LEC - 7.1 - ACEs & ARBs Flashcards
explain the RAAS System
Renin Angiotensin Aldosterone System
A system that kicks into place during hypotension
This involves the kidneys, liver, lungs, and heart
Hypotension activates prorenin which is converted to renin
Renin is turned into angiotensin in the liver
Angiotension becomes angiotensin I in the lungs
Angiotension I is introduced to angiotensin converting enzyme (ACE) to become angiotensin II
Angiotensin II - a powerful vasoconstrictor, to help address hypotension
Angiotensin II travels to the adrenal cortex and is converted to Aldosterone
Aldosterone - increases water reabsorption, meaning decreased urine output and increased blood pressure
A system that kicks into place during hypotension
Renin Angiotensin Aldosterone System
The RAAS involves which organs?
the kidneys, liver, lungs, and heart
___ activates prorenin which is converted to renin
Hypotension
Hypotension activates ___ which is converted to renin
prorenin
Renin is turned into ___ in the ___
angiotensin
liver
Angiotension becomes angiotensin I in the ___
lungs
Angiotension I is introduced to ___ to become angiotensin II
angiotensin converting enzyme (ACE)
this is a powerful vasoconstrictor, to help address hypotension
Angiotensin II
Angiotensin II travels to the ___ and is converted to ___
adrenal cortex
Aldosterone
this increases water reabsorption, meaning decreased urine output and increased blood pressure
Aldosterone
one of the body’s homeostatic mechanisms that helps to maintain blood pressure at nearly constant levels, it provides a rapid negative feedback loop in which an elevated blood pressure causes the heart rate to decrease
Baroreflex
130/90 BP = ?
Prehypertension
? BP = Prehypertension
130/90 BP
> 140/>90 BP = ?
Hypertension
? BP = Hypertension
> 140/>90 BP
Types of hypertension:
Essential
Secondary
Hypertension of unknown origin.
Essential Hypertension
Hypertension that results from other disease process
Secondary Hypertension
Environmental Factors that Cause Hypertension:
Stress
Increased sodium intake
Obesity
Smoking
This antihypertensive medication prevents ACE from converting angiotensin I to angiotensin II, a powerful vasoconstrictor and stimulator of aldosterone release. This action leads to a decrease in blood pressure and in aldosterone secretion, with a resultant slight increase in serum potassium and a loss of serum sodium and fluid.
ACE Inhibitor
Examples of ACE Inhibitors:
captopril (Capoten)
lisinopril (Zestril)
enalapril (Vasotec)
ramipril (Altace)
fosinopril (Monopril)
Pharmacokinetics:
Available only orally
70% - 75% is absorbed
Partly absorbed and partly excreted unchanged in urine
Food interferes with its absorption
Half life: 2 hours, but action stays for 6-12 hours
Captopril
Pharmacokinetics of Captopril:
Administration:
Absorption:
Excretion:
Teachings:
Half life:
Available only orally
70% - 75% is absorbed
Partly absorbed and partly excreted unchanged in urine
Food interferes with its absorption
2 hours, but action stays for 6-12 hours
Adverse Effects of Captopril
Cough – persistent brassy cough
Hyperkalemia in renal failure patients with K+ sparing diuretics, NSAID and beta blockers
Hypotension – sharp fall may occur with the 1st dose
Acute renal failure
Angioedema: swelling of lips, mouth, nose, etc.
Rashes, urticaria
Dysgeusia: loss or alteration of taste
term for the swelling of lips, mouth, nose, etc.
Angioedema
term for the loss or alteration of taste
Dysgeusia
Contraindications for Captopril
Pregnancy
bilateral renal artery stenosis
hypersensitivity and hyperkalemia
Advantages over captopril:
Longer half life and requires a 5-20 mg once daily dosage regimen
Absorption not affected by food
Rash and loss of taste are less frequent
Longer onset of action
Less side effects
Enalapril
Pharmacokinetics of Enalapril:
Administration:
Absorption:
Excretion:
Teachings:
Half life:
Longer onset of action
Absorption not affected by food
Rash and loss of taste are less frequent
Longer onset of action
Longer half life and requires a 5-20 mg once daily dosage regimen
No postural hypotension or electrolyte imbalance (no fatigue or weakness)
Safe in asthmatics and diabetics
Prevention of secondary hyperaldosteronism and K+ loss
Renal perfusion is well maintained
No hyperuraecemia or deleterious effect on plasma lipid profile
No rebound hypertension
Minimal worsening of quality of life – general wellbeing, sleep and work performance
1st line of Drug
Nursing Implementation for 1st line Drugs
Encourage patient to implement lifestyle changes
Monitor for hypotension
Let client rest in supine position beginning one hour after administration and for 3-4 hours after the first dose
Observe for hypersensitivity reaction, particularly angioedema
Monitor for neutropenia and signs of infection
Monitor for persistent dry cough or changes in cough pattern
Monitor for hyperkalemia
Monitor for liver and kidney function
These antihypertensive drugs selectively bind the angiotensin II receptors sites in vascular smooth muscle and in the adrenal gland to block vasoconstriction and the adrenal cortex release of aldosterone
These actions block the blood pressure – raising effects of the renin angiotensin system and lower blood pressure.
Angiotensin II Receptor Blockers (ARBs)
Examples of ARBs:
Candesartan ( Blopress)
Losartan ( Combizar)
Irbesartan (Aprovel)
Valsartan (Diovan)
Pharmacokinetics of ARBs:
Absorption not affected by food but unlike ACE Inhibitor its bioavailability is low
High first pass metabolism
Adverse effects of ARBs:
Foetopathic like ACE Inhibitors – not to be administered in pregnancy
Rare 1st dose effect of hypotension
Low dysgeusia and dry cough
Lower incidence of angioedema
Theoretical superiority of ARBs over ACEIs:
Cough is rare – no interference with bradykinin and other ACE substrates
Heart rate remains unchanged and CVS reflexes are not interfered
No significant effect in plasma lipid profile, insulin sensitivity and carbohydrate tolerance
Mild uricosuric effect