cardiac Output
- Is determined by heart rate, heart contractility, blood volume and venous return.
- An increase in any of these results in an increase in blood pressure.
- Many drugs are deigned to decrease CO which decreases BP

Peripheral Resistance
- Is determined by arteriolar constriction.
- Constriction of the arteries and arterioles will cause blood pressure to rise.
- Drugs are targeted to decrease peripheral resistance

Blood Pressure = Cardiac Output x Peripheral Resistance

Question 10

What are the 3 Systems that Regulate Blood Pressure?

Answer 10

1. The sympathetic nervous system.
2. The renin-angiotensin-aldosterone system (RAAS)
3. Renal Regulation of Blood Pressure

Question 11

1. The Sympathetic Nervous System

Answer 11

• Helps us respond to stress, i.e. the fight-or flight response.
• Is also constantly active to help keep body functions (including blood pressure) in homeostasis.
• The sympathetic nervous system has a reflex circuit called the baroreceptor reflex that helps keep blood pressure at a set level.

Sympathetic Response
- Pupils dilate (far vision)
- Eyes water
- Mouth becomes dry
- Increased sweating
- HR increases
- Adrenaline Rush
- Quicker Breathing
- Bronchial airways dilate
- Digestive functions inhibited
- Stomach activity decreases
- Bladder relaxes

Question 12

Baroreceptor Reflex

Answer 12

• Baroreceptors on the aortic arch and carotid sinus (in the carotid arteries of the neck) sense blood pressure and relay the information back to the brainstem.
• If BP is perceived to be too low, the brainstem sends impulses along sympathetic neurons that stimulate the heart to cause increased cardiac output and smooth muscle on arteries causing vasoconstriction.
  ○ This increases BP.
• If BP is perceived to be too high, sympathetic activity is decreased. This causes decreased cardiac output and vasodilation.
• In patients with chronic hypertension, the body adapts to the higher BP, resetting the baroreceptors’ “set point” to this elevated level. As a result, the baroreceptors perceive this high BP as normal.
  • The baroreceptor reflex responds rapidly (seconds or minutes) to changes in blood pressure.

Question 13

2. Renin-Angiotensin Aldosterone Pathway

Answer 13

• RAAS is comprised of a series of protein hormones.
• RAAS regulates blood pressure, blood volume and electrolyte balance.
• Activation of the RAAS affects the kidney and vascular smooth muscle to control blood pressure.
• The RAAS is a target for many blood pressure lowering drugs.
• Unlike the baroreceptor reflex, activation of the RAAS may take hours or days to influence blood pressure

Question 14

Components of RAAS

Answer 14

1) Renin - enzyme that cleaves angiotensinogen I to angiotensin I

2) Angiotensin I - inactive protein; no direct effect on BP

3) Angiotensin Converting Enzyme - converts angiotensin I into angiotensin II

4) Angiotensin II - active protein and potent vasoconstrictor
- Stimulates the release o aldosterone and antidiuretic hormone

a. Aldosterone

b. Antidiuretic Hormone

Question 15

Purpose of Renin

Answer 15

• Catalyzes the formation of angiotensin I from angiotensinogen.
• The rate-limiting step in angiotensin II formation.
• Renin is synthesized and secreted by the juxtaglomerular cells of the kidney into the blood.
  → juxtaglomerular cells - cells around the glomerulus that are present to sense the amount of sodium and BP in and around the glomerulus
  → For these cells, an increase in renin release will occur of they sense:
  1. Decreased blood volume.
     
     2. Low blood pressure.
     3. Stimulation of beta 1 receptors
        on juxtaglomerular cells of kidney.

*Note: juxtaglomerular = beside the glomerulus

Question 16

Function of Angiotensin Converting Enzyme

Answer 16

• Angiotensin converting enzyme (ACE) converts the inactive angiotensin I into the active angiotensin II.
• Activated Angiotensin II is:
  → potent vasoconstrictor by binding to its receptor (the AT1 receptor on smooth muscle cells) to produce vasoconstriction.
  → Stimulates release of aldosterone from the adrenal cortex.
• Aldosterone acts on the kidneys to increase sodium retention, which can increase water retention (which increased blood volume = increases CO = increases BP)
• Angiotensin II also acts on the posterior pituitary gland to release antidiuretic hormone (ADH also called vasopressin).
  → ADH causes water retention by the kidney

Question 17

Summary of RAAS Pathway

Answer 17

• The RAAS system is present to help our bodies regulate blood pressure.
• When the RAAS system is activated it causes vasoconstriction and renal
  retention of sodium and water.
• Vasoconstriction increases blood pressure by increasing peripheral
  resistance.
• Increased retention of water and sodium cause an increase in blood
  volume, which in turn increases cardiac output.

