Flashcards in Hypertension Deck (106):
Where are beta 1 receptors located?
In the heart (responsible for pulse)
Where are beta 2 receptors located?
In the bronchioles and blood vessels (responsible for vasodilation)
What is the minimum MAP needed to perfuse the brain?
CO = SV x HR
What is stroke volume (SV)?
amount ejected with each ventricular beat
(influences pulse pressure)
What is ejection fraction (EF)?
Fraction of end diastolic volume (EDV) ejected with a ventricular beat
(related to contractility)
What are changes in the HR by an increase or decrease in firing of SA node?
What are changes in conduction velocity at the AV node and influences the PR interval on EKG?
dromotrophy (how fast)
What happens if there is a sudden decrease in preload?
baroreceptor reflex activation resulting in reflex tachycardia and angina
What is known as the force of the contraction?
What mineral concentration effects inotropy?
(increased calcium increases force of contraction)
What is responsible for minute to minute BP regulation?
The goal of HTN management is to protect which four organs?
Which Rx meds can worsen control of BP?
stimulants for ADHD
tricyclic antidepressants (TCA)
Hypertensive urgency vs emergency
both have bp >180/110
Urgency DOES NOT target organ damage and hospital admission can be considered
Emergency DOES target organ damage and admitted for management
*Chlorthalidone, chlorothiazide, hydrochlorothiazide, indapamide and metolazone - Class?
*Thiazide Diuretic - MOA
inhibits reabsorption of Na and water by blocking Na/Cl co-transporter on the luminal side of the tubule = decreased plasma volume --> decreased preload
*Can Thiazide Diuretics be used as mono therapy?
yes, in early HTN
Thiazide diuretics - side effects
hyperuricemia --> gout
*Amiloride (Midamore) and Triamterene (Dyrenium) - class?
potassium sparing diuretics
*Potassium sparing diuretics - MOA
decrease in membrane permeability to Na by inhibiting epithelial sodium transport at the late distal tubule = bloks the Na and keeps the K
Are potassium sparing diuretics used as mono therapy?
used with thiazide diuretic to off set hypokalemia potential
*Eplerenone (Inspra) and spironolactone (aldactone) - class?
*Aldosterone antagonists - MOA
competitively binds to mineralcorticoid receptor in the distal tubule to prevent the intracellular gene transcription necessary to up regulate the critical components for Na and water reabsorption.
Teaching - why avoid salt subs for many anti-hypertensives?
high in K
Good drug choice if Chem 7 shows high Na and low K...
Aldosterone antagonists - side effects
gynecomastia (spironolactone - 10%)
Eplerenone (Inspra) - DDI
CYP450 substrate - caution with inhibitors (if a DDI increases eplerenone, hyper k can worsen)
Aldosterone Antagonists - contraindications
CrCl <50 for HTN
concurrent CYP450 inhibitors
*ACE inhibitors - MOA
inhibits ACE -->reduces formation of ATII
after load and preload are reduced and acts mainly as a functional vasodilator
*Captopril (Capoten), Enalapril (Vasotec), Lisinopril (Zestril)…-Class?
*ACEI or ARB in pregnancy?
No - D
Why are Thiazide diuretics not effective with low CrCl?
the drug has to get to the renal tubule to work and if CrCl<30 it will not
*ACEI and ARB - DDI
NSAIDS with decrease effectiveness of ACEI because prostaglandin blocking will constrict tubules and Jg cells will compensate by increase renin, increase aldosterone and decrease effectiveness.
*ACE inhibitors vs ARB - side effects
hypotension, angioedema (emergency b/c airway could close), hyperkalemia
only ACE has dry, non-productive cough (b/c accumulation of bradykinin is irritating)
*Angiotensin Receptor Blockers (ARB) - MOA
inhibits the ability of ATII to bind to the AT subtype 1 receptor
--> vasoconstriction, vascular remodeling (important in HF)
Very specific (AT1 subtype)
Same MOA as ACE inhibitors except does not inhibit bradykinin
*Candesartan, Eprosartan, Irbesartan…-class?
Why do new cardiac drugs have a T:P>50?
Can ACEI and ARB be used as mono therapy?
Yes because do not cause "pseudo" tolerance as with other vasodilators
*Tekturna (Aliskiren) - class?
The only renin inhibitor
(no clinically relevant benefits over other classes so not 1st line)
*Renin inhibitor in Pregnancy?
No - D
*Acebutolol, Atenolol, Bisoprolol, Esmolol, Metoprolol, Nebivolol - class?
beta blocker - B1 selective
*Nadolol, Pindolol, Propranolol - class?
beta blocker non selective B1 and B2
*Beta blockers - MOA (brain)
decrease sympathetic NS outflow - protects sudden cardiac death
*Beta blockers - MOA (heart)
effect phase 4 depolarization
decrease O2 demand so improves ischemia
decreases force of contraction
*Beta blockers - MOA (vessels)
inhibits B2 receptors - vasoconstriction
inhibits alpha1 and alpha2 - vasodilation
*better at HR control than BP
*Beta blockers - MOA (kidneys)
inhibits B1 receptors --> reduces renin --> reduces Na
*Beta blockers - side effects
AV heart block (prolonged PR interval)
bronchospasm in hyperactive airway disease
decreased sexual function
Mask hypoglycemia b/c won't get tachy
*Beta blockers in pregnancy?
