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vascular system Flashcards

1
Q

Renin

A
  • released by the kidneys in response to decrese perfusion
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2
Q

RAAS

A
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3
Q

Angiotensinogen

A
  • released by liver
  • converted to angiotensin I by renin
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4
Q

Angiotensin I

A
  • no known activity
  • converted to angiotensin II by ACE
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5
Q

Angiotensin II

A
  • causes vasoconstriction, salt retention, vascular growth
  • stimulates release of aldosterone
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6
Q

Medications classes effecting the RAAS

A

Direct renin inhibitor
ACEi
Angiotensin receptor blockers
Aldosterone antagonists

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7
Q

Direct Renin Inhibitor
Mechanism of action

A
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8
Q

Aliskerin

A

direct renin inhibitor

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9
Q

Aliskerin MOA

A

Direct renin inhibitor- prevent conversion of
angiotensinogen to angiotensin I

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10
Q

Aliskerin ADRs

A

Diarrhea, dyspepsia, Hypotension

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11
Q

aliskerin drug interactions
Increased levels with?

A

Increased levels when combined with CYP3A4 inhibitors like macrolide antibiotics

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12
Q

Aliskerin dental implications

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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13
Q

ACEi MOA diagrammed

A
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14
Q

ACEi suffix

A

-pril

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15
Q

ACE Inhibitors
Adverse drug reactions/ contraindications

mneumonic?

A

C: Cough (up to 10%)
A: Angioedema (<1%) / Agranulocytosis (rare)
P: Potassium excess (hyperkalemia 1-10%)/Proteinuria (rare)
T: Taste change (2-4%)
O: Orthostatic hypotension (~5%)
P: Pregnancy (contraindication)
R: Renal artery stenosis- bilateral (contraindication)
I: Increased serum creatinine (1-10%- transient)
L: Leukopenia (rare) / Liver Toxicity (rare

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16
Q

lisinopril MOA

A

inhibits the angiotensin converting enzyme blocking the
conversion of angiotensin I to angiotensin II

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17
Q

lisinopril ADRs

A

Cough, angioedema, hypotension, acute renal
insufficiency, hyperkalemia, taste disturbances/dry mouth(rare)

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18
Q

Lisinopril drug interactions:
* NSAIDs
* Alcohol
* General anesthesia

A
  • NSAIDs- reduced anti-hypertensive effect
  • Alcohol- increased anti-hypertensive effect
  • General anesthesia- increased anti-hypertensive effect
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19
Q

ACE Inhibitors
Dental Implications

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 proceduresdifficult
  • If dental surgery is anticipated evaluate risk of hypotensive episode
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20
Q

Angiotensin II Receptor Blockers
Mechanism of action diagram

A
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21
Q

Angiotensin Receptor blockers suffix

A

-sartan

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22
Q

Angiotensin Receptor Blockers
Adverse drug reactions

menumonic? do not cause?

A

Halt Dangerous Hypertension:
* Headache / Hypotension
* Dizziness
* Hyperkalemia

DO NOT CAUSE: Cough and Angioedema (probably)

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23
Q

candesartan MOA

A

Blocks the AT1 receptor of angiotensin II

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24
Q

candesartan ADRs

A

Hypotension, dizziness, and hyperkalemia

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25
Q

candesartan drug interactions:
* Sedative medications
* NSAIDs
* General anesthesia

A
  • Sedative medications- increased anti-hypotensive effects
  • NSAIDs- reduced anti-hypertensive effect
  • General anesthesia- increased anti-hypertensive effect
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26
Q

Angiotensin Receptor Blockers
Dental Implications

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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27
Q

angiotensin receptor neprilsyn inhibitor MOA

A
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28
Q

Sacubitril/Valsartan MOA’s

A
  • MOA: Sacubitril inhibits neprilysin resulting in elevated levels of B-type natriuretic peptide (BNP) and valsartan blocks the angiotensin II AT1 receptor
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29
Q

Sacubitril/Valsartan ADRs

A

Hypotension, hyperkalemia, angioedema

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30
Q

Sacubitril/Valsartan drug interactions:
ACEi?

A

ACE inhibitors- increased risk of angioedema

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31
Q

Sacubitril/Valsartan dental

A

Watch to hypotension upon rising

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32
Q

Aldosterone antagonists Mechanism of action
(where?)

A

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

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33
Q

ALDOSTERONE
Cardiac and renal effects

A
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34
Q

Aldosterone antagonists names

A

spironolactone
eplerenone

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35
Q

Spironolactone moa
also referred to as?