Question 18

Renal Blood Pressure Regulation

Answer 18

• The kidney is a critical organ in terms of blood pressure regulation.
• If blood pressure decreases for a prolonged time period, the kidney retains water.
• This increased water retention leads to increased blood volume.
• Increased blood volume causes increased cardiac output and therefore increased blood pressure.

Question 19

Non-Drug Treatments for Hypertension

Answer 19

• Non-pharmacological interventions are the initial recommendation for
  patients with a diastolic blood pressure of 90 – 95 mmHg.
• non-pharmacological treatments increase the effectiveness of
  drug therapy in patients with higher blood pressure.
• Non-pharmacologic interventions include:
  1. Decreasing body weight.
  2. Restricting sodium intake.
  3. Physical exercise.
  4. Potassium supplementation.
  5. The DASH diet.
  6. Smoking cessation.
  7. Alcohol restriction.

Question 20

1) Decreasing Body Weight

Answer 20

• There is a direct relationship between obesity and hypertension.
• Obesity is thought to cause hypertension by two mechanism:
  
  1. Obese patients have increased insulin secretion, which causes tubular reabsorption of Na+ and therefore water reabsorption and a higher blood volume.
     → Wherever Na goes, water goes
  2. Obese patients also have increased activity of the sympathetic nervous system.
     → SNS activates the heart to increase contractility and activates vasoconstriction
• Weight loss lowers blood pressure in majority of obese patients.

Question 21

2) Restricting sodium intake

Answer 21

• Salt is necessary to our bodies, however when sodium chloride (salt) intake is too high, it has a negative effect on blood pressure.
• The kidney regulates the amount of salt in our body, eliminating excess salt in the urine.
• When salt levels are too high, it causes water to be reabsorbed from the kidney into the blood.
  → To compensate for high salt content of blood
• This causes increased extracellular (blood) volume and therefore increased blood pressure.
• Limiting salt intake to 5 g per day decreases systolic BP by approximately 12 mmHg and diastolic BP by 6 mmHg.

Question 22

3) Physical exercise

Answer 22

• Regular exercise decreases blood pressure by an average of 10 mmHg.
• Regular exercise decreases extracellular fluid volume and circulating levels of plasma catecholamines (like epinephrine) which activate the heart and cause vasoconstriction.
• The benefits of exercise are seen even if patients don’t restrict sodium or lose weight during the training period

Question 23

4) Potassium supplementation

Answer 23

• Just as total body sodium levels are positively correlated with blood pressure, total body potassium levels are inversely correlated with blood pressure.
• This means high total body potassium results in lower blood pressure.
• High potassium diets decrease blood pressure by increasing sodium excretion, decreasing renin release and causing vasodilation.
• Preferred sources of potassium are fresh fruits and vegetables.
• IMPORTANT Patients taking ACE inhibitors should not be on a high potassium diet.

Question 24

5) The DASH Diet

Answer 24

• dietary approaches to stop hypertension studies.
• These studies gave subjects 1 of 3 diets and evaluated blood pressure.
• The 3 diets included:
  
  1. Standard North American diet
  2. Standard North American diet plus extra fruit and vegetables.
  3. A diet rich in fruits, vegetables, low fat dairy, lean meats (poultry and fish), whole grains, nuts and legumes. The diet also excluded foods high in saturated fat, total fat and cholesterol.
• Most patients achieving lower blood pressure within 14 days without lowering salt intake.
• The best results were seen in patients with prehypertension.
• Patients with severe hypertension are encouraged to stick to this diet in combination with blood pressure lowering medications.

Question 25

6) Smoking cessation.

Answer 25

- Smoking acutely elevates blood pressure but has not been linked to be causal in the development of hypertension. - Despite this, patients with hypertension should be encouraged to quit. - Both smoking and hypertension are risk factors for the development of cardiovascular disease.

Question 26

7) Alcohol restriction.

Answer 26

- Excessive alcohol consumption increases blood pressure. - It can decrease response to antihypertensive medications. - Patients with hypertension or prehypertension should consume < 2 drinks per day and < 14 drinks per week for men and 9 drinks per week for women.

