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Pharmacology > The Vascular System > Flashcards

The Vascular System Flashcards

1
Q
  • Renin
A
  • released by the kidneys in response to  perfusion
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2
Q
  • Angiotensinogen
    (2)
A
  • released by liver
  • converted to angiotensin I by renin
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3
Q
  • Angiotensin I
    (2)
A
  • no known activity
  • converted to angiotensin II by ACE
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4
Q
  • Angiotensin II
    (2)
A
  • causes vasoconstriction, salt retention, vascular growth
  • stimulates release of aldosterone
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5
Q

Direct renin inhibitor
(aliskiren)
MOA

A

Blocks renin activity on angiotensinogen

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6
Q

ACE inhibitors
(captopril, enalapril, etc..)
MOA

A

Prevents ACE from converting angiotensin I to
angiotensin II

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7
Q

Angiotensin receptor blockers
(candesartan, valsartan, etc..)
MOA

A

Blocks angiotensin II activity at the AT1 receptor

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8
Q

Aldosterone antagonists
(eplerenone and spironolactone)
MOA

A

Blocks the activity of aldosterone in the kidneys
and other tissues (i.e. heart, smooth muscle)

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9
Q

Aliskerin
Direct Renin Inhibitor
* Brand name: Tekturna®
* MOA:
* Use:
* ADRs: (3)
* Drug-Drug interactions:
* Increased levels when combined with

A

Direct renin inhibitor- prevent conversion of
angiotensinogen to angiotensin I
Hypertension
Diarrhea(frequent), dyspepsia(occasional), Hypotension
CYP3A4 inhibitors like macrolide
antibiotics

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10
Q

Aliskerin
Direct Renin Inhibitor- Dental Implications
(2)

A
  • Monitor vital signs
  • After supine positioning, have patient sit upright
    for at least 2 minutes before standing to avoid
    orthostatic hypotension
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11
Q

ACE inhibitors
Example: Lisinopril
* Brand name: Prinivil® or Zestril®
* MOA:
* Use: (4)
* ADRs: (6)
* Drug-Drug interactions:
(3)

A

inhibits the angiotensin converting enzyme blocking the
conversion of angiotensin I to angiotensin II
Hypertension, heart failure, post-MI, kidney disease
Cough, angioedema, hypotension, acute renal
insufficiency, hyperkalemia, taste disturbances/dry mouth(rare)

  • NSAIDs- reduced anti-hypertensive effect
  • Alcohol- increased anti-hypertensive effect
  • General anesthesia- increased anti-hypertensive effect
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12
Q

ACE Inhibitors
Dental Implications
(4)

A
  • Orthostatic hypotension: After supine positioning, have patient sit upright for
    at least 2 minutes before standing to avoid orthostatic
    hypotension
  • Monitor vital signs
  • ACE Inhibitor induced cough may make longer dental procedures
    difficult
  • If dental surgery is anticipated evaluate risk of hypotensive episode
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13
Q

Angiotensin Receptor Blockers
Example: Candesartan
* Brand name: Atacand®
* MOA:
* Use: (3)
* ADRs: (3)
* Drug-Drug interactions:
(3)

A

Blocks the AT1 receptor of angiotensin II
Hypertension, heart failure, kidney disease
Hypotension, dizziness, and hyperkalemia

  • Sedative medications- increased anti-hypotensive effects
  • NSAIDs- reduced anti-hypertensive effect
  • General anesthesia- increased anti-hypertensive effect
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14
Q

Angiotensin Receptor Blockers
Dental Implications
(3)

A
  • Orthostatic hypotension:
  • After supine positioning, have patient sit upright for
    at least 2 minutes before standing to avoid orthostatic
    hypotension
  • Monitor vital signs
  • If dental surgery is anticipated evaluate risk of hypotensive episode
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15
Q

Angiotensin Receptor Neprilsyn Inhibitor (ARNI)
Mechanism of action
(2)

A
  • Sacubitril inhibits neprilysin
    resulting in elevated levels of
    B-type natriuretic peptide
    (BNP)
  • Valsartan blocks the
    angiotensin II AT1 receptor
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16
Q

Sacubitril/Valsartan
Angiotensin Receptor Neprilsyn Inhibitor (ARNI)
* Brand name: Entresto®
* MOA:
* Use:
* ADRs:(3)
* Drug-Drug interactions:
* ACE inhibitors- increased risk of —
* Dental implications: (1)

A

Sacubitril inhibits neprilysin resulting in elevated levels of
B-type natriuretic peptide (BNP) and valsartan blocks the
angiotensin II AT1 receptor
Heart Failure reduced ejection fraction (HFrEF)
Hypotension (18%), hyperkalemia (12%), angioedema (1-2%)
angioedema
Watch to hypotension upon rising

