Anti-hypertensive Therapy (Th2 23/11) Flashcards Preview

Case 3: Hypertension > Anti-hypertensive Therapy (Th2 23/11) > Flashcards

Flashcards in Anti-hypertensive Therapy (Th2 23/11) Deck (23)
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1

You are seeing a 60-year-old man for the first time. He has untreated hypertension (168/106 mm Hg and blood pressure has been elevated on at least 3 occasions). There is currently no evidence of target organ dysfunction (heart, neurological, or eye grounds). From a therapeutic perspective, Select the best initial approach?

A. Initiate treatment with indapamide.

B. Consider initiating treatment with a 2-agent combination of drugs.

C. Delay pharmacologic intervention and treat with salt restriction.

D. Organize an Ambulatory Blood Pressure Monitor (ABPM) for a 24 hour period.

D. Organize an Ambulatory Blood Pressure Monitor (ABPM) for a 24 hour period.

From the information you have here we can’t really prescribe an appropriate regimen of drugs. We need to see if these measurements are valid and ensure the patient doesn’t have white-coat syndrome.

Therefore we must do an ABPM first

2

You evaluate a woman with chronic hypertension whose blood pressure remains above target despite a daily regimen of lisinopril, indapamide, and amlodipine.

Select what your next step should be:

A. Add an agent from another class, such as hydralazine or clonidine.

B. Characterize the patient as having resistant hypertension and initiate therapy with spironolactone (potassium levels permitting).

C. Add an ARB.

D. Switch from amlodipine to verapamil.

B. Characterize the patient as having resistant hypertension and initiate therapy with spironolactone (potassium levels permitting).

Resistant hypertension is defined as blood pressure not controlled on a complimentary 3-drug regimen with a diuretic as one of the agents. This patient is taking an ACE inhibitor, a calcium channel blocker and a diuretic and therefore has resistant hypertension. Spironolactone has become a “go-to” agent for treating resistant hypertension

3

You see a patient whose previous physician has retired. The patient is a 45- year- old man his blood pressure is not controlled on a regimen of nifedipine.

From a therapeutic perspective, Select the best initial approach?

A. Initiate treatment with indapamide in addition to the nifedipine.

B. Consider adding other medications hydralazine and atenolol.

C. Stop treating with nifedipine and try lisinopril instead

D. Add lisinopril to the treatment regimen.

D. Add lisinopril to the treatment regimen.

Adding an ACE inhibitor to the calcium channel blocker already in use should reduce the patients hypertension.

 

There was some speculation in the class amongst the tutors on reading the guidelines. They suggest that and ARB would be preferable over the ACE inhibitor. The answers in list here don’t include an ARB so this is not an option in this case.

 

We know the ACE inhibitor may have little effect in this particular patient because of his ethnicity. So it was suggested to skip the ACE inhibitor and jump straight to adding thiazide diuretic instead. This links nicely with your evidence based medicine session and the assessment of information available based on the evidence what do you think we should do?

 

On consultation with the clinical pharmacologist you would add the ACE inhibitor before the diuretic.

4

List the risk factors for hypertension?

  • Overweight: more weight, skeletal muscle has to work harder, metabolic deamd increases, increase SV/HR so CO increases, so HBP.
  • Stress with work: noradrenaline and adrenaline released, so vasoconstriction, mean arterial pressure increases, BP increases.
  • Diet: salt causes water retention.
  • No excercise: no seratonin.
  • Male
  • Age: arteries less elastic, more fatty deposits, atherosclorosis, lumen size decreases, high BP.

5

Why are people with high BP at higher risk of having kidney failure?  Explain your answer

 

 

  • When the force of blood flow is high, blood vessels stretch so blood flows more easily.
  • Eventually, this stretching scars and weakens blood vessels throughout the body, including those in the kidneys.
  • When the arteries become damaged, the nephrons do not receive the essential oxygen and nutrients — and the kidneys lose their ability to filter blood and regulate the fluid, hormones, acids and salts in the body. 
  • Also, damaged kidneys fail to regulate blood pressure.  The kidneys perceive the low perfusion/ renal blood flow due to atherosclorosis in arteries, and so they activate the renin- aldosterone sytem. They release prorenin- renin- angotensinogen- angiotensin 1- angiotensin 2 by ACE. Angiotensin 2 is a vasoconstrictor, and stimulates aldosterone release which causes sodium and water reabsorbtion while at the same time causing the excretion of potassium (to maintain electrolyte balance). This increases the volume of extracellular fluid in the body, which also increases blood pressure.
  • Also there is an increased risk of atherosclerosis causing occlusion of the renal artery: kidney tissue necrosis.

6

What is the rationale to reducing salt intake to control hypertension?  Explain your answer

Salt in the systemic circulation, hasn't been filtered yet, causes water to move from the interstitial space to the blood vessels, increasing BP.

7

Why would blocking the action of a vasoconstrictor lower blood pressure?

If vessels are wider then blood flows more easily, the heart doesn't have to pump as hard, and vessels aren't damaged.

8

What’s the mechanism of action of an ACE inhibitor?

ACE inhibitors prevent the conversion of angiotensin 1 to A2, so A2 can't cause vasoconstriction, and aldosterone release is not stimulated, so sodium and water isn't reabsorbed.

9

How do calcium channel blockers lower blood pressure? Explain your answer.

Calcium can't be used to cause muscle contraction, so CCB cause vasodilation, lower BP.

10

How do the heart cells contract- calcium induced calcium release?