Question 27

Antihypertensive Medications

Answer 27

- Remember that blood pressure is a product of cardiac output and peripheral resistance. - Drugs that decrease blood pressure do so by decreasing cardiac output or peripheral resistance. - Cardiac output is determined by heart rate, heart contractility, blood volume and venous return. Therefore decreasing any of these will decrease cardiac output and therefore decrease blood pressure. - Peripheral resistance is determined by artery/arteriolar constriction. Therefore decreasing constriction (or increasing dilation) will decrease blood pressure

Question 28

Sites of Action for Antihypertensive Medications

Answer 28

- Remember that blood pressure is a product of cardiac output and peripheral resistance. - Drugs that decrease blood pressure do so by decreasing cardiac output or peripheral resistance. - Cardiac output is determined by heart rate, heart contractility, blood volume and venous return. Therefore decreasing any of these will decrease cardiac output and therefore decrease blood pressure. - Peripheral resistance is determined by artery/arteriolar constriction. Therefore decreasing constriction (or increasing dilation) will decrease blood pressure Vascular Smooth Muscle - Ca channel blockers - Thiazide diuretics RAAS - Beta blockers - Direct renin inhibitors - ACE inhibitors - ARB's (angiotensin receptor blockers) - Aldosterone receptors antagonist Brainstem - Centrally acting alpha 2 agonist Heart - Beta blockers - Ca channel blockers Kidney - Thiazide diuretics - Loop diuretics - Potassium spring diuretics

Question 29

Diuretics

Answer 29

- Diuretics are the mainstay therapy for hypertension. - There are 3 main classes of diuretics: 1. loop diuretics 2. thiazide diuretics 3. potassium sparing diuretics/aldosterone antagonists - Diuretics work by blocking sodium and chloride ion reabsorption from the nephron of the kidney. - By preventing reabsorption of Na+ and Cl- diuretics make an osmotic pressure within the tubule (“attracts the water”) that prevents the reabsorption of water. - The retention of water within the nephron promotes excretion of water and sodium/chloride ions. - Excretion of water decreases blood volume = decreases CO = decreases BP

Question 30

Diuretics - Site of Action

Answer 30

- It also shows the percentage of sodium reabsorbed at each site. - Diuretics produce more effective decreases in blood pressure at sites of high sodium reabsorption. - ex. loop diuretics produce the largest decrease in blood pressure since 20% of sodium is reabsorbed at its site of action 1) Loop diuretics - act on ascending limb of loop of Henle - 20% of Na is absorbed - Prevent the reabsorption of Na out of the nephron - Bc so much Na is reabsorbed, they are effective drugs at decreasing blood volume 2) Thiazide diuretics - act in the distal tubule - Only 10% of na is absorbed - Not as good as loop diuretics because not as much Na is reabsorbed 3) Potassium diuretics - Act in late distal tubule or in collecting duct - Prevent Na reabsorption - 1-5% of Na reabsorbed - not as effective as other diuretics in terms of their effect on lowering BP

Question 31

Loop Diuretics

Answer 31

- The most effective diuretics available. - They act by blocking sodium and chloride ion reabsorption in the thick ascending limb of the loop of henle. - Loop diuretics are usually reserved for situations that require rapid loss of fluid such as: 1. Edema 2. Severe hypertension that does not respond to milder diuretics. 3. In severe renal failure. - Remember, this fluid is then excreted out in the urine Adverse effects include: 1. *Hypokalemia – may cause fatal cardiac dysrhythmias 2. Hyponatremia 3. Dehydration 4. Hypotension *The transporter responsible for reabsorbing Na+ and Cl-, also transports K+ into the blood which is why hypokalemia occurs

Question 32

Thiazide Diuretics

Answer 32

- The most commonly used class of drug to treat hypertension. - They act by 2 main mechanisms: 1. Blocking sodium and chloride ion reabsorption in the distal tubule. 2. Decreasing vascular resistance (the mechanism of which is unknown). - Blocks reabsorption of Na, so water and Na are excreted into urine which decreased blood volume and BP - The maximum amount of diuresis (i.e. urine production) is much less than loop diuretics. (preferred drug to treat BP) - For many hypertensive patients thiazide diuretics alone are enough to control blood pressure. Adverse Effects include: 1. Hypokalemia – may cause fatal cardiac dysrhythmias 2. Dehydration 3. Hyponatremia

Question 33

Potassium Sparing diuretics/ Aldosterone Inhibitors

Answer 33

- Produce minimal lowering of blood pressure. - Act by inhibiting aldosterone receptors in the collecting duct. - Aldosterone normally causes sodium reuptake and potassium secretion. - Blocking aldosterone receptors causes increased sodium excretion and potassium retention (hence “potassium sparing”) in the body. - Normal action of aldosterone is to increase amount of Na and K pump Na out of lumen into blood and K into nephron where it can be excreted - Potassium diuretics block action of aldosterone → Causes K to stay outside (in the blood) and Na stays in the nephron and gets excreted into urine Not effective at lowering BP, but effective at retaining K - used in combination with thiazide and loop diuretics to counteract the hypokalemia side effect - should not be used with ACE inhibitors or renin inhibitors as these drugs also conserve potassium. - The primary adverse event associated with potassium sparing diuretics is hyperkalemia, which may result in fatal dysrhythmias.

