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Pharmacology - cardiac - Antihypertensives (*RAAS inhibitors ACEIs and…
Pharmacology - cardiac - Antihypertensives
*RAAS inhibitors
ACEIs and ARBs
*ACE Inhibitors
end in "-pril"
Side effects
dry cough
--> due to build up of bradykynin
ACE normally breaks down Bradykinin
-->stoppping ACE stops breakdown of bradikinin
hypotension
--> common with ACEIs when first starting them to get hypotension --> need to start at a low dose and titrate up after this
ACE inhibitors Renal protective for CKD
especially for diabetics, ACEIs dilate the efferent arteriole of the kidney and lower the GFR pressure
--> prevents Glomerular damage
this is especially important for diabetics
ACE inhibitors Renal protective for CKD
Notes
:
note that
Clinical Case
Bradykinin Excess from ACIs
bradykinin is potent vasodilator
dry cough
angiodema
*Angiodemia
angio = blood vessels
--> swelling of the blood vessels
occurs in the lips, eyes and tongue
either mast cell degranulation
--> IgE type 1 reaction
--> IgE independent mast cell (drugs = oppioids)
ACEIs / bradykinin excess
Clinical Cases
Clinical Case
Notes
:
note that
Clinical Case
*Fetus Potter Sequence from Maternal ACEIs and ARBs
Angiotensin 2 is needed for proper renal development in the fetus
if mother using anti HTN that block Angiotensin 2 synthesis
--> get oligohydramnios
--> get Potter sequence
Starting ACEIs
watch for
Hypotension
--> so start low and titrate up titrate
in RAS patients
--> AKI is possible since you are removing the PDA ACE regulatory system that maintains the GFR
Hypotension S/E when starting ACEIs
need to start low dose and titrate up
--> start at 5 mg, then go up by 5s
ACEI and hypotension when starting case
Clinical Case
Notes
:
note that
PDA ACE Regulation of GFR
PDA = prostaglandins dilate afferent
ACE = Angiotensin 2 constricts the efferent
RAS starting on ACEIs
AKI is possible since you are removing the PDA ACE regulatory system that maintains the GFR
Clinical Cases
1 more item...
*ARBs
end in "-sartan"
-
"BARB, get behind me SATAN!"
--> ARBs = sartans
people who can't tolerate ACIs (especially for dry cough S/Es)
Side effects
unlike ACEIs, ARBs DO NOT have dry cough
--> they stop the RAAS one step after ACE
ACE normally breaks down Bradykinin
-->stoppping RAAS after ACE allows the normal breakdown of bradikinin
ARBs case
Clinical Case
Notes
:
note that
*BARB Sartan tx
--> for the RAAS system
B
= Beta blockers
A
= ACE Is
ARBs
= Angiotensin 2 blockers
*Beta Blockers
block the first step in the RAAS system for RAS BARB tx of HTN
JGC have beta1 receptors that when activated make the JGC release renin to kick off the RAAS system
*CCBs = Calcium Channel Blockers
dihydropyridines vs non-dihydropyridines
Why CCB's ONLY affect SM and Cardiac Muscle and NOT Skeletal Muscle?
since cardiac and SM rely on extracellular Ca++ to release their inner sarcoplasmic reticulum stores of Ca++
skeletal muscles are not reliant on outer Ca++
--> their DYP receptors are coupled directly to the RY receptors
SM and Cardiac Muscle
since cardiac and SM rely on extracellular Ca++ to release their inner sarcoplasmic reticulum stores of Ca++
think that cardiac cells need very tight control over their Ca++ and thus don't open RY receptors to the sarcoplasmic ret until there is ACTUAL Ca++ in the cell
Skeletal Muscle
skeletal muscles are not reliant on outer Ca++
--> their DYP receptors are coupled directly to the RY receptors
thus as soon as membrane is depoled by an AP
--> the DYP receptor opens the RY receptor and lets out inner Ca ++ stores
VERY salty DILL pickle Pirates
Ventricles = Verapamil > Diltiazem >> dihydros
verapamil
= works mostly at the LV
Diltiazam
= LV and periphery equally
dihydros
= no effect on the heart at all
Clinical Cases
Clinical Case
Notes
:
note that
Clinical Case
CCBs and HTN and Side effects case
Clinical Case
Notes
:
note that
think of pyrates for CCB dihydropyridines...
DAMN KNIFE NICKED my FELLOW PIRATE
DAMN
= amlodipine
KNIFE
= nifedipine
NICKED
= ncardipine
FELLOW
= felodipine
PYRATE
= dihydropyridines
Side effects
thiazide diuretics
--> gout and hyperuricemia (Dr. Obrien said more common than alcohol for gout)
--> always rule this out when there is gout with someone who has multiple heart problems and Hx
Ace Inhibitors
--> dry cough
--> angiodemia and hyperkalemia (need spironalactone)
CCBs
--> systemic vasodilation = peripheral edema
beta blockers
--> bronchospasm
--> bradycardia (beta blocker toxicity --> cardiogenic shock type)
--> sexual dysfunction
*Diuretics
1st line = thiazide diuretics
2nd line = potent loop diuretics
add ons = K+ sparing diuretics
--> check this?
Thiazide Diuretics
Hydrochlorothiazide, chlorthalidone
inhibit NaCl at the DCT
after the loop de loop get some cotton candy....
-->
thiazides give hyper GLUC side effects
after the loop de loop get some cotton candy....
hyper GLUC side effects
G = hyperglycemia
L = hyperlipidemia
U = hyperuremia
C = hypercalcemia
Clinical Cases
Clinical Case
Notes
:
note that
Clinical Case
K+ sparing Diuretics
K+ STAys.
spironalactone eplerenone, triamterene, amiloride
spironalactONE inhibit aldosterONE at the CD
K+ STAys.
Loop Diuretics
OHH DAANG, nice LOOP earings...
Loop earing hurt your
EARS
...
ottotoxicity
gout
, alkylosis, nephritis
FURIOUS BUM on the loop de loop...
furosemide, bumetinide, torsemide
Diuretics for other uses
Acetazolamide
= ACID causing diuretic
--> used for glaucoma and alkaline urine
Mannitol
= powerful MAN used for raised ICP, intracranial pressures causing diuretic
--> able to cross the blood BB
Acetazolamide
ACID causing diuretic
--> used for glaucoma and alkaline urine
Mannitol
powerful MAN used for raised ICP, intracranial pressures causing diuretic
--> able to cross the blood BB
