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SRNAPharmacology I > ANTIHYPERTENSIVES > Flashcards

ANTIHYPERTENSIVES Flashcards

1
Q

Should antihypertensives be stop?

A

Antihypertensive should be given up to the time of surgery

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2
Q

Selective Alpha 2 adrenergic agonists

A

Clonidine (ONLY DISCUSSED )
Dexmedetomine
Methyldopa
Apraclonidine

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3
Q

Selective alpha 2 agonists Properties

A 
Sedation
anxiolytics
Hypnosis
Analgesia
Sympatholysis effects
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4
Q

Selective Alpha 2 adrenergic agonists PROTOTYPE

A

CLONIDINE

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5
Q

CLONIDINE is

A

“CENTRALLY ACTING” selective partial alpha 2 adrenergic receptor agonist.

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6
Q

CLONIDINE alpha 2 to alpha 1 ratio

A

220:1

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7
Q

CLONIDINE also

A

sedative, anxiolytic, and ANALGESIC PROPERTIES (weak)

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8
Q

CLONIDINE is a ______ agent that _______The BBB

A

Lipid soluble

Penetrates

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9
Q

ANESTHESIA clinical use of CLONIDINE

A

Increases the duration of analgesia and reduces dose requirement for narcotic opioid pain medications
Reduces requirements for epidural infusion by 20 % - 60%

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10
Q

ANESTHESIA clinical use of CLONIDINE , and local anesthetics

A

Increases the duration of analgesia, reduce requirement for LOCAL ANESTHETICS

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11
Q

How CLONIDINE works : It prolongs what?

A

Prolongs effects of regional and neuraxial anesthesia via pre and post synaptic alpha 2 receptors

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12
Q

Alpha 2 receptors are both

A

PRE synaptic

POST synaptic

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13
Q

Clonidine ANESTHESIA USED:

A

decrease Requirements of anesthetics *Decrease MAC ) of inhaled and injected anesthetics
Blunt REFLEX TACHYCARDIA associated with tracheal intubation
Decreased fluctuation of BP and HR during anesthesia
AUGMENTS VASOPRESSOR RESPONSE to agents such as IV ephedrine and phenylephrine.

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14
Q

Clonidine for anesthesia can also used if demerol not effective:

A

SHIVERING (75 mcg IV)

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15
Q

The periooperative use reduces the incidence of

A

MI, myocardial ischemia

decrease mortality

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16
Q

ANESTHESIA:: The risk of ______ and risk of ______hemodynamic instability limits the use of clonidine in ______Cases

A

Fetal bradycardia
Maternal
Obstetric

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17
Q

**Most common use of CLONIDINE

A

TREATMENT OF HYPERTENSION

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18
Q

Clonidine can also be used to diagnosis

A

Pheochromocytoma.

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19
Q

ROUTE Of Administration clonidine

A

PO, IV

PACTH, EPIDURAL

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20
Q

Clonidine: Mechanism of action (MAIN)

A

Stimulate inhibitors alpha 2 receptors in the VASOMOTOR CENTER In the brain stem which results in a DECREASE in SNS outflow from this region (BRAINSTEM) to peripheral tissues resulting in
-decreased HR and Myocardiall contractility which decreased CO, peripheral vasodilation

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21
Q

Clonisinw on kidney

A

Decreased renin activity and circulating plasma catecholamine levels.

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22
Q

Clonidine Other mechanism of action

A

Pre synaptic inhibitory alpha 2 receptors in sympathetic peripheral nerve endings resulting in decreased BP and decrease circulating plasma cathecolamines.
COMBINATION of central and peripheral NS effects.

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23
Q

Clonidine antihypertensive effects are caused by a

A

combination of central AND peripheral

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24
Q

EPidurally clonidine produce

A

dose dependent analgesia effects
Because when administered , AGONIZE BOTH PRE AND POST adrenoceptors in the spinal cord .
REDUCES substance P

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25
Q

Clonidine : Mechanism of action on cell membrane.

A

Modifies function of K+ channels, cells membranes become HYPERPOLARIZED
Decrease Aqueous humor and IOP

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26
Q

Dexmetomodine (Precedex )does

A

Same action as CLONIDINE

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27
Q

Sympathetic reflexes

A

Baroreceptor reflexes are blunted by clonidine

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28
Q

Clonidine some affinity for peripheral post synaptic

this occur at doses _____that those required to stimulate central ______alpha 2 receptors. seen in

A

alpha 2 receptors (which can cause vasoconstriction, increased BP)
HIGHER; inhibitory; OVERDOSE

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29
Q

Pharmacokinetics of CLONIDINE:

Half life? peak hypotensive when?, Lipid soluble? duration? distribution? protein binding?