Question 34

Beta Blockers

Answer 34

- Beta blockers are effective at treating hypertension by two distinct mechanisms: 1. Blocking cardiac beta 1 receptors → Binding of catecholamines (i.e. epinephrine, norepinephrine) to cardiac beta receptors causes increased cardiac output. (increases BP) → Blocking beta receptors decreases cardiac output and therefore decreases blood pressure. 2. Blocking beta 1 receptors on juxtaglomerular cells → Juxtaglomerular cells release renin which activates the RAAS pathway causing vasoconstriction. → Beta blockers decrease renin release therefore decreasing RAAS mediated vasoconstriction (peripheral resistance). - Beta blocker drugs all have the suffix “olol”. For example propanolol, metoprolol etc. **Remember, these are antagonists since they block receptors!

Question 35

Classes of Beta Blocker Drugs

Answer 35

- Beta blockers can be classified as either first generation or second generation. 1st generation beta blockers - These drugs produce non-selective blockade of beta receptors. - Inhibit both beta 1 (in the heart and juxtaglomerular cells) and beta 2 (in the lung) receptors. 2nd generation beta blockers - These drugs produce selective blockade of beta 1 receptors

Question 36

Adverse Effects of Beta Blockers

Answer 36

1) Selective beta 1 receptor blockers have the following adverse events: - Bradycardia (slow heart rate) - Decreased cardiac output o Heart failure (rare) - Rebound hypertension/cardiac excitation if withdrawn abruptly. - The dose of beta blockers should be tapered slowly over 10 – 14 days to prevent this. 2) Non-selective beta blockers have the same adverse events as selective beta blockers but also cause: - Bronchoconstriction due to blockade of beta 2 receptors in the lung. - Non-selective beta blockers should be avoided in patients with asthma or other pulmonary diseases. - Inhibition of hepatic and muscle glycogenolysis. → This can be dangerous in patients with diabetes if they accidentally take too much insulin.

Question 37

Angiotensin Converting Enzyme Inhibitor

Answer 37

- ACEI decrease blood pressure by 2 mechanisms: 1. Decreasing the production of angiotensin II → Angiotensin II is a potent vasoconstrictor so decreasing it causes vasodilation. → Decreased angiotensin II also decreases total blood volume, therefore ACEI reduce cardiac output and peripheral resistance. 2. Inhibiting the breakdown of bradykinin. → Elevated levels of bradykinin cause vasodilation - ACE breaks down bradykinin into inactive product - ACE inhibitors → Decreased angiotensin II = vasodilation and decreased blood volume → Increased bradykinin = vasodilation - ACEI all have the suffix “pril” ○ Ex. captopril, ramipril.

Question 38

Adverse Effects of ACE Inhibitors

Answer 38

- ACEI are generally well - Adverse effects can be linked to the reduction of angiotensin II or elevated bradykinin. 1. Side effects from decreased angiotensin II - 1st dose hypotension – first few doses should be low. - Hyperkalemia – decreased angiotensin II causes decreased aldosterone release. → Decreased aldosterone leads to potassium retention. → Potassium supplements and use of potassium sparing diuretics should be avoided. 2. Side effects from increased bradykinin - Persistent cough (in 5-10% of patients). - Angioedema (rare but potentially fatal). - Use with certain NSAIDs may decrease the effect of ACE inhibitors.

Question 39

Angiotensin Receptor Blockers (ARB's)

Answer 39

- ARBs have a similar action to ACEI in that they decrease the actions of angiotensin II, although the mechanism differs. - ARBs act by blocking the binding of angiotensin II to its receptor (the AT1 receptor). - Therefore ARB’s block the actions of angiotensin II but do not affect its synthesis. - ARBs cause vasodilation by blocking the action of angiotensin II on arterioles. - ARBs decrease aldosterone release from the adrenal cortex causing increased sodium and water excretion. - ARBs all have the suffix “sartan”. Ex. losartan, valsartan etc.

