Anti-hypertensive drugs Flashcards

1
Q

What is the recommendations for HTN targets for people over the age of 60?

A

Initiate pharmacological treatment to lower SBP under 150 and DBP under 90. Goal to have both within the 150/90 range

Grade A recommendation

All ranges are greater or equal to to treat

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2
Q

What is the HTN target for treatment in people under the age of 60?

A

In people under 60 initiate treatment to lower DBP that is above 90mmHg to lower to less than 90mmHg

Strong recommendation A for 30-59, E for 18-29

Lower SBP in those under 60 to under 140mmHg. This is expert opinion- Grade E recommendation

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3
Q

What is the target range for when to initiate treatment in CKD and diabetes?

A

CKD and DM in people over 18, initiate treatment to lower SBP greater than 140 or DBP greater than 90 get both within 140/90.

Grade E= expert opinion

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4
Q

What did the sprint trial show?

A

It showed that intensive HTN control (SBP lower than 120) led to less CVD events mortality and adverse events than normal control (SBP lower than 140)

It did lead to some syncope, hypotension, and acute kidney injury but NNT 61 and 90

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5
Q

What is the MOA of thiazide diruretics?

A

poison a pump in the distal convoluted tubule that reabsorbs sodium chloride= net loss of sodium and potassium

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6
Q

What are the thiazide diruretics and the thiazide like diuretics? What did the ALLHAT trial say about effectiveness?

A

Thiazides
Chlorothiazide
Hydrochrolothiazide

Thiazide-like
Metolazone- very potent
Chlorthalidone- ALLHAT showed better outcomes with chlorthalidone than amlopidine or lisinopril, first line tx. If can’t tolerate move to ACEi, CCB, BB
Indapamide

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7
Q

What are indications for thiazide diuretics?

A

poison a pump in the distal convoluted tubule that reabsorbs sodium chloride= net loss of sodium and potassium

net reabsorption of calcium= useful in hypocalcemia, recurrent urinary stones(decrease Ca2+ in urine), and nephrogenic Diabetes insipidus

First line choice in patients for HTN bc cheap and used for long time

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8
Q

What are side effects/ contradictions to thiazide diuretics?

A

cause a metabolic alkalosis

HYPOKALEMIA
HYPOMAGNESEMIA
HYPERURICEMIA
HYPERCALCEMIA

Sunlight sensitivity, dizziness, lightheadedness, weakness

Use with caution in gout- increase in uric acid

Use a different class in renal failure, sulfur allergy, or pregnancy

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9
Q

What is the MOA of CCB?

A

CCB all bind intracellularly on the the alpha-1 subunit of the transmembrane voltage-gated L-type calcium channel, but the two groups bind at different sites. Binding of the drug reduces the frequency of opening of the calcium channel in response to depolarization of the membrane. This decreases calcium influx, resulting in relaxation of muscle. In cardiac muscle, this also results in reduction of contractility, decreases in sinus node rate of firing, and AV nodal conduction. Skeletal muscle is relatively unaffected by CCBs since they have such a huge intracellular pool of calcium and are not as dependent on influx from outside the cell.

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10
Q

What is the site of action for dihydropyridines and what drugs are in this class?

A
Dihydropyridines- tend to act on the periphery 
Amlodipine
Nicardipine
Nifedipine
Isradipine
Clevidipine
Allow for vasodilation while having little effect on vascular permeability all have selectivity for peripheral tissue smooth muscle and act on vascular smooth muscle much more than on myocytes or the electrical conduction of the heart. They are thus used for HTN and not for arrythmias! The main difference between these agents is their half life; when starting amlodipine, it will work sometime next week vs. that day. It's great for compliance, though, because it can be taken once a day. So, other agents need to be used while waiting for the amlodipine to take effect.
Short-acting CCBs from this class are also used to treat Raynaud's phenomenon or coronary vasospasm and angina. 
Nifedipine is a preferred drug for HTN in pregnancy.
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11
Q

What are the non-dihydrophyridine CCB? Where do they act?

