Anti-hypertensives Flashcards
What are the BP thresholds and goals for:
Always treat to which goal?
Or, for which conditions do you begin treatment at 130/80 and which for 140/90?
Always treat to goal of <130/80
What do you start with for stage 1 HTN?
When do you initiate a 2-drug regimen?
SPB 130-139 / 80-80
—thiazide diuretic
—CCB
—ACE/ARB
Use two drugs if stage 2 HTN (>140/>90) and BP 20/10 above target
What are the preferred first line agents for these populations/conditions? [must know]
—CAD incl stable angina, and previous MI —2
—HF —4
—CKD stage 3+ or stage 1-2 w/albuminurian —1
—DM — 3
—African Americans —2
—Afib — 1
DM / CKD — know they should be on an ACE or ARB
Dr Chu said pt having angina episode, you would prescribe CCB
Who would be treated with these drugs?
What are the follow up guidelines after prescribing an anti-HTN med?
—low risk no pharm — f.u 3-6mo
—stage 1 and 2 — f.u 1 mo
—BP measurement and lab values pertinent to meds
Familiarise yourself with this
What is BP?
BP = HR x SV x SVR
What are the 3RAAS inhibitors?
ACEIs — ends in? Give 3 examples
ARBs — ends in? Give 4 examples
Aldo antagonist?
Can’t use ACE/ARB together because work on the same pathway, but could use with? What type of anti-HTN med is this?
ACE inhibitors end in pril — without exception — BLR
—benazepril
—lisinopril
—ramipril
ARBs all end in sartan — VOLI
—valsartan
—olmesartan
—losartan
—irbesartan
Only use one or the other, not two together. Because they work on the same pathway.
Could use with an aldosterone antagonist spironolactone = K-sparing diuretic
Where do ACE inhibitors work in the RAAS system?
What about ARBs?
What about spironolactone?
Aliskiren?
What side effect could be associated with ACEI, why? [must know this]
ACEI
—inhibit conversion of angiotensin I to angiotensin II
ARBS
—inhibit effects of angiotensin II (vasoconstriction and aldosterone secretion)
Spironolactone
—works even further down to inhibit Na+ and H2O retention
Alikiren came to market but not used as much
What is this?
What is it attributed to?
What are the risk factors?
Onset?
Treatment?
ACEI-induced angioedema, increased risk in black patients
Bradykinen build up ➡️ peptide & histamine release 🟰 inflammation
It can occur at any time, even if a patient has been on a medication for years! Not necessary a new drug reaction.
Direct to ER ASAP, patient might need to be intubated.
Provider will be hesitant to use an ARB in the future, because they work in a similar way, just on a different part of the pathway.
Where do ACEIs and ARBs work?
What could we see on labs as a result of the MOA of these medications ?
What would you do if you prescribed these meds?
—angiotensin II normally constricts the efferent arteriole (EA) (leaving the glomerulus)
—ACEI/ARBs dilate the EA (which on the one hand is nephroprotective)
—and in doing so we often see a bump in SCr and K+
—so check SCr and K+
CALL them back to check their labs!!
What would you want to monitor in acutely ill patients if you prescribed ACEI or ARBs?
Serum creatinine
Potassium
Could see an increase if on ACEIs and ARBS
What is a side effect of NSAID use in terms of the kidney?
This leads to?
—NSAIDs and renal stenosis constrict afferent arteriole — going TO the glomerulus (restricted flow)
—ARBs/ACEIs dilate the EA — so increase flow away from the glomerulus
—additive effect is dangerous drop in GFR — leads to kidney injury
Can ARBs/ACEI be used in pregnancy?
Absolutely not!
What is the MOA of spironolactone/Eplerenone? Specific type in this category?
Where in the kidney does it act?
Diuretic effect
—work at the end of the nephron
—promotes excretion of NaCl and water from distal renal tubules
—normally aldosterone would retain Na and thus water.
—spironolactone is an aldosterone antagonist of this action so Na+ is excreted, water follows 👉 diuretic
—it is potassium sparing!!
What are the side effects of spironolactone?
Spir⭕️n⭕️lactone = two boobs.
Lactone = think milk from boobs!
👉gynecomastia
What are the diuretic medications?
