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CRNA Pharmacology > Anti-Hypertensive Agents > Flashcards

Anti-Hypertensive Agents Flashcards

1
Q

Attenuation of SNS and ↓ in BP during anesthesia caused by ____ ?

A

1) Acute blood loss
2) Body position changes
3) ↓ Venous return d/t positive pressure ventilation of the lungs

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2
Q

General uses of A1 agonists

A

1) Sedation (↓ activity, to make calm and relax)
2) Anxiolysis
3) Hypnosis (to put to sleep)
4) Analgesia
5) Sympatholysis

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3
Q

Clonidine characteristics

A

1) Selective partial A2 receptor agonist
2) Belongs to Imidazoline subclass
3) Antihypertensive agent with sedative, anxiolytic, and analgesic properties
4) Lipid Soluble

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4
Q

*What is the effect of combining Clonidine with opioids/local anesthesia?

A

1) ↑ duration of analgesia and ↓ requirements for opioids

2) Prolongs effects of regional and Neuraxial anesthesia via pre and post synaptic A2 receptors

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5
Q

Pre-anesthetic medication use of Clonidine

A

1) ↓ MAC of inhaled and injected anesthetics
2) Blunts reflex tachycardia assoc. with intubation
3) ↓ Fluctuations in BP during anesthesia
4) ↑ Vasoconstriction even more when given in the presence of Ephedrine and Phenylephrine

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6
Q

Why is the use of Clonidine limited in Obstetrics?

A

The risk of fetal bradycardia and maternal hemodynamic instability is increased with the use of Clonidine

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7
Q

What are the advantages of the preoperative use of Clonidine?

A

It reduces the incidence of myocardial ischemia, infarction, and mortality after cardiovascular surgery.

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8
Q

Can Clonidine be used for Post-operative shivering?

A

Yes - 75mcg/IV

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9
Q

*What is the most common use for Clonidine?

A

Tx of HTN

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10
Q

Other clinical uses of Clonidine besides HTN

A

1) Tx of opiate, benzo, and alcohol withdrawal
2) Dx of pheochromocytoma
3) Smoking cessation
4) Comined with opiates into an Epidural form to treat cancer

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11
Q

Routes of administration for Clonidine

A

1) Oral - 2.5 to 5mcg/kg 30-90mins before induction)
2) Transdermal
3) Epidural (75 to 150mcg)
4) Intrathecal
5) IM (rarely used)
6) IV (rarely used)

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12
Q

Clonidine MOA

A

1) Binds presynaptic A2 receptors which ↓ SNS outflow via ↓ NE
2) ↓ HR, contractility, CO, SVR and BP, vasodilation

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13
Q

Which receptors in the CNS does Clonidine bind? What happens when they bind?

A

Imidazoline receptor in the CNS - Contributes to clonidine’s sympathy-inhibitory response

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14
Q

Effect of Epidural Clonidine

A

1) Produces dose-dependent analgesia
2) Analgesia produced at pre-synaptic and post junctional A2 adrenoreceptors in spinal cord, which prevent tx of pain signal to brain
3) Inhibits substance P release

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15
Q

Explain the mechanism by which Clonidine ↓ requirements for anesthetics and other agents like Dexmedetomidine

A

Modifies the function of K+ channels in the CNS resulting in membranes becoming hyper polarized

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16
Q

What is the effect of Clonidine on the eyes?

A

↓ Aqueous humor secretion which results in ↓ Intra ocular pressure

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17
Q

What effect does Clonidine have on the Baroreceptor reflexes?

A

Baroreceptor reflexes are blunted by Clonidine

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18
Q

What happens when Clonidine is administered at higher doses than those required (overdose/toxicity) to stimulate central inhibitory A2 receptors?

A

Clonidine will have an affinity for peripheral post synaptic A2 receptors.

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19
Q

Effects of Clonidine binding peripheral post-synaptic A2 receptors?