A

T 1/2 ~ 12 hours
Peak hypotensive 1-3 hours
Duration of hypotensive effect after oral dose ~ 8 hours
HIGH VOLUME Distribution: HIGLY LIPID SOLUBLE crosses into CNS
Protein binding : LOW

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30
Q

NOT EVERY LIPOPHILLIC DRUG Is

A

HIGHLY PROTEIN Bound

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31
Q

**Clonidine adverse effects when administered EPIDURALLY and as an INJECTION

A

BRADYCARDIA

HYPOTENSION

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32
Q

CNS side effects of CLONIDINE

A

Sedation and

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33
Q

Clonidine side effects and HYPERTENSIVE

A

IMPOTENCE

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34
Q

Most COMMON side effects of CLONIDINE is

A

Xerostomia sedation and drowsiness

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35
Q

***Adverse effects BLACK BOX FDA EPIDURAL and INJ for CLONIDINE

A

Not recommended
OBSTETRICAL
POSTEPARTUM
PERI-OPERATIVE pain management

RISKS outweighs benefits.

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36
Q

**Clonidine withdrawal Syndrome (can be dangerous)
caused by ___________
How soon after discontinuation ________
with ____Dose (PO, IV, IM, TD)

A

Sudden abrupt discontinuation of clonidine may cause withdrawal , 18-36 hours after discontinuation
ORAL

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37
Q

***Symptoms of clonidine withdrawal syndrome include

Massive ________ _____

A

Massive sympathetic surge

******REBOUND HYPERTENSION****
Apprehension
Nervousness
Abdominal pain
Sweating
Headache
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38
Q

REBOUND HYPERTENSION risk is increased if oral dose was greater than

A

1.2mg /day

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39
Q

• Treatment of the clonidine induced rebound hypertension _______

  1. Restart clonidine if non-life threatening situation
  2. Administer___________
  3. Beta-adrenergic blocking agents (especially nonselective betaadrenergic agents) SHOULD NOT be used alone in this setting, why?
A

1.urgency of reducing the arterial blood pressure:
2. Administering vasodilators such as ***hydralazine, sodium nitroprusside or a combination of α- and β adrenergic blockade (Labetalol IV)
because they may accentuate the rebound hypertension by allowing unopposed α1 adrenergic vasoconstriction caused by activation of the SNS and elevated circulating catecholamines

40
Q

RENIN ANGIONTENSIN-ADOLSERONE SYSTEM

A

Renin (Juxoglomerular cells) BETA -1 receptors kidney afferent

41
Q

Renin converts

Rate limiting step

A

Angiotensinogen to Angiotensin 1 (rate limiting step)

42
Q

Renin secretion increased by

A

Hypotension
Decreased renal perfusion
Decreased Blood Volume (hemorrhage)
Reduction of NA concentration in early distal tubule

43
Q

ACE is a ______Enzymes converting_______

A

Dipeptidyl peptidase enzyme that converts angiotensin I to angiotensin II
Also acts on BRADYKININ , vasodilation substance

44
Q

ACE found in 2 places?

A

Membrane bound in endothelial cells which line blood vessels

LUNGS

45
Q

Tissues with highest concentration of membrane bound ACE

A

Lungs

46
Q

Angiotensin II is

A

POTENT VASOCONTRICTION hormone (more potent than EPI and NE)

47
Q

Angiotensin II binds to ___ ____ ___ receptors

A

AT1, AT2, AT4

48
Q

Angiotensin II Metabolized to Angiotensin

A

III, less potent physiologic responses compared to Angiotensin II

49
Q

Angiotensin II can also produced by

A

non-ACE or Non Ace pathways.

50
Q

Angiotensin II effects mediated via

A

Angiotensin II binding to AT 1 receptor
acts directly on both arteries and veins
Stimulated the synthesis & secretion of ALDOSTERONE from adrenal cortex

51
Q

Aldosterone effects.

A

Increase sodium and water retention

Increase EXCRETION of potassium and hydrogen

52
Q

RAAS Angiotensin II (4 main actions)

A

Stimulate posterior pituitary gland to secrete ADH
Stimulate SNS –> Increase vascular tone
Stimulate ALDOSTERONE
INHBITS renin release, (once enough has occured)

53
Q

ACE inhibitors available agents

A

ends in PRIL

Except ENALAPRILAT not enalapril

54
Q

ACE inhibitors mechanism of action

A

Inhbit ACE conversion angiotensin I to angiotensin II

Prevents angiotensin II mediated vasoconstriction and stimulation

55
Q

Bradykinin levels increases a result of

A

ACE inhibition

56
Q

BRADYKININ levels are too______leading to 2 main side effects ____ and _______

A

HIGH: COUGH and angioedema

57
Q

Most ACEI are

A

prodrugs.