A

Competitively inhibits the action of aldosterone
* May also be referred to as a potassium-sparing diuretic

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36
Q

sprionolactone ADRs

A

Hyperkalemia, renal insufficiency, gynecomastia(males), dry mouth

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37
Q

spironolactone drug interactions:
NSAIDs

A
  • NSAIDs: reduced anti-hypertensive effect and Increased risk of nephrotoxicity
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38
Q

Aldosterone Antagonists
Dental Implications

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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39
Q

Vascular Smooth Muscle Tone
Key Mediators of constriction and dialation

A
  • Vasoconstriction: Angiotensin II and Endothelin-1
  • Vasodilation: Nitric oxide and Prostaglandin
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40
Q

vacular smooth mm cell contraction mechanism

A
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41
Q

Endothelins in Vascular Tone

A

Endothelin 1, 2, and 3 involved working on ET A and B receptors

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42
Q
  • Endothelin-1

produced where?

A
  • Produced in vascular tissue, smooth muscle, brain,
    kidney, intestines, and adrenal gland
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43
Q

Endothelin-2

produced in?

A
  • Produced in kidney and intestine
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44
Q

Endothelin-3

A
  • Produced in brain, kidney, intestine, adrenal gland
45
Q

ETA actions

A

vasoconstriction, bronchoconstriction, increased aldosterone secretion

46
Q

ETB actions

A

vasodilation, inhibition of platelet aggregation

47
Q

Nitric Oxide moa

A

Activates guanylyl cyclase resulting in increased cGMP = decreased [Ca++] leading to relaxation

48
Q

prostaglandins of vascular tone

A

PGI2, PGG2 and PGH2

49
Q

PGI2
additional name?
MOA?
can also cause?

A

prostacyclin
* Binds to I prostanoid receptor (IP)
* Activates adenylyl cyclase resulting in increased cAMP= decreasd [Ca++] leading to relaxation
* Also inhibit platelet aggregation

50
Q

PGG2 and PGH2

A

prostaglandin endoperoxide intermediates
* Have some constricting activity

51
Q

Direct Acting Vasodilators and MOAs

A
  • Calcium Channel Blockers- lower intracellular Ca++ concentration- Dihydrodpyridine type are more selective for smooth muscle
  • Minoxidil- opens KATP channels- turns off voltage-dependent Ca++ channels
  • Nitroprusside (and other nitrates) - increases intracellular nitric oxide (NO) concentration
    * Hydralazine- blocks intracellular release of Ca++
  • Ethanol- unclear- probably thru alteration of centrally controlled vasodilation
52
Q

Calcium Channel Blockers names/ classes

53
Q

Dihydropyridine CCB MOA

A
  • More selective for calcium channels in peripheral
    vasculature
  • More effective for hypertension
    -dipines
54
Q

Non-Dihydropyridine CCB MOA

A
  • More selective for calcium channels in myocardium
  • More effective for arrhythmias
    dialtezem and verampril
55
Q

amlodipine moa

A

Blocks L-type calcium channel in the vascular
smooth muscle (Dihydropyridine type)

56
Q

amlodipine ADRs

A

Edema, dizziness, lightheadedness, hypotension, flushing, gingival enlargement

57
Q

amlodipine interactions:
* sedatives, opioids, general and inhaled anesthetics?
* NSAIDS?

A
  • Hypotension with sedatives, opioids, general and inhaled anesthetics
  • NSAIDS reduce blood pressure lowering effect
58
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
59
Q

Minoxidil
Mechanism of action

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
60
Q

Minoxidil ADRs

A

Hair growth, edema, photosensitivity (rare)

61
Q

Minoxidil interactions:
* Reduced anti-hypertensive effect with?
* Increased anti-hypertensive effect with?

A
  • Reduced anti-hypertensive effect with NSAIDs and
    sympathomimetic
  • Increased anti-hypertensive effect with sedatives and other drugs used for conscious sedation
62
Q

Minoxidil Dental Implications

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
63
Q

Sodium Nitroprusside
Mechanism of action

other forms?

A
  • Sodium Nitroprusside
  • Only available for intravenous administration
  • Used for acute control of hypertension
  • Oral/topical nitrate formulation
  • Used mainly for angina
  • Not effective as anti-hypertensive agent, but may have hypotensive side effects
64
Q

Sodium Nitroprusside MOA

A

increase intra cell NO

65
Q

Sodium Nitroprusside ADR

A

Methemoglobinemia, hypotension, dizziness, thiocyanate toxicity

66
Q

Sodium Nitroprusside interactions

A
  • PDE-5 inhibitors (i.e. sildenafil)
67
Q

Hydralazine Proposed MOA:

A

interference with action of IP3 on calcium release
from sarcoplasmic reticulum

68
Q

Hydralazine ADRs

A

Headache
palpitations
GI disturbances
flushed face (rare)

69
Q

hydralazine interactions:
Reduced anti-hypertensive effect with?

A

Reduced anti-hypertensive effect with NSAIDs and sympathomimetic

70
Q

Hydralazine Dental Implications

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 vasoconstricto
71
Q

Pulmonary Hypertension
* rare?
* Estimated prevalence?
* Defined by?