A

Non-dihydropyridines
Verapamil
Diltiazem

Reduce vascular permeability while also affecting cardiac contractility and conduction. mainly cardiac effects

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12
Q

When are non dihydopyridines used? CCB is general?

A

Verapamil in particular suppresses the HR and cardiac output. Remember when I told you that you had to remember which agents besides BBs decrease the heart rate? this is one of them! Its major use is as an antiarrythmic- like atrial fibrillation
Diltiazem has less cardiac effect but still some, and can also be used for antiarrythmic purposes or less commonly for HTN.

CCB=preferred to control BP in patient w/ COPD and asthma b/c oppose tracheobronchial constriction and do not increase airway secretions

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13
Q

What are the side effects and toxicities of CCB?

A

Edema- most notorious effect
Verapamil- 25% with constipation
Avoid non-dihydropyridines in heart failure, sick-sinus syndrome, or heart block (if conduction problems don’t want to slow down further)

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14
Q

What is the MOA of ACE inhibitors?

A

Block the conversion of angiotensin I to angiotensin II-

Angiotensin II blocks the efferent arteriole, so blocking AngII vasodilates increasing renal flow

blocking aldosterone stops it from saving Na and dumping K+

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15
Q

What are the effects of ACEi?

A

Main: inhibits pathological cardiac remodeling, inhibits aldosterone and Na dumping (naturesis)
lower arteriolar resistance
increase in venous capicatnace
decrease CO CI stroke work and cardiac volume
decrease renal Protein kinase C - protects from DM neuropathy

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16
Q

What is the suffix for ACEi

A

=pril

lisinopril enalapril etc

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17
Q

What are the common side effects of ACEi

A

Main: cough or angiodema- must class switch

act both by inhibiting the angiotensin pathway and effects of angiotensin II, but also by increasing the effect of bradykinin, which is vasodilatory. All affect renal perfusion by affecting the ability of the kidney to autoregulate the efferent arteriole, and dosage should be decreased in renal disease.

Also: hyperkalemia
renal impairment

18
Q

When are ACEi contradicted?

A

pregnancy, acute kidney injury, or aortic stenosis

19
Q

What is the good thing about using an ARB vs. ACEi (hint has to do with its MOA). Also when ARBs need

A

ARB can block the AT1 receptor which blocks the bad things Angiotensin II can do- vasoconstriction, SNS activation, cell proliferation, aldo release, Na saving
Block atherosclerosis and HTN.

But it can keep AT2 spared- vasodilation, inhibit cell growth, promote apoptosis. Can lead to Regression of a dilated aortic root and fibrosis in liver heart and lungs

Used in patients who can’t tolerate ACEi bc of cough from bradykinin build up

20
Q

When are Beta blockers indicated?

A

1) control of cardiac arrhythmias
2) protect heart from second MI (secondary prevention)- shown to decrease mortality sp MI. Used after acute heart failure exacerbations to improve mortality
3) control of HTN as third or later line therapy

21
Q

What are the classes of BB?

A

Non selective: N-Z: Nadolol, propranolol, timolol, pindolol

Beta 1 selective: A-M Atenololm bispropolol, esmolol, metropolol, (nebivolol)- reduce HT and contraction

With alpha blocking: carvedilol, labetalol- vasodilation properties

22
Q

What are side effects of BB?

A

bronchospasm, bradycardia, hypotension
Heart failure and heart block,
ED and insomina

Carvedilol associated with edema
B1 block of macula dense is associated with hyponatremia and hyperkalemia

23
Q

Contradictions of BB?

A

not good for coke overdose, only blocks beta and alpha can cause BP to go higher

24
Q

Define hypertensive urgency. what is goal of tx?

A

BP greater or equal to 180/120 which is asymptomatic

Reduce SBP by 25-30% over first 24 hours- usually to 160/100

25
Q

What is hypertensive emergency? What can it lead to in pregnancy

A

BP greater or equal to 180/120 with associated end organ damage

In pregnancy can lead to eclampsia (high BP with protein in urine). could lead to severe eclampsia called HELLP- hemolysis, elevated liver enzymes, low platelet count

26
Q

What is the goals of treatment in hypertensive emergency? Any exceptions? What drugs do you use?