A

1) Vasoconstriction
2) ↑ TPR (total peripheral resistance)
3) ↑ BP

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20
Q

What is Clonidine’s Half Life, Peak and Duration

A

1) Half Life - 12hrs
2) Peak - 1 to 3hrs
3) Duration - 8 hrs

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21
Q

Clonidine’s Distribution, Metabolism, Excretion

A

1) Distribution - Lipid soluble and 20 to 40% protein bound
2) Metabolism - 50% hepatic
3) Excretion - 50% unchanged in urine

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22
Q

Clonidine’s Adverse Effects

A

1) Most Common: Xerostomia, sedation/drowsiness

2) Bradycardia, hypotension, dizziness, dry eyes and nose, fluid retention, skin rash, impotence

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23
Q

*Which 2 adverse effects of Clonidine can be common when administered epidurally?

A

Hypotension and Bradycardia

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24
Q

What is the black Box warning that comes with Clonidine?

A
  • Epidural Clonidine not rec. for obstetrical, postpartum, or preoperative care
  • Hypotension and bradycardia risks are high
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25
Q

What time frame do Clonidine withdrawal symptoms manifests after abrupt/sudden discontinuation of the drug?

A

18 to 36 hrs

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26
Q

*Symptoms of Clonidine withdrawal Syndrome

A

1) Rebound HTN and tachycardia
2) Headache and abdominal pain
6) Nervousness, tremors and diaphoresis

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27
Q

What increases the risk of Rebound Hypertension in Clonidine Withdrawal PTs?

A

If the oral dose was more than 1.2mg/day

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28
Q

Tx of Clonidine induced Rebound HTN depends on what? How is it treated accordingly?

A
  • Tx depends on the urgency of reducing arterial
    1) Restart clonidine if non-lifethreatening situation
    2) Administer vasodilators such as hydralazine, Na-Nitroprusside, or a combo of A and B blockers i.e. Labetalol
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29
Q

How is Clonidine used to diagnose Pheochromocytoma?

A
  • Since Pheochromocytoma is a tumor that releases excess EPI and NE
  • Clonidine binds A2 receptors on pre-synaptic nerves which inhibits release of EPI and NE
  • If giving the PT clonidine ↓ BP, then the PT has Pheochromocytoma.
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30
Q

Why should you not use beta blockers alone to treat rebound HTN in clonidine withdrawal PTs.

A

Allowing unopposed A1 vasoconstriction caused by activation of the SNS and elevated circulating catecholamines will make HTN worse

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31
Q

Steps of RAAS system

A

↓BP&raquo_space;> Renin release&raquo_space;> (Renin Δs angiotensinogen to angiotensin I)&raquo_space;> (ACE Δs angiotensin I to Angiotensin 2)&raquo_space;> (Angiotensin II goes to effector organs)

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32
Q

What are the effector organs of Angiotensin II and what are its actions there?

A

1) Kidneys - causes secretion of aldosterone from the zone glomerulosa of the adrenal cortex.
2) Vessels - vasoconstriction
3) Pituitary - ADH secretion
4) SNS - ↑ SNS activity

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33
Q

What is Renin? Where is it produced? What is its primary role?

A
  • Renin is an enzyme
  • Produced primarily by the Juxtaglomerular (JAG) cells of the kidney’s afferent arteriole.
  • Converts angiotensinogen to the inactive peptide angiotensin I
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34
Q

*What is the Rate Limiting Factor in the Angitensin II production?

A

When Renin converts ngiotensinogen to the inactive peptide

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35
Q

Renin secretion is increased by what?

A

1) Hypotension
2) ↓ Blood volume (i.e. hemorrhage)
3) ↓ Na+ in early distal tubule
4) ↑ Binding of catecholamines to B1 receptors on JAG cells

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36
Q

What is ACE, what are its roles?

A
  • ACE means Angiotensin Converting Enzyme
  • It is a dipeptidyl peptidase enzyme
  • It converts angiotensin I to angiotensin II
  • It also breaks down bradykinin
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37
Q

What is Bradykinin?

A

A vasodilation substance

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38
Q

Where is ACE found

A

1) Lungs - membrane-bound form of ACE found in endothelial cells which line BVs of lung
2) Blood - soluble form of ACE that circulates in blood stream

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39
Q

What is Angiotensin II (Ang II)? Which receptors does it bind?

