HTN 2 Drugs 1 Flashcards
Blood pressure is determined by the product of
BP = CO x PVR
CO=cardiac output which is equal to
SV X HR
The Primary physiologic factors that determine blood pressure are
Renin-angiotensin-aldosterone system Sympathetic nervous system Plasma volume (largely mediated by kidneys)
CO will Increase
Increase venous constriction:
Sympathetic nervous system overactivity
Excess stimulation of Renin-angiotensin aldosterone system
Increase in cardiac preload include
Increased Fluid volume from excess Na
PVR increase by these factors
Increasing vascular constriction and hypertrophy
Excess stimulation of RAAS
SNS overactivity
Endothelial dysfunction due to decreases Nitric Oxide and increases endothelial
Most pts with essential HTN have a normal CO but increased
peripheral resistance
Peripheral resistance is determined by small arterioles
responsible for blood flow distribution to organs
Arteriole walls contain layers of
endothelial cells
Vasodilator
Nitrico oxide
Vasoconstrictor are
ENDOTHELIUM and ANGIOTENSIN 2
When there is damage in endothelial
blood starts to aggregate in the damage part and become plaque
Angiotensin 2 positive and negative effects
The postive effects if angiotensin 2 are it plays the major part homeostasis, decrease thrombosis, decrease platelet aggregation but when endothilial is damage it does the oppsite cause thrombosis, platelet agregation and plaque.
Excess stimulation of Renin angiotensin-aldosterone
system (RAAS) can lead to:
Increased sympathetic activity
Increased PVR (arteriolar vasoconstriction)
Water / salt retention
Lead to elevated BP
Inhibiting RAAS leads to
lowering BP
ACE INHIBITOR MOA
block conversion of angiotensin 1 to angiotensin 2
The ace inhibitor also inhibits and break down
BRADYKININ
which means the bredykinin level increase
The inhibition of Bradykinin by ACE-1 leads to
Cough, hperkalemia and Angioedema
ACE inhibitor meds are
Lisinopril (Prinivil, Zestril) 10 – 40MG Daily
Enalapril (Vasotec) 5 – 40MG 1-2 times daily
The ACE inhibitor is also considered
First-line therapy in HTN guidelines (without compelling indication)
When someone already has a heart attack and they are established. what ACE will do
improves their chance of second heart attack and reduces hospitalization.
Compelling use of an ACE inhibitor
Post-MI & HFrEF
renal protection for patients with protein-related DM DKD or CKD
Elevated UACR (> 30mg/g)
eGFR < 60
It helps patients with post-MIT, hfref AND protects kidney
When they already have it then we use it but we cannot use to prevent it from happening.
When not to use ACE
HTN: less efficacy as monotherapy in Black patients, consider combo therapy when used (need adequate dose!)
Contraindicated in pregnancy Especially in the 2nd and 3rd trimester
Pt with Bilateral Renal Artery Stenosis
ARB Angiotensin Receptor Blocker MOA
Block the activity of Angiotensin 2 at the Type 1 receptor
Stimulation of AT1 ________ Inhibiton of At1 _________
Vasoconstriction, Vasodilation
ARB does not cause what side effect
Bradykinin
ARB meds are
Irbesartan (Avapro) 150 – 300 Daily
Lorsartan (Cozaar) 50 – 100 1-2 times daily
Valsartan (Diovan) 80 – 320 Daily
Special compelling for ARB are
Compelling use in Post-MI & HF •Compelling use in renal protection for patients with protein-related DM DKD or CKD •Elevated UACR •eGFR < 60
ARB has ONE extra advantage and why
•Consider losartan in pts with PMH of gout due to increased urinary uric acid excretion
ACEI / ARB Adverse Drug Events (ADE)
Slight rise in SCr at initiation (<30% rise from
baseline acceptable)
• Hyperkalemia have Increased risk in pt with CKD
Dry Cough* (Can be DELAYED) –> Asian Americans have a higher incidence of ACE inhibitor–induced cough.
Angioedema* (Rare: <1%)
Contraindicated: of ACEI / ARB are
Pregnancy Category D & Bilateral Renal
Artery Stenosis
cough and angioedema are less common with _____ but have a chance of happening
ARBs
Lisinopril-induced cough will not be effected by cough suppressant the solution is
Change to ARB.
Lisinopril-induced angioedema can be cure by
changing to ARB means wait 6 week wash out period.
than change to ARB
ACE/ARB Drug Interactions are
Effect k+ so not use with K+ sparing dieuretics or supplements
ACE/ARB monitoring include
B.P. SCr, BUN, K+, angioedema and cough
Asses blood test for electorlytes and renal function 2 to 4 weeks after initiating therapy
Direct Renin Inhibitor MOA
Block RAAS at its initial point of activation and prevent formation of ATI AND ATII
Direct Renin drug (cousin of ARB/ACE) name is
Aliskirn
One imporant thing about Direct Renin Inhibitor is
Do not use with ARB/ACE as it will increase K+ level
ALDOSTERONE Antagonist MOA
Inhibit aldosterone receptor in distal tubule, and increasing NaCl & H20 excretion while conserving K+.
Block effect of aldosterone on arteriolar smooth muscle
(Work on fluid balance and smooth muscle)
Aldosterone Antagonists are
Spironolactone (Aldactone) 25 – 100mg/day 1-2times/day
Aldosterone antagonist should be avoided in
someone has elevated K+
or less kidney fuction
Alodosterone antagonist is effective in
Heart failure with reduce ejection fraction
Primary aldostronsim ( elevated eldostrone)
Resistant HTN
Spironolactone adverse effect are
Hyperkalemia Hyponaterima Gynecomastia ( main issue in males) impotence Hpotension
Excess stimulation of Renin-angiotensinaldosterone system (RAAS) can lead to
Increased sympathetic activity
Increased PVR (arteriolar vasoconstriction)
Water / salt retention
Lead to elevated BP
Inhibiting RAAS lead s to
Leads to lowering BP
Adverse effects specific to Aldosteron antagonist are
Hyponaterima
Gynecomastia ( main issue in males)
