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PHARMACOLOGY > LEC - 7.1 - ACEs & ARBs > Flashcards

LEC - 7.1 - ACEs & ARBs Flashcards

1
Q

explain the RAAS System

A

Renin Angiotensin Aldosterone System
A system that kicks into place during hypotension
This involves the kidneys, liver, lungs, and heart
Hypotension activates prorenin which is converted to renin
Renin is turned into angiotensin in the liver
Angiotension becomes angiotensin I in the lungs
Angiotension I is introduced to angiotensin converting enzyme (ACE) to become angiotensin II
Angiotensin II - a powerful vasoconstrictor, to help address hypotension
Angiotensin II travels to the adrenal cortex and is converted to Aldosterone
Aldosterone - increases water reabsorption, meaning decreased urine output and increased blood pressure

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2
Q

A system that kicks into place during hypotension

A

Renin Angiotensin Aldosterone System

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3
Q

The RAAS involves which organs?

A

the kidneys, liver, lungs, and heart

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4
Q

___ activates prorenin which is converted to renin

A

Hypotension

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5
Q

Hypotension activates ___ which is converted to renin

A

prorenin

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6
Q

Renin is turned into ___ in the ___

A

angiotensin

liver

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7
Q

Angiotension becomes angiotensin I in the ___

A

lungs

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8
Q

Angiotension I is introduced to ___ to become angiotensin II

A

angiotensin converting enzyme (ACE)

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9
Q

this is a powerful vasoconstrictor, to help address hypotension

A

Angiotensin II

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10
Q

Angiotensin II travels to the ___ and is converted to ___

A

adrenal cortex

Aldosterone

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11
Q

this increases water reabsorption, meaning decreased urine output and increased blood pressure

A

Aldosterone

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12
Q

one of the body’s homeostatic mechanisms that helps to maintain blood pressure at nearly constant levels, it provides a rapid negative feedback loop in which an elevated blood pressure causes the heart rate to decrease

A

Baroreflex

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13
Q

130/90 BP = ?

A

Prehypertension

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14
Q

? BP = Prehypertension

A

130/90 BP

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15
Q

> 140/>90 BP = ?

A

Hypertension

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16
Q

? BP = Hypertension

A

> 140/>90 BP

17
Q

Types of hypertension:

A

Essential

Secondary

18
Q

Hypertension of unknown origin.

A

Essential Hypertension

19
Q

Hypertension that results from other disease process

A

Secondary Hypertension

20
Q

Environmental Factors that Cause Hypertension:

A

Stress

Increased sodium intake

Obesity

Smoking

21
Q

This antihypertensive medication prevents ACE from converting angiotensin I to angiotensin II, a powerful vasoconstrictor and stimulator of aldosterone release. This action leads to a decrease in blood pressure and in aldosterone secretion, with a resultant slight increase in serum potassium and a loss of serum sodium and fluid.

A

ACE Inhibitor

22
Q

Examples of ACE Inhibitors:

A

captopril (Capoten)

lisinopril (Zestril)

enalapril (Vasotec)

ramipril (Altace)

fosinopril (Monopril)

23
Q

Pharmacokinetics:
Available only orally
70% - 75% is absorbed
Partly absorbed and partly excreted unchanged in urine
Food interferes with its absorption
Half life: 2 hours, but action stays for 6-12 hours

A

Captopril

24
Q

Pharmacokinetics of Captopril:
Administration:
Absorption:
Excretion:
Teachings:
Half life:

A

Available only orally

70% - 75% is absorbed

Partly absorbed and partly excreted unchanged in urine

Food interferes with its absorption

2 hours, but action stays for 6-12 hours

25
Q

Adverse Effects of Captopril

A

Cough – persistent brassy cough

Hyperkalemia in renal failure patients with K+ sparing diuretics, NSAID and beta blockers

Hypotension – sharp fall may occur with the 1st dose

Acute renal failure

Angioedema: swelling of lips, mouth, nose, etc.

Rashes, urticaria

Dysgeusia: loss or alteration of taste

26
Q

term for the swelling of lips, mouth, nose, etc.

A

Angioedema

27
Q

term for the loss or alteration of taste

A

Dysgeusia

28
Q

Contraindications for Captopril

A

Pregnancy

bilateral renal artery stenosis

hypersensitivity and hyperkalemia

29
Q

Advantages over captopril:
Longer half life and requires a 5-20 mg once daily dosage regimen
Absorption not affected by food
Rash and loss of taste are less frequent
Longer onset of action
Less side effects

A

Enalapril

30
Q

Pharmacokinetics of Enalapril:
Administration:
Absorption:
Excretion:
Teachings:
Half life:

A

Longer onset of action

Absorption not affected by food

Rash and loss of taste are less frequent

Longer onset of action

Longer half life and requires a 5-20 mg once daily dosage regimen

31
Q

No postural hypotension or electrolyte imbalance (no fatigue or weakness)
Safe in asthmatics and diabetics
Prevention of secondary hyperaldosteronism and K+ loss
Renal perfusion is well maintained
No hyperuraecemia or deleterious effect on plasma lipid profile
No rebound hypertension
Minimal worsening of quality of life – general wellbeing, sleep and work performance

A

1st line of Drug

32
Q

Nursing Implementation for 1st line Drugs

A

Encourage patient to implement lifestyle changes

Monitor for hypotension

Let client rest in supine position beginning one hour after administration and for 3-4 hours after the first dose

Observe for hypersensitivity reaction, particularly angioedema

Monitor for neutropenia and signs of infection

Monitor for persistent dry cough or changes in cough pattern

Monitor for hyperkalemia

Monitor for liver and kidney function

33
Q

These antihypertensive drugs selectively bind the angiotensin II receptors sites in vascular smooth muscle and in the adrenal gland to block vasoconstriction and the adrenal cortex release of aldosterone

These actions block the blood pressure – raising effects of the renin angiotensin system and lower blood pressure.

A

Angiotensin II Receptor Blockers (ARBs)

34
Q

Examples of ARBs:

A

Candesartan ( Blopress)
Losartan ( Combizar)
Irbesartan (Aprovel)
Valsartan (Diovan)

35
Q

Pharmacokinetics of ARBs:

A

Absorption not affected by food but unlike ACE Inhibitor its bioavailability is low

High first pass metabolism

36
Q

Adverse effects of ARBs:

A

Foetopathic like ACE Inhibitors – not to be administered in pregnancy

Rare 1st dose effect of hypotension

Low dysgeusia and dry cough

Lower incidence of angioedema

37
Q

Theoretical superiority of ARBs over ACEIs:

A

Cough is rare – no interference with bradykinin and other ACE substrates

Heart rate remains unchanged and CVS reflexes are not interfered

No significant effect in plasma lipid profile, insulin sensitivity and carbohydrate tolerance

Mild uricosuric effect

PHARMACOLOGY (24 decks)

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