A
  • A very POTENT vasoconstriction hormone (40x more potent that EPI)
  • Binds AT1, AT2 and AT4 at it target organs
40
Q

Metabolization of Ang II

A

Metabolized to Angiotensin III by the enzyme aminopeptidase

41
Q

Explain the physiology of Ace-escape in PTs who take ACE inhibitors?

A
  • AngII can be produced by non-ACE’s or non-ACE pathways

- Since ACE inhibitor ↓ BP by inhibiting ACE, if ACE is created some other way, then the PTs BP will ↑

42
Q

Which receptors does aldosterone bind to? What are the effects of the binding?

A
  • Aldosterone binds mineralocorticoids receptors in the distal and convoluted tubules of the kidneys
  • Binding ↑ Na+ and H2O retention and ↑secretion of K+ and H+
43
Q

The stimulant effect of Ang II on aldosterone secretion is reduced by what and increased by what?

A

1) Increased by hyponatremia, hyperkalemia, and adrenocorticotropic hormone
2) Reduced by hypernatremia or hypokalemia

44
Q

Ace Inhibiters: Current Available Agents

A

1) Captopril
2) Lisinopril
3) Enalaprilat
- —————————–
4) Enalapril
5) Benazepril
6) Ramipril
7) Quinapril
8) Moexipril
9) Trandolapril
10) Perindopril
11) Fosinopril

45
Q

What is unique about Captopril as an Ace Inhibitor?

A

It is the only one that contains Sulfhyryl moiety and it’s the shortest acting ACE-I

46
Q

What is the only ACE-I that is available in IV form? What else is important to know about this drug?

A

Enalaprilat - It is the active metabolite of the prodrug Enalapril (vasotec)

47
Q

ACE-I MOA

A
  • Inhibit ACE

- Prevents Ang II from vasoconstriction, stimulation of SNS, ADH and Aldosterone secretion

48
Q

Why are Bradykinin levels increased in PTs receiving ACE-I?

A

ACEs are responsible for breaking down bradykinin, if the they are inhibited then levels of bradykinin goes up and resulting inflammation does too

49
Q

Why do ACE-I’s induce a cough and angioedema?

A

↓ACE&raquo_space;> ↑Bradykinin&raquo_space;> ↑ vasodilation&raquo_space;> ↑ angioedema and ↑ cough (from vasodilation in respiratory system)

50
Q

Most of the ACE-I’s are ester prodrugs broken down in the liver by esterases. Which 3 aren’t ester prodrugs?

A

1) Captopril
2) Lisinopril
3) Enalaprilat

51
Q

Ace Inhibitors: Clinical Effects

A

1) Dilate vessels via bradykinin
2) ↑ Renal secretion of aldosterone, which ↑ BP
3) ↓ SNS activity
4) ↑ ADH which promotes reabsorption of Na+ and water

52
Q

*What are ACE-I’s effect on cardiac output and heart rate?

A

Although they ↓ SNS activity, they have NO effect on CO and HR.

53
Q

What are the benefits of ACE-I’s over other HTN drugs?

A

1) Lacks CNS effects i.e. depression, insomnia and sexual dysfunction
2) Doesn’t cause CHF, bronchospasm, bradycardia, and exacerbation PVD
3) No metabolic changes like those assoc. with diuretics i.e. hyperglycemia and hypokalemia
4) Rebound HTN and tachycardia doesn’t not occur with ACE-Is use

54
Q

Ace Inhibitors Side Effects

A

1) Dry cough
2) Angioedema
3) Renal Insufficiency and hyperkalemia
4) Maculopapular skin rash
5) Dysguesia (can’t taste)
6) Neutropenia
7) Agranulocytosis

55
Q

How do ACE-I’s cause hyperkalemia

A

ACE-I’s cause ↓ in aldosterone, which retains urine, which we usually excrete in urine.

56
Q

How is life-threatening Angioedema from taking ACE-I’s treated?

A

EPI 0.3 to 0.5mL of a 1:1000 solution SQ

57
Q

*What causes angioedema when taking ACE-I’s?