58
Q

ACEI esterified in the liver by

A

Hepatic Esterases NOT CYP 450 enzymes

59
Q

Only active ACE is

A

Captopril
Lisonopril
ENALAPRILAT

60
Q

Which ACEI is the shortest acting ACEI

A

CAPTOPRIL

61
Q

ACEI clinical effects

A

dilate arteries and veins by blocking angiotensin II formation and inhibiting BRADYKININ METABOLISM

62
Q

ACEI decreases both

A

PRELOAD
AFTERLOAD
Decreased MAP< SBP and DBP

63
Q

ACEI and HR

A

DO NOT TOUCH HR

64
Q

Clinical Effects continued ACEI

A

Decreases renal efferent arteriole vasoconstriction

bly blocking angiotensin II formation and angiotensin II

65
Q

ACEI and kidney : Promote renal ______ of _____and ________ by doing what? and by blocking ________ stimulation of ________

A

Promote renal excretion of sodium and water, by blocking angiotensin II in the kidney and by blocking angiotensin II stimulation of aldosterone secretion

66
Q

For HF ACEI: to vascular

A

Reduced vascular remodeling

67
Q

ACEi lacks

A

side effects common with other antihypertensive drugs such as Depression, IMPOTENCE

68
Q

DO Not occur with ACEi

A

CHF, bronchospasm, bradycardia or PVD

DO NOT CAUSE HYPERGLYCEMIA & HYPOKALEMIA

69
Q

ACEI SIDE effects (Acutely)

A
  1. HYPOTENSION
    DRY COUGH
    **HYPERKALEMIA
    **    ANGIOEDEMA
70
Q

Drug induced angioedema caused by (leading cause)

A

ACEi

71
Q

The clinical features of ACEi ANGIOEDEMA are related to what

A

ELEVATED levels of BRADYKININ

72
Q

Angioedema is life threatening treated with

A

Epinephrine 0.3-0.5 ml of 1:1000 Solution SC

73
Q

ACEi should NEVER be given to (3 contraindications)

A

BILATERAL RENAL ARTERY STENOSIS
Pregnant
Previous angioedema

74
Q

Pre-op management with ACEi

A

Hypotension

Hemodynamic instability

75
Q

ACEI Inhibitors * NOT IMPORTANT

A

HTN
HF
MI
LV dysfunction post MI

76
Q

ARB’s

A

Angiotensin II receptor Blocks (ARBs)

77
Q

ARBs blocs which receptor

A

AT1 Angiotensin II

78
Q

ARBs All ends in

A

-sartan

79
Q

ARBs MOA short

A

Selective antagonist of Angiotensin II at the AT1 receptors

80
Q

ARBs mechanism of action

A

Block and interfered with RAAS by blocking the binding of angiotensin II to the AT 1 receptor on th cell membrane, Thereby inhibitor the action of angiotensin II

81
Q

ARBs

A 
Same action of ACEi
Decrease vasoconstriction
Decrease NE released
Decreased ADH and aldosterone release
decreased AFTERLOAD AND PRELOAD
82
Q

ARBs action

A 
Same action of ACEi
Decrease vasoconstriction
Decrease NE released
Decreased ADH and aldosterone release
decreased AFTERLOAD AND PRELOAD
83
Q

Adverse effects of ARB

A

HYPERKALEMIA (K* sparring diuretic)’

84
Q

ABRs side effects less incidence of _____

A

Less incidence of cough and AnGIOEDEMA

85
Q

ARB precautions

A

Attenuated by NSAIDs.

86
Q

NSAIDS

A

decrease BP

87
Q

Direct RENIN Inhibitor

A

Inhibits RAAS first step RENIN

88
Q

ALISKIREN (Tekturna(

A

The first in a new class of orally effective direct renin inhibitors f or the treatment of HTN

89
Q

Tektruna MOA

A

Aliskiren works at the first and rate-limiting step of the reninangiotensin-aldosterone system.
It binds to the active site of renin
and blocks the conversion of angiotensinogen to Ang I, decreasing Ang I levels which subsequently decreases the production of Ang II
• Aliskiren is a highly selective, potent competitive inhibitor of renin

90
Q

Adverse effects Aliskiren

A

Diarrhea HYPERKALEMIA

91
Q 
DRUGS class affecting RAAS
CA-BA-DA
A 
ACE
ARBs
Beta BLOCKERS
ALDOSTERONE antagonists
Direct renin Inhibitors 
Clonidine
92
Q

NEPRILYSIN INHBITOR ______

A

Sacubitril is a neprilysin inhibitor that acts as an enhancer of the natruiretic peptide neurohormonal pathway

93
Q

Sacubitril is only combined with _______in the brand name product ______ and is only use in _______

A

Valsartan
Entresto
Heart failure.

94
Q

Sacubitril MOA
______ rapidly metabolized by _______into active metabolites then inhibits ________
Leads to increased _______ and other vasoactive substances such as _______

A

Prodrugs rapidly by esterase enzyme into the active metabolite–> inhibits NEPRILYSIN
Leads to increase natriuretic petides and other vasoactive substance such as BRADYKININ.

95
Q

Increased levels of bradykinin and the natruiretic peptides results in

A

Increased level of cGMP,
vasodilation (art and veins)
Natriuresis, diuresis
Suppression of aldosterone

96
Q

SACUBITRIL main adverse effects

A

HYPOTENSION

SRNAPharmacology I (29 decks)

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