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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
Q

Side effects with captopril

A

Loss of taste
Neutropenia
Oral lesions

In addition to the others for all ace inhibitors

25
Q

What are contraindications of ace inhibitors

A

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
Q

Angiotensin receptor antagonists

A

-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
Q

There are four sites of control for blood pressure:

A

arterioles (resistance),
venules capacitance),
heart (pump output),
and kidney (volume)

28
Q

Treatment for HTN - step 0

A 
Lifestyle changes 
⬇Na intake 
⬆Exercise 
⬇Smoking
⬇Alcohol
29
Q

HTN treatment step 1 - diuretics

A

diuretics- lower blood pressure by increasing Na+ excretion and thus reduce bloodvolume -> ⬇preload ->⬇co

30
Q

HTN treatment step 2 - agents that alter sympathetic nervous system function

A
  • lower blood pressure by reducing peripheral vascular resistance, reducing cardiac function, and increasing
    venous pooling in capacitance vessels
31
Q

HTN treatment step 3 direct vasodilators

A

lower pressure by relaxing vascular smooth muscle increasing capacitance

⬇TPR

32
Q

HTN treatment RAAS inhibitors

A

⬇TPR

⬇Blood volume ➡⬇preload

33
Q

Thiazide diuretics - what do they do and use

A

⬇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
Q

Thiazide diuretics - side effects

A

Side effects : hypokalemia
Hypomagnesia
Hyperglycemia - k channels play a role in insulin channels in pancreas

36
Q

Loop diuretics - what are they, uses

A

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
Q

K sparing diuretics side effects, uses , what are they

A

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
Q

Side effects of loop diuretics

A 
Side effects 
Hypokalemia 
Ototoxicity - ringing in ears reversible 
Hyperglycemia 
Hyperuricemia
38
Q

Aquaretics

A

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
Q

β1-adrenergic receptor antagonists (β-blockers)

A

Used for mild HTN

  • ⬇hr
  • ⬇inotropy
  • ⬇renin release

propanolol, metoprolol, atenolol

41
Q

β1-adrenergic receptor antagonists (β-blockers)

Side effects

A 
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
Q

α1-adrenergic receptor antagonists (α-blockers)

A

prazosin, terazosin, doxazosin

Vasodilators - ⬇TPR and ⬇preload
Don’t have metabolic side effects
Orthostatic hypotension ( first day)

Only use alpha 1 selective

43
Q

Central adrenagric inhibitors

A

Clonidine( alpha 2 agonist)
⬇NE release

Reserpine - deplete NE - ⬇NE release
Methyldopa - never will use

44
Q

Direct vasodilators

A 
Relax smooth muscle 
⬇TPR 
⬆Venous capacitance 
Might get reflex tachycardia 
Not first line therapy but as an adjunct therapy with something
45
Q

Calcium channel blockers

A

Verapamil , diltiazm, DHP

No reflex tachy b( v and d) bc neg inotropy

DHP does have a risk of reflex tachy

46
Q

K channel openers

A

Hydralazine, minoxidil ( rogaine)

Vasodilators
Arterial dilator

Not used anymore for HTN treatment

47
Q

How do you choose the treatment of HTN ??

A

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
Q

Sympatholytics that treat HTN

A

β1-adrenergic receptor antagonists (β-blockers)
α1-adrenergic receptor antagonists (α-blockers)
central adrenergic inhibitors

Julie Pharm (14 decks)

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