A
  • A rare disorder
  • Estimated prevalence of 15-50 cases per million persons
  • Defined by a mean pulmonary artery pressure ≥ 25mmHg at rest
72
Q

classifications of pul HTN

A

Sub-divided into five classifications depending in etiology
* Group I- Pulmonary arterial HTN (PAH) – primary pulmonary HTN
* Group II- Pulmonary HTN due to left heart disease
* Group III- Pulmonary HTN due to lung disease
* Group IV- Chronic thromboembolic pulmonary HTN (CTEPH)
* Group V- Pulmonary HTN with unclear mechanism

73
Q

World Health Organization Functional Class of pul htn

74
Q

Drug Therapies for PAH

classes of drugs

A

Endothelin receptor antagonists (ERA)
Phosphodiesterase 5 (PDE5) inhibitors
Prostacyclin analogue
Soluble guanylate cyclase stimulator
selective prostacyclin IP receptor agonist

75
Q

PDE5 inhibitors names

A

Sildenafil
Tadalafil

76
Q

prostacylin analogues/ forms

A

Epoprostenol, Available: IV
Iloprost, Available: Inhalation (Inh)
Treprostinil, Available: PO, Inh, IV, and SQ

77
Q

soluble GC stimulator

78
Q

selective prostacyclin IP receptor agonist

79
Q

what Rx can cause dose dependent jaw pain?

A

Prostacyclin analogues:
Epoprostenol
Iloprost
Treprostinil

80
Q

endothelin receptor antag names

A

All end in -entan
Ambrisentan
Bosentan
Macitentan

81
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

82
Q

Bosentan moa

A

Endothelin 1 receptor antagonist

83
Q

bosentan adrs

A

Headache, flushed face, dyspepsia, liver dysfunction

84
Q

bosentan interactions:
Increased levels when used with?

A

Increased levels when used with ketoconazole

85
Q

bosentan preg category

86
Q

Endothelin receptor antagonists-Dental Implications

A
  • Monitor vital signs
  • High risk patient
  • Acute pulmonary hypertension could occur
  • Bleeding gums has been reported
  • Limit or avoid vasoconstrictors
  • Low risk of orthostatic hypotension
87
Q

Phosphodiesterase 5 (PDE5) inhibitors
Mechanism of Action

A
  • 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

88
Q

Sildenafil moa

A

Phosphodiesterase 5 inhibitor

89
Q

Sildenafil ADR

A

Headache, flushed face, dyspepsia, rash

90
Q

Sildenafil interactions:
* Sodium Nitroprusside?
* Increased levels with?

A
  • Sodium Nitroprusside- avoid combination- severe hypotension
  • Increased levels with CYP 3A4 inhibition (i.e. erythromycin, clarithromycin, etc.)
91
Q

Sildenafil
Phosphodiesterase 5 (PDE5) inhibitor Dental Implications

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
92
Q

Prostacyclin analogues
Mechanism of Action

A
  • 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
93
Q

Treprostinil moa

A

Prostacyclin analogue

94
Q

Treprostinil adrs

A

Headache, flushing, hypotension, infusion site pain
* jaw pain, inhibition of platelet aggregation (increased r/o bleeding)

95
Q

Treprostinil interactions:
Other drugs that?

A
  • Other drugs that increased r/o bleeding (i.e. NSAIDS
96
Q

Prostacyclin analogues Dental Implications

A
  • Monitor vital signs
  • High risk patient: Acute pulmonary hypertension could occur and Continuous infusion can not be interrupted
  • Increased risk of bleeding: Inhibits platelet aggregation
  • Limit or avoid vasoconstrictors
97
Q

Selexipag
Mechanism of Action

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
98
Q

Selexipag moa

A

IP receptor agonist

99
Q

Selexipag adrs

A
  • Flushing, Headache, diarrhea
  • Jaw pain
100
Q

Selexipag interactions

101
Q

Selexipag- Selective prostacyclin IP receptor agonist
dental

A
  • Monitor vital signs
  • High risk patient: Acute pulmonary hypertension could occur
  • Limit or avoid vasoconstrictors
102
Q

Soluble guanylate cyclase stimulator
Mechanism of Action

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
103
Q

Riociguat moa

A

Soluble guanylate cyclase stimulator

104
Q

Riociguat adrs

A
  • Hypotension, dyspepsia, headache, edema
105
Q

Riociguat interactions:
* Avoid combination with?
* Decrease effects with?

A
  • Avoid combination with PDE5 inhibitors
  • Decrease effects with CYP 3A4/2C8 inducers
106
Q

Riociguat and pregnancy

A

category x

107
Q

Riociguat
Soluble guanylate cyclase stimulator-Dental Implications

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
108
Q

Jaw Pain ADR
* Unique side effect to? why?
* Often occurs with?
* dose limiting?
* Management?

A
  • Unique side effect to prostacyclin pathway therapies
  • Prostacyclin is a mediator in inflammation and pain- May produce hyperalgesia
  • Often occurs with 1st bite of meal
  • Generally, not dose limiting
  • Management:
  • Taking slow bites
  • Sucking on a saltine cracker or hard candy, or chewing gum before eating

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