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Julie Pharm > Antihypertensives > Flashcards

Antihypertensives Flashcards

0
Q

What is angiotensinogen

A

a plasma glycoprotein which is synthesized in many organs, includingliver, kidney, brain, and fat. It is the only known substrate of renin

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1
Q

What is renin

A

a protease synthesized and stored in the renal juxtaglomerular apparatus.

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2
Q

What is angiotensin I (Ang I)

A

a decapeptide formed by proteolysis of angiotensinogen by renin.Has weak vasoconstrictor activity

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3
Q

angiotensin II (Ang II)

A

an octapeptide formed by proteolysis of Ang I by angiotensinconverting enzyme (ACE). A very potent vasoconstrictor.

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4
Q

angiotensin converting enzyme (ACE)

A

a peptidase located in several tissues, althoughthe highest levels are found in lung epithelial cells, which are considered the major
source of circulating Ang II.

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5
Q

angiotensin III (Ang III)

A

a heptapeptide formed by the action of an aminopeptidase onAng II; has less vasoconstrictor activity than Ang II.

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6
Q

angiotensin receptors

A

there are two classes of angiotensin receptors: AT1 and AT2. All known postnatal physiological effects of angiotensin appear to be mediated by AT1
receptors.

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7
Q

AT1 receptors

A

Angiotensin 2 is ligand G protein coupled receptors. IP3/DAG cascade

Release of calcium - vasoconstrictor activity
Mitogenic activity - stimulate growth
Clinical target

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8
Q

AT2 receptor

A

G protein coupled - activate phosphodiesterase
High expression in fetus
Postnatally their function is unknown

Not a clinical target

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9
Q

bradykinin

A

a peptide with potent vasodilator activity. While not part of the renin-angiotensin system, it is a substrate for ACE, which converts bradykinin to an inactive fragment

Opposite effect of angiotensin
Bradykinin gets broken down by ACE

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10
Q

How does ang II effect the blood pressure

A

blood pressure:
intravenous infusion of Ang II produces a strong pressor responsewithin 10-15 seconds. The pressor response is primarily due to vasoconstriction of vascular smooth muscle mediated by angiotensin receptors on the muscle cells.
-Resets the baroreceptors ( no reflex Brachy or tachy)

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11
Q

How does ang II effect adrenal cortex

A

adrenal cortex: Ang II acts directly on the zona glomerulosa of the adrenal cortex to stimulate aldosterone biosynthesis and release, which in turn increases renal sodium
reabsorption and blood volume.

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12
Q

How does ang II effect the CNS

A

central nervous system:
Ang II exerts a CNS- mediated pressor response caused by increased central efferent sympathetic activity to the periphery.
Aka - increase NE release from ANS
It also stimulates thirst (dipsogenic effect)
the secretion of vasopressin and ACTH.

  • increase vasopressin release -> increase. H20 reabsorption
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13
Q

How does ang II effect cell growth

A

cell growth: Ang II exerts mitogen activity for vascular and cardiac muscle cells, andmay contribute to cardiac hypertrophy.

  • cardiac remodeling and HF
  • fetal growth ( AT1)
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14
Q

What is the rate limiting step in renin secretion

A

Renin release is the rate-limiting step in the formation of Ang II, and can be controlledby either local renal mechanisms or through the CNS:

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15
Q

What do renal vascular receptors do for regulation

A

renal vascular receptor: functions as a stretch receptor, and reductions in stretch
caused by a decrease in renal perfusion pressure leads to increased renin release

Decrease stretch -> increase renin release

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16
Q

What does macula densa do for regulation of renin

A

b.) macula densa: receptors here are sensitive to rate of sodium delivery to the distal
tubule; reductions in sodium delivery stimulate renin release

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17
Q

How does the sympathetic nervous system regulate renin release

A

c.) sympathetic nervous system: norepinephrine stimulates renin release via direct action on β-adrenergic receptors on the juxtaglomerular cells

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18
Q

How does ang II regulate renin release

A

d.) angiotensin II: Ang II acts on juxtaglomerular cells to reduce renin release, forming a short-loop negative feedback system.

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19
Q

What are the four points of intervention for renin ang system

A
  • renin release : ⬇symp output ⬇release
  • formation of Ang I by renin (renin inhibitors): no more effective and induces reactive renin release
  • formation of Ang II by ACE (ACE inhibitors) : ang II is blocked
    (-pril)
  • AT1 receptors (AT1 receptor antagonists)
20
Q

What are the three classes of ace inhibitors

A

Class 1 - Captopril - active by its self (-SH) sulfhydro group
Class 2 Pro drugs
- enalapril ➡enalaprilat
Liver metabolism

Class 3 - lisinopril - active drugs
More water soluble longer half life

21
Q

Actions of ace inhibitors

A

⬇BP by ⬇ TPR
Ace inhbs don’t induce sympathetic reflex ( ok for ischemic heart disease)
⬆Bradykinin bc ace also breaks down bradykinin
- symptoms skin rash and dry cough

22
Q

When do you use ace inhibitors

A

All states of heart failure ( ⬇mortality)