*Diltiazem and Verapamil - class?
act on heart and periphery
*Amlodipine, Nicardipine, Nifedipine, Nimodipine…-class?
Dihydropyridine (DHP) CCB
act on periphery
*CCB - MOA
inhibits Ca entry by blocking channels in the SA and AV nodes
-->decreased force of contraction
decreases O2 demand
*CCB for HF?
No! does not protect against sudden death because no remodeling
*CCB - 2 drugs with DDI because sub/inhib CYP3A4
Diltiazem and Verapamil
*CCB - side effects
AV heart block
*lower extremity edema*
CCB in WPW?
caution! can worsen condition because has accessory pathways around AV node and can cause increased pulse because bypasses
*Which 2 Mixed Beta Blockers require tedious titration?
Esmolol and Carvedilol
*Clonidine and Methyldopa - class?
Alpha 2 receptor agonist
*Preferred HTN treatment in pregnancy
*Alpha 2 receptor agonist - MOA?
work in CNS to decrease sympathetic outflow onto the heart, blood vessels and kidneys
Reduce preload and after load
*Alpha 2 receptor agonist - side effects
*rebound HTN and tachy if abruptly stopped
What is the most commonly prescribed Thiazide diuretic?
HCTZ - Pregnancy?
Yes - B
Why might Chlorthalidone be more effective than HCTZ?
greater lowering of BP
maybe less cardiac events
Digoxin - what needs to be monitored?
Levels b/c narrow TI
What 2 classes are known substrates of CYP2D6?
Beta Blockers (anti-hypertensive) and antiarrhythmics
Which 2 populations are at greatest risk for being a poor metabolizer of CYP2D6?
Blacks and Asians
How does amiodarone increase risk for hyperthyroidism?
contains a large amount of iodine. Get baseline TSH and repeated levels q 6-12 mos.
Licorice contains glycyrizzhic acid and can cause...
Garlic for HTN - dosing
Kwai (garlic powder) 600-900 mg/day
Beta blockers - inhibit sympathetic or parasympathetic NS?
BP goal for non-DM or chronic kidney disease (CKD)
BP goal if DM or CKD
Garlic for HTN - MOA
(some pts reduce BP by >20%)
Why can diabetics still sweat on beta blockers?
postganglionic sympathetic nerve fibers secrete Ach (most sympathetic responses are related to norepinephrine)
Which beta blocker do patients tend to feel worse before better?
Garlic - effect on blood vessels
dilates (lowers BP)
Which aldosterone antagonist has more DDI (CYP450)?
Treatment secondary hypertension r/t hyperaldosteronism and what labs would you see?
Lab: high na, low k
Why do thiazides diuretics potentially cause more hyponatremia?
Work on the last place for reabsorption - distal tubule
What does aldosterone do?
Changes the cell membrane so more Na can be reabsorbed.
What does angiotensin do?
Vasoconstricts and remodels
What enzyme facilitates conversion of angiotensin I to II?
Why are thiazide diuretics useful in osteoporosis?
Improves Ca reabsorption
Which diet is recommended for hypertension?
ACEI or ARB as mono therapy?
Yes, very good
Why are ACEI or ARB less effective as mono therapy in AAs?
Make less renin (combo therapy is not an issue)
How do ACEI and ARB confer "renal protective effects" in diabetics?
Decrease glomerular filtration pressures --> Block angio 2 vasoconstriction and decreases pressure.
Why does ARB not have cough as ADE if MOA is same as ACEi?
Same but does not inhibit bradykinin --> buildup causes cough in ACEI.
Are renin inhibitor used as first line?
No advantage over ACEI and ARB. Only one drug (aliskiren)
Same ADE, preg,etc.
Why is it beneficial to reduce remodeling of the myocardium?
Leads to angina
Disorganized myocardial fibers make contraction less effective
Which classes of anti hypertensives reduce remodeling?
Not DHP CCB (dilt and verapamil)
Preferred class for HF?
Are BB effective as BP lowering?
No, better at rate control b/c don't have the beta 2 vasodilation effect.
What happens when renin is released?
Release aldosterone --> Na/water reabsorption and increase plasma volume.
What are the only 3 BB FDA approved for HF?
Which non selective BB is hydrophilic (renal), long T 1/2 (qd dosing)?
Be careful in renal pts
Which non selective BB is lipophilic (liver), has more DDI, short t1/2?
Careful in cirrhosis and decreased hepatic function.
Can you crush metoprolol succinctness (toprol XL)?
No, but can break on scored line.
CCB - phase if action
BB phase of action
Which DHP CCB can be used as a tocolytic?
Clonus one, guanfacine, methyldopa - class?
Alpha 2 receptor agonist
Non stimulant options for ADHD (alpha 2 Receptor agonist)
Which alpha 2 receptor agonist can be used for opiate/benzo/ethos withdrawal?