Hypertension Medication Flashcards
ACEi
- ACE inhibitor
How it works ? ACE tends to be found in the luminal surface of capillary endotelial cells, predominantly in the lungs. THe inhibitor limits the conversion of AT1 to AT2. A reduction in AT2 results in vasodilation (so a decrease in afterload) , reduction in aldosterone release (more sodium and water excretion), reduced ADH (more water excretion) and reduced cell growth and proliferation.
Bradykinin is also a substrate for ACE. Using ACEi therefore potentiates bradykinin- causing vasodilation via NO and PGI2.
Example – lisinopril and ramipril
Side Effects – hypotension, dry cough, hyperkalaemia (low aldosterone could increase potassium using the pump), angioedema (caused by bradykinin and more common in black population) and renal failure (especially in renal artery stenosis where constriction of efferent arteriole needed)
Don’t give? Renal artery stenosis, AKD, pregnancy and breastfeeding (pressure effects and could cause damage to skeletal bone and skulls) and caution in CKD
Warning? High potassium drugs, NSAID’s and other antihypertensive agents
ARB’s
How it works ? ACE is not the only way that this conversion can happen, chymases can also be used to form angiotensin 2 making ARB’s important. Angiotensin 2 acts via Angiotensin 1 and Angiotensin 2 receptors. AT1 are important in relation to cardiovascular regulation. Binding at AT1 usually causes vasoconstriction, stimulation of aldosterone, cardiac and vascular muscle cell growth and ADH release. Directly targeting these receptors allows for a more effective inhibitor at the AngII mediated vasoconstriction. Unlike ACEi, it has no effect on bradykinin so less likely to have dry cough and angioedema and is less effective in low renin hypertensives.
Example – candesartan and losartan
Don’t give? Renal artery stenosis, AKD, pregnancy, breastfeeding and caution in CKD
Warning? High potassium drugs, NSAID’s and other antihypertensive agents
CCBs - dihydropyridine
CCB’S ARE THE PRIMARY CHOICE ANTIHYPERTENSIVE IN LOW RENIN PATIENTS The LTCC (VOCC) are usually expressed throughout the body including vascular smooth muscle cells and cardiac myocytes plus the SA and AV node and lead to CICR. The three classes of CCB’s interact with different sites on subunits of VOCC. THey each have a selectivity for vascular smooth muscle or myocardium
Dihydropyridine class
How it works ? Dihydropyridines are selective for the peripheral vasculature and have little chronotropic or inotropic effects (first line CCB for hypertension). They are used for subarachnoid haemorrhages as they have a selectivity for the cerebral vasculature
Example – Amlodipine (longer half life and is the most prescribed) , nifedipine and nimodopine (particularly selective for cerebral vasculature)
Side effects – ankle swelling, flushing and headaches (vasodilation) ,palpitations (compensatory tachycardia so are not useful in unstable angina)
Don’t give? Unstable angina, severe aortic stenosis
Warning? Don’t give with simvastatin (as it can increase effects of statins) or other antihypertensive agents.
CCB’s - phenylalkylamines
negative inotropy. THey are a class IV anti arrhythmic agent. They prolong the action potential and have an effective refractory period. It is used for arrhythmia and angina especially along with hypertension. Example – verapamil Don’t give? Poor LV function (cardiologist must be involved) , AV nodal conduction delay Warning? Beta blockers (work in a similar way to these CCB’s so don’t give together), other antihypertensive and antiarrhythmic agents
CCB’s benzothiazepines
How it works ? In the middle, effect on both peripheral and myocardium.
Example- diltiazem
Diuretics
How it works ? Thiazide and thiazide like diuretics are chemically different. These inhibit the NCCT channel in the DCT. RAAS must compensate for the reduction in sodium and water. The long term effects are mediated by sensitivity of vascular smooth muscle to vasoconstrictors.
Example - bendroflumethiazide and indapamide
Side effects – hypokalaemia, hyponatraemia, hyperuricemia and arrhythmia
Don’t give? - hypokalaemia, hyponatraemia
Warning? NSAID’s and potassium decreasing drugs
Aldosterone receptor antagonist
- Aldosterone Receptor Antagonist
How it works ? Reduce levels of aldosterone
Example – Spironolactone
Don’t give? Hyperkalaemia, Addison’s
Warning? Potassium increasing drugs inc ACEi and ARB
beta adrenoreceptor blockers
If the potassium levels are high, instead of ARA, use sympathetics:
How it works ? These decrease sympathetic tone and reduce myocardial contraction. THis will decrease cardiac output. It may also bind to B1 receptors and lead to a decrease in renin secretion
Example - labetalol, bisoprolol, metoprolol
Side effects – bronchospasm, heart block, Raynauds, lethargy, impotence, can mask tachycardia
Don’t give? Asthma, COPD, haemodynamic instability, hepatic failure (dose monitoring)
Warning? Non-dihydropyridine CCB as it could cause asystole when used together
Alpha adrenoreceptors
How it works ? Selective antagonism of alpha 1 adrenoreceptors. This will reduce peripheral vascular resistance. It is relatively safe to use in renal disease
Example – doxazosin , tamsulosin (BPH)
Side effects – postural hypotension, dizziness, syncope, headache and fatigue
Don’t give? - postural hypotension
Warning? - dihydropyridine CCB’s as they could cause oedema
Diabetics and race
Black African or African Caribbean and elderly patients tend to have a low renin level, so it is futile to target these systems. Therefore, initially, we don’t prescribe the drugs related to RAAS.
Type 2 diabetics – taking the medication will lead to a reduction in diabetic nephropathy, CKD and proteinuria. This is a two-pronged approach as there is dilation of efferent glomerular arteriole reducing proteinuria but also contributing to decrease blood pressure within the glomerulus. Therefore, ACEi/ARB’s are the first line for diabetes regardless of race or age.
In Step 4, if none of the medication has worked, consider
Nice guideline pathway
ARB’s, Ace