T hiazide and thiazide-like 2
Loop 1
K+ sparing 1
Aldosterone antagonist 1
Where do thiazide diuretics act on the nephron?
What about the loop diuretics?
Loop diuretics — act on the loop
Thiazide — act on the distal tubule (later)
How do thiazides and loop diuretics generally work?
DCT — where you start reabsorbing Na+ and Cl- so thiazide diuretics act here and you lose Na+ and with that H2O follows
Loop diuretics — ascending loop of Henley — where ions are reabsorbed, loop diuretics blunt this and they are kicked out.
target sodium reabsorption — water follows
K-sparing diuretics
What do they do? (MOA)
Which examples - 4
Used in combo with
What could you get as a result?
What would you do if your patient experiences low K+?
—Potassium-sparing diuretics act to prevent sodium reabsorption in the collecting tubule by either binding ENaCs (amiloride, triamterene)
—OR by inhibiting aldosterone receptors (spironolactone, eplerenone).
—This prevents excessive excretion of K+ in urine and decreased retention of water, preventing hypokalemia.
—You lose some K+ as well when you lose Na and Cl so there are some drugs that will make sure you don’t lose potassium as well. K+ stays in the blood
—must make sure the patient doesn’t become HYPERkalemic
What are loop and thiazide diuretics associated with a risk of?
hyperuricemia and gout flares
Sulfa allergies
What are they mainly referring to?
What anti-HTN meds could you still likely prescribe even though they may have sulfa in them?
Know that sulfamide in ANTIBIOTICS specifically vs other sulfa containing drugs
It’s mainly referring to Bactrim but patients could still take meds like thiazide/loop diuretics etc
But you’ll see warnings when you’re trying to prescribe a sulfa-containing non abx medication
Exception might be SJS ;)
What do calcium channel blockers target? (Both groups)
Give 2 examples for each
DHP
—~dipine endings (DHP = DDDipine)
—they target SVR — they mainly vasodilate
—amlodipine & nifedipine
Non-DHP:
—mainly target HR and SV
—lower HR and stroke volume, so for example could cause bradycardia but the -dipine drugs wouldn’t
—verapamil & diltiazem
Where specifically do CCBs target? Both groups
Ca++ important in muscle contraction — when CCBs block this, the muscle tissue is affected
-dipines:
—targets vasculature SVR, blood vessels relax, BP goes down
—amlodipine & nifedipine
Non-DHP:
—affect the SA/AV nodes send electrical signals
— decreases chronograph, SV & HR
—i.e verapamil, diltiazem
What are the notable CCB side effects for DHPs
and non-DHPs? What would you not give with non-DHPs? Which condition would you also not give these meds for?
(Think about their MOA to determine this)
What do you need to keep in mind for Nifedipine?
What about for HF patients ?
Recommend compression and elevation
DHP
—works by decreasing systemic vascular resistance, dilating peripheral vasculature, therefore makes sense that you could end of w/peripheral edema
non-DHP
—acts on SV and HR
—so it makes sense that a possible ADR would be bradycardia and hypotension, the med is working TOO well
—avoid w/ BBs which also makes sense, this would be an additive effect of slowing the HR down too much
—which could exacerbate CHF
What are common combinations of anti-HTNs?
What are the pros/cons?
sp: maxzide
Make sure you know which classes they are in
What are examples of
Beta-blockers 4
A1-blockers 1
A2-agonists? 1
BB w/ A1? 1
Know the difference between the two metoprolols!
Succinate is extended release, given once a day
succinate sticks around
Tartrate: twice a day, acute care setting
Where do beta-blockers work?
Directly on the heart?
Explain the difference between B1 and B2 BBs?
B1
—🫀heart
—⬇️ contractility and HR
B2
—🫁 lungs
— bronchoconstriction
BBs starting with N-Z are B1 & B2: avoid in pts with respiratory conditions like asthma
—propanalol
—carvedilol
—labetalol
What are the side effects of BBs?
What guidance should you give all patients on BBs? What should they not do?
Propanalol — gets into the CNS so used for migraine prophylaxis, stage fright, anxiety
gradual tapering is required!
Do not abruptly D/C the medication
Alpha receptors — where are they found?
What do A1 receptors do normally? What do antagonists do?
Example?