 

  1. An action potential causes voltage gated sodium channals to open. Sodium enters the cell.
  2. Action potential travels down the t-tubule untill it reaches a L-type calcium channel called a dihydropyridine receptor..
  3. The dihydropyridine receptor is activated to allow calcium through to the sarcoplasm.
  4. The dhp-receptor is coupled with another called a ryanadine receptor which is activated by the calcium. This opens this receptor, and allows calcium stored in the sarcoplasmic reticulum to leave and go to the sarcoplasm.
  5. Calcium activates tropomyosin.

 

11

How does smooth muscle contract?

  • The membrane of smooth muscle has different types of calcium channels
  • An action potential causeds calcium to enter the cell.
  • It binds with calmodulin which then activates myosin light chain kinase
  • MLCK adds a phosphate to myosin and this activates it for contraction to happen.
  • Smooth muscle is different to skeletal muscle. In skeletal muscle the myosin is always active, but the binding sites on actin are covered by tropomyosin. In smooth muscle the myosin is always inactive, but the actin binding sites are always available.

12

Tell me some facts about hypertension?

  • Each 2 mmHg rise in systolic blood pressure is associated with a 7% increased risk of mortality from ischaemic heart disease and a 10% increased risk of mortality from stroke.
  • Diastolic pressure is more commonly elevated in people younger than 50.
  • With ageing, systolic hypertension becomes a more significant problem, as a result of progressive stiffening and loss of compliance of larger arteries.
  • At least one quarter of adults (and more than half of those older than 60) have high blood pressure.

13

How is hypertension diagnosed?

  • If the clinic blood pressure is 140/90 mmHg or higher, offer ambulatory blood pressure monitoring (ABPM) to confirm the diagnosis of hypertension.
  • Ensure that at least two measurements per hour are taken during the person's usual waking hours (for example, between 08:00 and 22:00).
  • Use the average value of at least 14 measurements taken during the person's usual waking hours to confirm a diagnosis of hypertension

14

What is stage one treatment for hypertension?

  • If under 55, ACE. If ACE not tolerated, eg due to dry cough, switch to low cost ARB
  • If over 55 or african-carribean, CCB. If a CCB is not suitable, for example because of oedema or intolerance, or if there is evidence of heart failure or a high risk of heart failure, offer a thiazide-like diuretic. 
  • Beta-blockers are not a preferred initial therapy for hypertention.

Stage 2 treatment: If blood pressure is not controlled by step 1 treatment, offer a CCB in combination with either an ACE inhibitor or an ARB

S3: If treatment with three drugs is required, the combination of ACE inhibitor or angiotensin II receptor blocker, calcium-channel blocker and thiazide-like diuretic should be used.

S4 if BP still is over 140/90 after doing the above. This is resistant hypertension. Consider adding a fourth antihypertensive drug and/or seeking expert advice.

15

How does anti-hypertensive medication work?.

There are two types of hypertension drugs. Those that interfere with the renin-angiotensin-aldosterone sytem, and those drugs that interfere with the sympatheic NS. There is one other class: nitrates induce venodilation.

Renin-angiotensin-aldosterone sytem drugs:

  • Angiotensin Converting Enzyme Inhibitors prevent the coversion of angiotensin 1 to angiotensin 2.
  • There are three classes of diuretics: pottasium sparing, loop and thiazide. They interfere with renal sodium absorption.
  • Angiotensin Receptor Blockers stop the action of angiotensin 2.
  • Aldosterone antagonists (bind to aldosterone receptors without activating them) so aldosterone would be the agonist (binds to receptor and activates it).
  • Direct renin inhibitors.

Sympatheic NS drugs:

  • Beta blockers: inhibit noradrenaline and adrenaline activity at beta-adrenergic receptors, normally responsible for increasing HR and myocardial contractility
  • Alpha blockers: inhibit noradrenaline and adrenaline activity on alpha adrenergic receptors, normally responsible for vasoconstriction.
  • Dihydropyridines: a type of calcium channel blocker that inhibits vasoconstriction
  • Non- dihydropyridines: a type of calcium channel blocker that reduce HR and contractility.
  • Centrally active alpha-2 agonists: clonidine and methyldopa, inhibit sympathetic NS in the brain stem.

16

How do you know if a drug is an Angiotensin Converting Enzyme Inhibitor, and what side effects do they have?

  • they end in -pril
  • E.G. lisinopril, benazepril, etc
  • Dry cough
  • Renal dysfunction

17

How do you know if a drug is an thiazide diuretic, and what side effects do they have?

  • There are three: hydrochlorothiazide, chlorthiazide and chlorthalidone.
  • S.E are hypokalemia (low potassium) hyponatremia (low sodium) renal dysfunction and increased insulin resiatance (makes type 2 diabetes worse).

18

How do you know if a drug is a loop diuretic, and what side effects do they have?

  • There are three: furosemide, bumetanide, torsemide.
  • Hypokalemia, hponatremia, renal dysfunction.

19

How do you know if a drug is a dihydropyridine, and what side effects do they have?

  • endi in -dipine
  • SE: constipation, lower extremity oedema

20

How do you know if a drug is a non-dihydropyridine, and what side effects do they have?

  • There are only two types: diltiazem and verapamil
  • SE: decreases cardiac contractility and bradycardia

21

How do you know if a drug is an ARB, and what side effects do they have?

  • endi in -sartan
  • can cause renal dysfunction

22

How do you know if a drug is a beta-blocker, and what side effects do they have?

  • end in -olol
  • SE: acutely cause lowered myocardial contractility, but increase it in the long run, depression, sexual dysfunction, fatigue and bradycardia.

23

How do you know if a drug is an apha blocker, and what side effects do they have?

  • endi in -osin
  • Cause orthostatic hypotension