A

HTN emergency- go to ICU, lower BP by 10-20% in first hour, lower 5-15% in next 23 hours

Except in ischemic stroke- lowered slowly if at all
Aortic dissection- lower rapidly, 20 minutes SBP 120-100

Nicardipine, BB, hydralazine, enalapril, and nitrates useful in treating it. Later in HTN soft chalk: use nitroprusside! This increases cGMP and relaxes

27
Q

What drugs are safe to use for HTN in pregnancy?

A

methlydopaa, hydralazine, labetalol, some CCB, HCTZ

28
Q

What is the action of clonodine and what is it used for?

A

A central acting alpha 2 agonist- decrease peripheral vascular resistance by lowering NE levels

Can be used in a test to dx pheochromocytoma

29
Q

PQ: a 57 yo Male with poor controlled HTN and CAD presents with 190/100 BP and new onset left weakness in arm and leg with facial droop. CT shows ischemic stroke. What is best tx?

A

To admit to ICU and provide supportive care

don’t want to reduce BP right away or maybe at all bc he is malperfused in part of his brain

30
Q

PQ: 47 yo male with obesity and DM has 148/91 BP and then 151/99 a week later. what is first line tx for him?

A

Lifestyle modification is always first line treatment- mediterrean diet, activity etc

31
Q

PQ: what is the best drug to reduce proteinuria?

A

ACEi- bc they are going to keep Ang II from clamping down on efferent arterioles and vasodilate arterioles of kidney and let more blood flow

32
Q

What is a side effects of all diuretics?

A

They increase serum uric acid levels and can precipitate gout

33
Q

How long does it take for diuretics to start working fully? Why?

A

It takes 6-8 weeks after initiation of diuretic therapy for the barorecptor SNS increase from the decrease in CO or blood volume to wear off. SNS compensation includes smooth muscle constriction (slight increase in PVR to counter the volume loss) and increase in RAAS

34
Q

What are two differences in thiazide and loop diuretics?

A

Loop diuretics work at TAL of LOH, cause Ca2+ excretion

Thiazides cause a net resorption of Ca2+ and work at DCT

35
Q

Describe how clonodine works and what side effects can result/

A

Clonodine is mainly an alpha 2 agoinst- reduces SNS tone and increases PSNS tone. This can decrease BP (desired effect) and decrease HR and decrease catecholamine release. Decrease in HR is important as can throw someone into cardiogenic shock, NEVER USE WITH BB OR NON DIHYDRO CCB that also lower HR

36
Q

What are side effects shared by methly dopa and clonodine

A

Both act like alpha 2 agonist centrally so depression, sedation are side effects.

Methyldopa also inhibits prolactin- lactation

Clonidine- treats drug withdrawl by reducing SNS but given with SNS depressant can lead to toxicity. Stopping suddenly can have reflex SNS like anxiety, tachy hypertension crisis

37
Q

What drugs are non selective alpha blockers? What are they used to tx?

A

Phentolamine is reversible, phenoxybenzamine is a irreversible prodrug

They are used to treat pheochromocytoma

They can cause reflex tachycardia

38
Q

What drug specifically is used in HTN and BPH

A

Tamsulosin is selective for alpha 1 and used in HTN and BPH

39
Q

What kind of drug is propranolol and what is it used to treat

A

Non specific beta blocker, used in migraine headaches and essential tremor, performance anxiety

40
Q

What beta 1 specific drugs do we need to know? What do they treat?

A

Metopropolol, atenolol, esmolol

Esmolol is short acting for tachyarrythmias or HTN crisis

Met and aten are very cardio specific in reducing muscle contractility and Ca influx

41
Q

What are the beta blockers with alpha blocking?

A

Labetalol- 3:1 beta to alpha. Alpha1 block causes vasodilation with beta still blocked, less likely to cause tachy- used in HTN emergency, first line in HTN in pregnancy

Carvedilol- peripheral alpha and beta blokcer, better anti HTN than beta1 selective BB. Used in patients with CHF bc decrease mortality

42
Q

What is main use of timolol?

A

Eyedrops for glaucoma

Non selective beta blocker