A2 receptors normally do what?
A2 AGONISTS do what?
Example?
All over vasculature
A1
—normal activity of A1 receptor ➡️ vasoconstriction
—antagonist/block A1 ➡️ vasodilation
—~zosins ➡️ prAzos1n is an a1 blocker
A2
—receptors on the SNS, normal activity inhibits the release of norepi.
—so agonise the activity of A2 ➡️ less norepi, which means less SNS activity
—Clonidine is an A2 AGONIST
Not used a lot
What are nitrates? 3
What is the MOA? 2
Main indication? 2
What is the main contraindication??
NO responsible for promoting dilation of blood vessels.
Relaxation of smooth muscles
—isosorbide mononitrate (ISMN)
—isosorbide d’initiateur (ISDN)
Increases NO
Rarely used for HTN
Major side effects
do you use viagra?
Can have an additive effect — profound dilation
Good for angina
Nitrate side effects 3
—cerebral dilation — headache 🤕 😵💫 (Nitrate/noggin’)
—Know methemoglobinemia
—tachyphylaxis (when you continue using it, it’ll stop working =tolerance 😐)
Methomoglobinemia
—diminution of the oxygen-carrying capacity
—nitrate converted to nitrite in blood.
—nitrite reacts with blood to create methemoglobin.
—the more methemoglobin in the blood, the worse that blood is at carrying oxygen where it is needed
—produces chocolate coloured blood when exposed to air
—antidote: methylene blue
HTN in black patients
Preferred 1st agents 2
Thiazide diuretics
CCB
Limited use of RAAS (ACEIs and ARBS) and BBs
HTN urgency & emergency
What are the criteria
> 180/120
End organ damage: stroke, CHF, kidney failure etc.
Emergency = end organ damage, ADMIT to ICU
What are the 4 medications for HTN urgency? Route?
Which are safe in pregnancy
Which is good for ACES
Which work faster (how fast?)
Which work slightly slower (how slow?)
ORAL
Pregnancy: labetalol, nifedipine (really, only pregnancy and preeclampsia)
Asthma/COPD, no A&B blocker!
HTN EMERGENCY 🚑
What are the drug options? And for which diseases?
DHP CCBs
Nitrates
Vasodilators
BBs
diseases
—flash pulmonary edema 3
—(pre) eclampsia 5
—stroke, incl hemorragic 4
—acute renal disease 2
—aortic dissection 2
Patient on diltiazem for HR control d/t afib. Recent MI. Taken off diltizem and put on carvedilol and lisinopril.
Understand why
2017 guidelines for HTN
Diuretics
What is preferred ?
When are loop diuretics preferred?
What is preferred in patients with low K+?
What is preferred for primary aldosteronism and resistant HTN?
—chlorthalidone (HCTZ) (due to long half life and reduction of CVD risk)
—loop → HF and when GFR <30
—amiloride and triamterene + thiazides → pts with low K+ b/c these are K+ sparing HTN meds
—spironolactone or eplerenone (aldosterone antagonists) → primary aldosteronism & resistant HTN
primary aldosteronism — adrenals make too much aldosterone ➡️ too much H2O retention 🟰 ⤴️ BP
2017 guidelines for HTN
RAAS inhibitors
What do they increase the risk of?
What is a big contraindication?
What can an ARB also help with?
—do not use ACI/ ARBs or any other renin inhibitor in combination
—hyperkalemia in CKD and w/ supplementary K+ or K+ sparing drugs
—pregnancy
—prevention of recurrence of afib.
2017 guidelines HTN
beta blockers
These are not first line, except when?
Which agents are preferred in HTN w/ HFrEF
Which is preferred in HFrEF
—not first line except in CAD and HRrEF
—avoid abrupt cessation
—bisoprolol and metoprolol succincinate are preferred in HTN w/ HFrEF
—BB w/ both alpha and beta receptor activity such as carvedilol are preferred in HFrEF
What do alpha 1 blockers do?
Example?
Indicated for?
ADR?
—a1 blocker: prAzos1n ➡️ vasoconstriction
—indicated for men with symptoms of benign prostatic hyperplasia
—rarely used in cardiac conditions
—tend to cause orthostatic hypotension (low pressure when standing from sitting/laying)