A

Bradykinin increase as a result of ACE decrease, which causes vasodilation and fluid shift.

58
Q

Ace Inhibitor induced angioedema most commonly affects which body parts?

A

1) Lips
2) Tongue
3) Face
4) Upper airway

59
Q

Which ACE-I is can cause angioedema? what doses cause the angioedema?

A

Angioedema occurs with all ACE-I’s and is not dose dependent

60
Q

Contraindications for using Ace Inhibitors?

A

1) Previous angioedema
2) Pregnancy
* 3) Bilateral renal artery stenosis

61
Q

How can the use of Ace Inhibitors cause renal failure?

A
  • ACE-I’s prevent the conversion go Ang I to Ang II - Ang II usually causes constriction of the efferent arteriole to maintain GFR
62
Q

How soon before surgery should the use of ACE-I’s surgical PTs?

A

They should be continued up until morning before surgery

63
Q

When is it acceptable to hold ACE-I’s before surgery?

A

ACE-I’s should be held for surgeries involving large blood loss or suspected fluid shift.

64
Q

How is hypotension related to ACE Inhibitor use treated?

A
  • Crystalloid infusion
  • Sympathomimetics i.e. ephedrine or phenylephrine
  • If not responsive to ephedrine or phenylephrine, treat with vasopressin
65
Q

How do NSAIDs affect use of ACE-I’s and ARBs?

A

NSAIDs antagonize/reduce the antihypertensive effects of ACE-I’s and ARBs.

66
Q

Ace Inhibitors is the first line of treatment for which clinical disorders?

A

1) HTN
2) HF
3) MI
4) LV dysfunction post MI

67
Q

Other uses of ACE-I?

A

1) Diabetic & non-diabetic nephropathy
2) Tx of coronary artery disease
3) Sclerodema renal crisis

68
Q

Angiotensin II Receptor Blockers (ARBs) drugs

A

1) Candesartan
2) Irbesartan
3) Losartan
4) Olmesartan
5) Telmisartan
6) Vasartan
7) Eporsartan
8) Azilsartan

69
Q

ARBs MOA

A
  • Selective antagonists of Ang II at the AT1 receptor, which inhibits the the actions of Ang II
70
Q

Do ARBs inhibit ACE or affect levels of Bradykinin?

A

ARBs do not inhibit ACE or effect levels of Bradykini

71
Q

What is the advantage of ARBs over ACE-I’s?

A
  • ARBs block the effect of Ang II regardless of how Ang II is generated since ARBs are blocking AT1 receptors.
  • ACE can be created via ACE-escape methods, which can bring back the PTs HTN
72
Q

Which ACE inhibitor is a prodrug?

A

Enalapril

73
Q

What dosage forms are ARBs available in?

A

Oral only

74
Q

ARBs Clinical Effects

A

1) ↓ Vasoconstriction
2) ↓ NE release
3) ↓ SNS activation
4) ↓ Aldosterone release
5) ↓ ADH release
6) ↓ Efferent arteriole vasoconstriction
7) ↓ Cellular hypertrophy & hyperplasia
8) ↓ SVR, preload and after load
9) ↓ MAP, SBP, DBP

75
Q

ARBs Side Effect

A

1) Dizziness and fatigue
2) Headache, hypotension and hyperkalemia
3) Renal insuficiency
* 4) Less incidence of cough
* 5) Less incidence of angioedema

76
Q

What is cross reactivity in regards to ACE-I’s and ARBs?

A

When someone who’s allergic to ACE-I’s has a reaction to ARBs as well.

77
Q

Aliskiren MOA

A

1) Selective, competitive direct Renin inhibitor

2) Binds to active site of renin and blocks conversion of angiotensinogen to Ang I

78
Q

Aliskiren’s effect on ACE-I’s and AT1 receptors?

A

Aliskiren does not affect either

79
Q

Aliskiren’s Clinical Effects?