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17
Q

Aldosterone antagonists
Mechanism of action

A

Competitive antagonist of the
aldosterone receptor
(myocardium, arterial walls, kidney)

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18
Q

Aldosterone Antagonist
Example: Spironolactone
* Brand name: Aldactone®
* MOA:
* May also be referred to as a —
* Use: (5)
* ADRs: (4)
* Drug-Drug interactions:
(3)

A

Competitively inhibits the action of aldosterone
potassium-sparing diuretic
Hypertension, heart failure, liver failure, edema, primary
hyperaldosteronism
Hyperkalemia, renal insufficiency, gynecomastia(males), dry
mouth

  • NSAIDs
  • reduced anti-hypertensive effect
  • Increased risk of nephrotoxicity
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19
Q

Aldosterone Antagonists
Dental Implications
(2)

A
  • Monitor vital signs
  • Assess salivary flow as a factor in caries,
    periodontal disease, and candidiasis secondary to
    dry mouth from diuretic effect
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20
Q

Key Mediators
* Vasoconstriction
(2)
* Vasodilation
(2)

A
  • Angiotensin II
  • Endothelin-1
  • Nitric oxide
  • Prostaglandin
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21
Q

Increase [Ca++] activates myosin light-chain kinase
(3)

A

1) Phosphorylation of myosin
2) Sensitization of the myofilaments to calcium
3) Inhibition of myosin phosphatase

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22
Q
  • Endothelin-1
A
  • Produced in vascular tissue, smooth muscle, brain,
    kidney, intestines, and adrenal gland
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23
Q
  • Endothelin-2
A
  • Produced in kidney and intestines
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24
Q
  • Endothelin-3
A
  • Produced in brain, kidney, intestine, adrenal gland
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25
Q
  • Receptor types
  • ETA- (3)
  • ETB- (2)
A

vasoconstriction, bronchoconstriction, increase
aldosterone secretion

vasodilation, inhibition of platelet aggregation

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26
Q

Nitric Oxide

A
  • Activates guanylyl cyclase
    resulting in  cGMP   [Ca++]
    leading to relaxation
27
Q

Prostaglandins

A
  • PGI2- prostacyclin
  • Binds to I prostanoid receptor (IP)
  • Activates adenylyl cyclase
    resulting in increase cAMP = decrease [Ca++]
    leading to relaxation
  • Also inhibit platelet aggregation
  • PGG2 and PGH2- prostaglandin
    endoperoxide intermediates
  • Have some constricting activity
28
Q

Direct Acting Vasodilators
(5)

A
  • Calcium Channel Blockers-
  • Minoxidil-
  • Nitroprusside (and other nitrates) -
  • Hydralazine-
  • Ethanol-
29
Q
  • Calcium Channel Blockers-
A

lower intracellular Ca++ concentration

30
Q
  • Dihydrodpyridine type are more selective for
A

smooth muscle

31
Q
  • Minoxidil-
A

opens KATP channels- turns off voltage-dependent Ca++ channels

32
Q
  • Nitroprusside (and other nitrates) -
A

increases intracellular nitric oxide (NO)
concentration

33
Q
  • Hydralazine-
A

blocks intracellular release of Ca++

34
Q
  • Ethanol- unclear-
A

probably thru alteration of centrally controlled vasodilation

35
Q

Dihydropyridine CCB
(2)

A
  • More selective for calcium
    channels in peripheral
    vasculature
  • More effective for
    hypertension
36
Q

Non-Dihydropyridine CCB
(2)

A
  • More selective for calcium
    channels in myocardium
  • More effective for
    arrhythmias
37
Q

Calcium channel blockers- ex: Amlodipine
Direct Acting Vasodilators
* Brand name: Norvasc®
* MOA:
* Use: (2)
* ADRs:
(6)
* Drug-Drug interactions:
(2)

A

Blocks L-type calcium channel in the vascular
smooth muscle (Dihydropyridine type)
Hypertension, and angina
* Edema (common), dizziness, lightheadedness, hypotension, flushing,
gingival enlargement (rare- more common with DHP type)

  • Hypotension with sedatives, opioids, general and inhaled anesthetics
  • NSAIDS reduce blood pressure lowering effect
38
Q

Calcium channel blockers
Dental Implications

A
  • Gingival hyperplasia (up to 10%)
  • Place on frequent recall to monitor for gingival hyperplasia
  • Monitor vital signs
  • Orthostatic hypotension:
  • After supine positioning, have patient sit upright for at least 2
    minutes before standing to avoid orthostatic hypotension
  • Use vasoconstrictors and inhaled anesthetics with caution
39
Q

Minoxidil
Mechanism of action:
(5)