Question 40

Adverse Effects of Angiotensin Receptor Blockers

Answer 40

- ARBs don’t inhibit bradykinin breakdown as well as ACEI do, so they don’t produce persistent cough. - Incidence of angioedema is much lower than with ARBs than with ACEI. - ARBs still cause hyperkalemia due to the same mechanism as ACEI

Question 41

Direct Renin Inhibitors (DRI's)

Answer 41

- DRI’s bind to renin and block the conversion of angiotensinogen to angiotensin I. - Since conversion of angiotensinogen to angiotensin I is the rate-limiting step in the RAAS pathway, DRIs can influence the entire pathway. - Despite DRI’s decreasing plasma renin activity by 50-80%, its blood pressure lowering effect is the same as other classes of drugs (i.e. ACEI and ARBs).

Question 42

Adverse Effects of Renin Inhibitors

Answer 42

- Hyperkalemia – should not be used in combination with other drugs that may cause hyperkalemia (i.e. potassium sparing diuretics, ACEI) and potassium supplements. - Very low incidence of persistent cough and angioedema (much lower than ACEI). - Diarrhea

Question 43

Calcium Channel Blockers

Answer 43

- Calcium channels bring calcium from outside the cell to inside the cell. - In the heart and smooth muscle that surrounds arteries, calcium is essential for contraction. - the activity of calcium channels plays an important role for contraction of the heart and smooth muscle that surrounds the arteries and arterioles. - Calcium channel blockers block the entry of calcium into heart cells and smooth muscle cells, therefore decreasing contraction. - Calcium channel blockers are classified into 2 categories: 1. Dihydropyridine calcium channel blockers 2. Non-dihydropyridine calcium channel blockers

Question 44

1) Dihydropyridine Calcium Channel blockers

Answer 44

- Dihydropyridine calcium channel blockers significantly decrease calcium influx into smooth muscle of arteries. - This results in relaxation of the muscle around the arteries and causes vasodilation. - At therapeutic doses they do not act on the heart. → Effect of these drugs is exclusively on smooth muscle surrounding arteries - Suffix of drug names is always “dipine” Ex. nifedipine, felodipine etc.

Question 45

Adverse Effects of Dihydropyridine Ca Channel blockers

Answer 45

- Flushing - Dizziness - Headache - Peripheral edema - Reflex tachycardia - Rash

Question 46

2) Non-dihydropyridine Calcium Channel blockers

Answer 46

- These drugs block calcium channels in both the heart and smooth muscle of the arteries. - in addition to producing vasodilation of arteries, non-dihydropyridine calcium channel blockers also decrease cardiac output

Question 47

Adverse Effects of Non-dihydropyridine Calcium Channel blockers

Answer 47

- Constipation - Dizziness - Flushing - Headache - Edema - May compromise cardiac function. → Should be used with caution in patients with cardiac failure.

Question 48

Centrally Acting Alpha 2 Receptor Agonists

Answer 48

- These drugs bind to and activate alpha 2 receptors in the brainstem. - Activation of these receptors decreases sympathetic outflow to the heart and blood vessels. - Sympathetic activity normally causes increased cardiac output and vasoconstriction. - By inhibiting sympathetic outflow, centrally acting alpha 2 receptor agonists decrease cardiac output and peripheral resistance.

Question 49

Adverse Effects of Centrally Acting Alpha 2 Receptor Agonists

Answer 49

- Drowsiness - Dry mouth - Rebound hypertension if withdrawn abruptly.

Question 50

Treatment Algorithms

Answer 50

- Deciding how to treat patients with hypertension can be difficult. - The target blood pressure that most patients should achieve is less than 140/90 mmHg. - Patients with diabetes or chronic kidney disease should achieve a blood pressure less than 130/80 mmHg. - Keeping blood pressure below 130/80 mmHg in patients with chronic kidney disease slows the progression of kidney damage. → In patients with severe renal disease, thiazide diuretics are ineffective so loop diuretics should be used. - Treatment algorithms exist for patients with just hypertension and for patients with hypertension plus diabetes or kidney disease. These algorithms help guide dosing.

Question 51

Treatment Algorithms - Hypertension

Answer 51

Prehypertension - Lifestyle modifications - If not effective, use thiazide diuretic Stage 1 Hypertension - Lifestyle modifications - If not effective, use thiazide diuretic - If not effective, thiazide diuretic + another class of drug (ACEI, ARB, BB, CCB) Stage 2 Hypertension - Lifestyle modifications + thiazide diuretic + another class of drug (ACEI, ARB, BB, CCB)

Question 52

Treatment Algorithms - Diabetes and Renal Disease

Answer 52

Moderate Renal disease or diabetes - Lifestyle modifications + thiazide diuretic + another class of drug (ACEI, ARB, BB, CCB) Severe Renal Disease - Lifestyle modifications + Loop diuretic + ACE or ARB