A

1) Dose-dependent ↓ in BP
2) Ang I and Ang II
3) ↑ plasma Renin concentrations due to the negative feedback loop
4) ↓ Plasma and urinary aldosterone levels which ↓ Na+ and water retention
5) Enhances naturesis

80
Q

Aliskiren Side Effects

A

1 ) Common - Diarrhea, cough and rash

2) Less Common - Hypotension, impaired renal fx, hyperkalemia, angioedema

81
Q

6 Class of drugs that act as antagonists to the RAAS System?

A

1) Ace Inhibitors
2) ARBs
3) BBs
4) Aldosterone antagonists
5) Direct renin inhibitors
6) Clonidine (central A2 agonists)

82
Q

How do BBs antagonize the RAAS system?

A

Renin is usually secreted in response to Beta Adrenergic stimulation of JAG cells in the kidney, which then cleaves plasma angiotensinogen to produce angiotensin I.

83
Q

Sacubitril MOA

A
  • Sacubitril is a prodrug that is metabolized by esterases
  • Its active metabolite is LBQ657, which inhibits neprilysin
  • Inhibits neprilysin, which acts as an enhancer of NP and bradykinin
84
Q

Effects of increased Bradykinin and NP

A
  • Increased levels of cGMP
  • Vasodilation
  • Natriuresis and diuresis
  • Supression of aldosterone levels
  • Inhibition of cardiac fibrosis and hypertrophy
85
Q

Sacubitril Clinical Use

A
  • Combined with Valsartan in the brand name Entresto

- Used in certain types of HF

86
Q

Sacubitril Adverse Effects

A
  • Hypotension and angioedema (rare)
87
Q

Hydralazine MOA?

A
  • Direct relaxation of vascular smooth muscles and arterioles
  • Hyperpolarization of cells by opening high conductance Ca2+-activated K+ channels
  • Also, activated guanylate cyclase increases cGMP
  • All leads to inhibition of the accumulation of intracellular Ca2+
88
Q

Hydralazine Cardiovascular Effects

A

1) ↓ SVR/afterload, which ↓ BP (more DBP than SBP)
2) Vasodilation more pronounced in coronary, cerebral, renal, and splanchnic circulation
3) Reflex tachycardia
4) Tachyphylaxis

89
Q

How does Hydralazine’s trigger of the baro-receptor mediated reflexes counteract its antihypertensive effect.

A
  • Hydralazine induced vasodilation triggers the baro-receptor mediated reflexes which results in:
    1) ↑ HR and FOC
    2) ↑ Renin activity which ↑ fluid retention
    3) ↑ SV and CO
90
Q

Cardiac warning when administering IV Hydralazine to PTs with CAD.

A

Myocardial ischemia may result in an MI

91
Q

Why is hydralazine usually given with a BB and a diuretic for long term therapy?

A
  • It limits the SNS activity produced by hydralozine, prevents tachycardia, and increased renin release
92
Q

Hydralazine Metabolism

A

1) Extensive 1st pass effect
2) Acetylation via N-acetyltransferasse
3) t 1/2 - 2 to 3 hours
4) Excretion - < 15% excreted as unchanged drug by kidneys

93
Q

Why is it so important to closely monitor PTs for up to 12 hrs after administration of Hydralazine?

A

Antihypertensive effects do not correlate with t 1/2 and usually last 3-6 hrs but can persist for up to 12 hrs.

94
Q

*Hydralazine Side Effects

A

1) Tacycardia
2) Hypotension and headache
3) Flushing
4) N and V
5) Flushing
6) Angina pectoris
7) Dizziness and vertigo
8) Sodium and water retention
9) ECG changes
10) SLE-like syndrome
11) Positive ANA test
12) Drug-induced fever, urticaria, polyneuritis, anemia and pancytopenia (all rare)

95
Q

Hydralazine Clinical Uses

A

1) Introperative HTN - 2 to 10 mg IV bolus
2) Eclampsia/pre-eclampsia - 5 to 10mg IV q10 to 20 mins prn
3) HF (usually given with isosorbide denigrate for HF)

96
Q

Hydralazine should be used with extreme caution when used in which PT populations?

A

1) PTs with ↑ ICP, aortic dissection, and rheumatic heart disease
2) Elderly
3) CAD

CRNA Pharmacology (8 decks)

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