A
  • Opening KATP channels
  • Resulting in hyperpolarization of
    cells
  • Turns off voltage dependent Ca++
    channels
  • Lowering the intracellular Ca++
    concentration
  • Resulting in vascular smooth
    muscle relaxation
40
Q

Minoxidil
Direct Acting Vasodilator
* Brand name: Loniten®
* MOA:
* Use:
* ADRs: (3)
* Drug-Drug interactions:
(2)

A

causes smooth muscle relaxation by opening KATP
channels
Severe resistant hypertension
Hair growth, edema, photosensitivity(rare)

  • Reduced anti-hypertensive effect with NSAIDs and
    sympathomimetic
  • Increased anti-hypertensive effect with sedatives and other drugs
    used for conscious sedation
41
Q

Minoxidil
Dental Implications
(3)

A
  • Monitor vital signs
  • Orthostatic hypotension:
  • After supine positioning, have patient sit upright for at least
    2 minutes before standing to avoid orthostatic hypotension
  • Avoid or limit dose of vasoconstrictor
42
Q
  • Sodium Nitroprusside
    (2)
A
  • Only available for intravenous
    administration
  • Used for acute control of
    hypertension
43
Q
  • Oral/topical nitrate formulation
    (2)
A
  • Used mainly for angina
  • Not effective as anti-hypertensive
    agent, but may have hypotensive
    side effects
44
Q

Sodium Nitroprusside
Direct Acting Vasodilators
* Brand name: Nitropress®
* MOA:
* Use: (1)
* ADRs: (4)
* Drug-Drug interactions:
(1)
* Dental implications:
(1)

A

causes smooth muscle relaxation by increasing
intracellular nitric oxide concentrations
Hypertensive crisis
Methemoglobinemia, hypotension, dizziness, thiocyanate
toxicity
* PDE-5 inhibitors (i.e. sildenafil)
* none

45
Q

Hydralazine
Mechanism of action(maybe)
Proposed MOA:

A

interference with action
of IP3 on calcium release
from sarcoplasmic
reticulum

46
Q

Hydralazine
Direct Acting Vasodilator
* Brand name: Apresoline®
* MOA:
* Use: (2)
* ADRs:
(4)
* Drug-Drug interactions:
(1)

A

Direct acting vasodilator thru interference with action of
IP3 on calcium release from sarcoplasmic reticulum
Hypertension, and heart failure
* Headache, palpitations, GI disturbances, flushed face(rare)
* Reduced anti-hypertensive effect with NSAIDs and
sympathomimetic

47
Q

Hydralazine
Direct Acting Vasodilator-Dental Implications
(3)

A
  • Monitor vital signs
  • Orthostatic hypotension:
  • After supine positioning, have patient sit upright for at least
    2 minutes before standing to avoid orthostatic hypotension
  • Avoid or limit dose of vasoconstrictor
48
Q

Pulmonary Hypertension
* A rare disorder
* Estimated prevalence of — cases per million persons
* Defined by a mean pulmonary artery pressure ≥ — at rest

A

15-50
25mmHg

49
Q

Pulmonary Hypertension
Sub-divided into five classifications depending in etiology
* Group I-
* Group II-
* Group III-
* Group IV-
* Group V-

A

Pulmonary arterial HTN (PAH) – primary pulmonary HTN
Pulmonary HTN due to left heart disease
Pulmonary HTN due to lung disease
Chronic thromboembolic pulmonary HTN (CTEPH)
Pulmonary HTN with unclear mechanism

50
Q

Endothelin receptor antagonist (ERA)
Mechanism of Action

A

Mechanism of action:
* Block the ETA receptor
* Decreasing the formation of IP3
* Lowering the intracellular Ca++
concentration
* Resulting in vascular smooth
muscle relaxation
Most ERAs block both ETA and ETB
- but have a high affinity for ETA

51
Q

Bosentan
Endothelin receptor antagonists
* Brand name: Tracleer®
* MOA:
* Use:
* ADRs:
(4)
* Drug-Drug interactions:
(1)
* Pregnancy category- –

A

Endothelin 1 receptor antagonist
Pulmonary hypertension WHO FC III and IV
* Headache, flushed face, dyspepsia, liver dysfunction
* Increased levels when used with ketoconazole
X

52
Q

Bosentan
Endothelin receptor antagonists-Dental Implications
(5)

A
  • Monitor vital signs
  • High risk patient
  • Acute pulmonary hypertension could occur
  • Bleeding gums has been reported with endothelin receptor
    antagonists (no specific reports with bosentan)
  • Limit or avoid vasoconstrictors
  • Low risk of orthostatic hypotension
53
Q