HTN ( dont impair insulin sensitivity so

23
Q

Side effects of ace inhibitors

A 
Hyperkalemia - ⬇ in aldosterone release 
Hypotension 
Renal failure due to ⬇ BP 
Angioedema - very rare 
Teratogenic 
Skin rash - ⬆bradykinin   Most common 
Dry cough -⬆ bradykinin.  Most common
24
Side effects with captopril
Loss of taste Neutropenia Oral lesions In addition to the others for all ace inhibitors
25
What are contraindications of ace inhibitors
Pregnancy Bilateral renal stenosis ( need high systemic BP to press blood into the kidneys) Hyperkalemia Severe renal failure ( won't be able to perfuse kidney)
26
Angiotensin receptor antagonists
-All end in -sartan -They avoid bradykinin mediated side effects -don't inhibit AT2 receptor effect (losartan, valsartan) - orally active - not superior to ace inhibitors
27
There are four sites of control for blood pressure:
arterioles (resistance), venules capacitance), heart (pump output), and kidney (volume)
28
Treatment for HTN - step 0
``` Lifestyle changes ⬇Na intake ⬆Exercise ⬇Smoking ⬇Alcohol ```
29
HTN treatment step 1 - diuretics
diuretics- lower blood pressure by increasing Na+ excretion and thus reduce bloodvolume -> ⬇preload ->⬇co
30
HTN treatment step 2 - agents that alter sympathetic nervous system function
- lower blood pressure by reducing peripheral vascular resistance, reducing cardiac function, and increasing venous pooling in capacitance vessels
31
HTN treatment step 3 direct vasodilators
lower pressure by relaxing vascular smooth muscle increasing capacitance ⬇TPR
32
HTN treatment RAAS inhibitors
⬇TPR | ⬇Blood volume ➡⬇preload
33
Thiazide diuretics - what do they do and use
⬇Na reabsorption in the dct Low ceiling diuretics Classic example : hydrochlorthiazide Increase urine output 3 x Use: HTN 1st line for mild HTN Chef when edema is mild Osteoporosis - ⬇urinary calcium loss
34
Thiazide diuretics - side effects
Side effects : hypokalemia Hypomagnesia Hyperglycemia - k channels play a role in insulin channels in pancreas
36
Loop diuretics - what are they, uses
Furosemide and ethacrynic acid, bumetanide, torsemide ⬆8 x urine output high ceiling diuretics ( pee like a race horse) Use : Chf- when edema is real bad HTN - lower doses than w. edema
36
K sparing diuretics side effects, uses , what are they
spironolactone/ eplerenone - aldo recept antagonist amiloride/ triamterene. - inhibit ENac Not as good as loop diuretics ⬇Na intake ``` Use Chf ( spironolactone or eplerenone ) ``` Side effects Hyperkalmia Metabolic acidosis ( not common) spironolactone- gynecomastia or impotence in males
37
Side effects of loop diuretics
``` Side effects Hypokalemia Ototoxicity - ringing in ears reversible Hyperglycemia Hyperuricemia ```
38
Aquaretics
inhibit the vasopressin V2 receptors, which promote the synthesis and translocation of aquaporin-2 (AQP2) in the collecting duct. When AQP2 is present, water is retained and the urine becomes more concentrated; when it is absent, water isnot retained, and the urine becomes more dilute and urinary output is increased. In addition, plasma Na+ levels rise. conivaptan and tolvaptan. Conivaptan is amixed V1 and V2 antagonist and it delivered IV, while tolivaptan is an oral V2 antagonist. The major clinical use of these two compounds is to treat hyponatremia.
40
β1-adrenergic receptor antagonists (β-blockers)
Used for mild HTN - ⬇hr - ⬇inotropy - ⬇renin release propanolol, metoprolol, atenolol
41
β1-adrenergic receptor antagonists (β-blockers) | Side effects
``` Side effects ⬇Cardiac function Bronchoconstriction ( beta 2) bc it's not super selective CNS: sedation (propranolol ) Metabolic effects: Hyperglycemia ⬆Tg ⬇Hdl ``` Rebound hypersensitivity - upregulation of beta receptors on the end organ so can't abruptly remove pt from beta blockers
42
α1-adrenergic receptor antagonists (α-blockers)
prazosin, terazosin, doxazosin Vasodilators - ⬇TPR and ⬇preload Don't have metabolic side effects Orthostatic hypotension ( first day) Only use alpha 1 selective
43
Central adrenagric inhibitors
Clonidine( alpha 2 agonist) ⬇NE release Reserpine - deplete NE - ⬇NE release Methyldopa - never will use
44
Direct vasodilators
``` Relax smooth muscle ⬇TPR ⬆Venous capacitance Might get reflex tachycardia Not first line therapy but as an adjunct therapy with something ```
45
Calcium channel blockers
Verapamil , diltiazm, DHP No reflex tachy b( v and d) bc neg inotropy DHP does have a risk of reflex tachy
46
K channel openers
Hydralazine, minoxidil ( rogaine) Vasodilators Arterial dilator Not used anymore for HTN treatment
47
How do you choose the treatment of HTN ??
Start with best initial drug - depends on pt Diabetics : avoid beta blockers and high dose diuretic/ use acei dyslipidemias : avoid beta blockers and diuretics / alpha may help Old ppl - everything is good in low doses Angina - avoid reflex tachy ( DHP, acei, arb) Post mi - b blockers , acei and arb - preferred stop remodeling
48
Sympatholytics that treat HTN
β1-adrenergic receptor antagonists (β-blockers) α1-adrenergic receptor antagonists (α-blockers) central adrenergic inhibitors

Julie Pharm (14 decks)

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