Phosphodiesterase 5 (PDE5) inhibitors
Mechanism of Action

A

Mechanism of action:
* Inhibit action of PDE5
* Increase intracellular cGMP
concentration
* Lowering the intracellular Ca++
concentration
* Resulting in vascular smooth
muscle relaxation
PDE5 inhibitors are also used
(more commonly) to treat erectile
dysfunction

54
Q

Sildenafil
Phosphodiesterase 5 (PDE5) inhibitor
* Brand name: Revatio™(PAH) or Viagra®(ED)
* MOA:
* Use: (3)
* ADRs:
(4)
* Drug-Drug interactions:
(2)

A

Phosphodiesterase 5 inhibitor
Pulmonary hypertension, erectile dysfunction, and BPH
* Headache, flushed face, dyspepsia, rash

  • Sodium Nitroprusside- avoid combination- severe hypotension
  • Increased levels with CYP 3A4 inhibition (i.e. erythromycin,
    clarithromycin, etc.)
55
Q

Sildenafil
Phosphodiesterase 5 (PDE5) inhibitor-Dental
Implications
(5)

A
  • Monitor vital signs
  • High risk patient- if using for PAH
  • Acute pulmonary hypertension could occur
  • Limit or avoid vasoconstrictors
  • Avoid use of nitroglycerin of nitroprusside
  • Low risk of orthostatic hypotension
56
Q

Prostacyclin analogues
Mechanism of Action
(5)

A

Mechanism of action:
* Bind to prostacyclin receptor (IP)
* Stimulate activity of adenylate
cyclase (AC)
* Increase intracellular cyclic AMP
levels
* Lowering the intracellular Ca++
concentration
* Resulting in vascular smooth
muscle relaxation

57
Q

Treprostinil
Prostacyclin analogue
* Brand name: Orenitram®(PO), Tyvaso™(INH), Remodulin™(IV/SQ)
* MOA:
* Use:
* ADRs:
(6)
* Drug-Drug interactions:
(1)

A

Prostacyclin analogue
Pulmonary hypertension
* Headache, flushing, hypotension, infusion site pain
* jaw pain, inhibition of platelet aggregation (
increase r/o bleeding)

  • Other drugs that increased r/o bleeding (i.e. NSAIDS)
58
Q

Prostacyclin analogues
Dental Implications
(4)

A
  • Monitor vital signs
  • High risk patient
  • Acute pulmonary hypertension could occur
  • Continuous infusion can not be interrupted
  • Increased risk of bleeding
  • Inhibits platelet aggregation
  • Limit or avoid vasoconstrictors
59
Q

Selexipag
Mechanism of Action
Mechanism of action:
(5)

A
  • Selective prostacyclin IP receptor
    agonist
  • Stimulate activity of adenylate
    cyclase (AC)
  • Increase intracellular cyclic AMP
    levels
  • Lowering the intracellular Ca++
    concentration
  • Resulting in vascular smooth
    muscle relaxation
60
Q

Selexipag
Selective prostacyclin IP receptor agonist
* Brand name: Uptravi®
* MOA:
* Use:
* ADRs:
(2)
* Drug-Drug interactions:
(1)

A

IP receptor agonist
Pulmonary hypertension Group I
* Flushing, Headache(65%), diarrhea (42%)
* Jaw pain (26%)
* None noted

61
Q

Selexipag
Selective prostacyclin IP receptor agonist
(3)

A
  • Monitor vital signs
  • High risk patient
  • Acute pulmonary hypertension could occur
  • Limit or avoid vasoconstrictors
62
Q

Soluble guanylate cyclase stimulator
Mechanism of Action
Mechanism of action:
(4)

A
  • Sensitizes guanylyl cyclase to nitric
    oxide but also directly activates
    guanylyl cyclase
  • Increase intracellular cGMP
    concentration
  • Lowering the intracellular Ca++
    concentration
  • Resulting in vascular smooth
    muscle relaxation
63
Q

Riociguat
Soluble guanylate cyclase stimulator
* Brand name: Adempas®
* MOA:
* Use:
* ADRs:
(4)
* Drug-Drug interactions:
(2)
* Pregnancy category- —

A

Soluble guanylate cyclase stimulator
Pulmonary hypertension group 1 and 4 (CTEPH)
* Hypotension, dyspepsia, headache, edema

  • Avoid combination with PDE5 inhibitors
  • Decrease effects with CYP 3A4/2C8 inducers
    X
64
Q

Riociguat
Soluble guanylate cyclase stimulator-Dental Implications
(4)

A
  • Monitor vital signs
  • High risk patient
  • Acute pulmonary hypertension could occur
  • Limit or avoid vasoconstrictors
  • Increased risk of bleeding
  • Risk of unanticipated bleeding during procedure

Pharmacology (13 decks)

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