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vascular system Flashcards

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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
candesartan drug interactions: * Sedative medications * NSAIDs * General anesthesia
* Sedative medications- increased anti-hypotensive effects * NSAIDs- reduced anti-hypertensive effect * General anesthesia- increased anti-hypertensive effect
26
Angiotensin Receptor Blockers Dental Implications
* 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
27
angiotensin receptor neprilsyn inhibitor MOA
28
Sacubitril/Valsartan MOA's
* MOA: Sacubitril inhibits neprilysin resulting in elevated levels of B-type natriuretic peptide (BNP) and valsartan blocks the angiotensin II AT1 receptor
29
Sacubitril/Valsartan ADRs
Hypotension, hyperkalemia, angioedema
30
Sacubitril/Valsartan drug interactions: ACEi?
ACE inhibitors- increased risk of angioedema
31
Sacubitril/Valsartan dental
Watch to hypotension upon rising
32
Aldosterone antagonists Mechanism of action (where?)
Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney)
33
ALDOSTERONE Cardiac and renal effects
34
Aldosterone antagonists names
spironolactone eplerenone
35
Spironolactone moa also referred to as?
Competitively inhibits the action of aldosterone * May also be referred to as a potassium-sparing diuretic
36
sprionolactone ADRs
Hyperkalemia, renal insufficiency, gynecomastia(males), dry mouth
37
spironolactone drug interactions: NSAIDs
* NSAIDs: reduced anti-hypertensive effect and Increased risk of nephrotoxicity
38
Aldosterone Antagonists Dental Implications
* Monitor vital signs * Assess salivary flow as a factor in caries, periodontal disease, and candidiasis secondary to dry mouth from diuretic effect
39
Vascular Smooth Muscle Tone Key Mediators of constriction and dialation
* Vasoconstriction: Angiotensin II and Endothelin-1 * Vasodilation: Nitric oxide and Prostaglandin
40
vacular smooth mm cell contraction mechanism
41
Endothelins in Vascular Tone
Endothelin 1, 2, and 3 involved working on ET A and B receptors
42
* Endothelin-1 | produced where?
* Produced in vascular tissue, smooth muscle, brain, kidney, intestines, and adrenal gland
43
Endothelin-2 | produced in?
* Produced in kidney and intestine
44
Endothelin-3
* Produced in brain, kidney, intestine, adrenal gland
45
ETA actions
vasoconstriction, bronchoconstriction, increased aldosterone secretion
46
ETB actions
vasodilation, inhibition of platelet aggregation
47
Nitric Oxide moa
Activates guanylyl cyclase resulting in increased cGMP = decreased [Ca++] leading to relaxation
48
prostaglandins of vascular tone
PGI2, PGG2 and PGH2
49
PGI2 additional name? MOA? can also cause?
prostacyclin * Binds to I prostanoid receptor (IP) * Activates adenylyl cyclase resulting in increased cAMP= decreasd [Ca++] leading to relaxation * Also inhibit platelet aggregation
50
PGG2 and PGH2
prostaglandin endoperoxide intermediates * Have some constricting activity
51
Direct Acting Vasodilators and MOAs
* **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
Calcium Channel Blockers names/ classes
53
Dihydropyridine CCB MOA
* More selective for calcium channels in peripheral vasculature * More effective for hypertension -dipines
54
Non-Dihydropyridine CCB MOA
* More selective for calcium channels in myocardium * More effective for arrhythmias dialtezem and verampril
55
amlodipine moa
Blocks L-type calcium channel in the vascular smooth muscle (Dihydropyridine type)
56
amlodipine ADRs
Edema, dizziness, lightheadedness, hypotension, flushing, gingival enlargement
57
amlodipine interactions: * sedatives, opioids, general and inhaled anesthetics? * NSAIDS?
* Hypotension with sedatives, opioids, general and inhaled anesthetics * NSAIDS reduce blood pressure lowering effect
58
Calcium channel blockers Dental Implications
* 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
Minoxidil Mechanism of action
* 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
Minoxidil ADRs
Hair growth, edema, photosensitivity (rare)
61
Minoxidil interactions: * Reduced anti-hypertensive effect with? * Increased anti-hypertensive effect with?
* Reduced anti-hypertensive effect with NSAIDs and sympathomimetic * Increased anti-hypertensive effect with sedatives and other drugs used for conscious sedation
62
Minoxidil Dental Implications
* 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
Sodium Nitroprusside Mechanism of action | other forms?
* 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
Sodium Nitroprusside MOA
increase intra cell NO
65
Sodium Nitroprusside ADR
Methemoglobinemia, hypotension, dizziness, thiocyanate toxicity
66
Sodium Nitroprusside interactions
* PDE-5 inhibitors (i.e. sildenafil)
67
Hydralazine Proposed MOA:
interference with action of IP3 on calcium release from sarcoplasmic reticulum
68
Hydralazine ADRs
Headache palpitations GI disturbances flushed face (rare)
69
hydralazine interactions: Reduced anti-hypertensive effect with?
Reduced anti-hypertensive effect with NSAIDs and sympathomimetic
70
Hydralazine Dental Implications
* 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
Pulmonary Hypertension * rare? * Estimated prevalence? * Defined by?
* A rare disorder * Estimated prevalence of 15-50 cases per million persons * Defined by a mean pulmonary artery pressure ≥ 25mmHg at rest
72
classifications of pul HTN
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
World Health Organization Functional Class of pul htn
74
Drug Therapies for PAH | classes of drugs
Endothelin receptor antagonists (ERA) Phosphodiesterase 5 (PDE5) inhibitors Prostacyclin analogue Soluble guanylate cyclase stimulator selective prostacyclin IP receptor agonist
75
PDE5 inhibitors names
Sildenafil Tadalafil
76
prostacylin analogues/ forms
Epoprostenol, Available: IV Iloprost, Available: Inhalation (Inh) **Treprostinil, Available: PO, Inh, IV, and SQ**
77
soluble GC stimulator
riociguat
78
selective prostacyclin IP receptor agonist
selexipag
79
what Rx can cause dose dependent jaw pain?
Prostacyclin analogues: Epoprostenol Iloprost Treprostinil
80
endothelin receptor antag names
All end in -entan Ambrisentan Bosentan Macitentan
81
Endothelin receptor antagonist (ERA) Mechanism of Action
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
Bosentan moa
Endothelin 1 receptor antagonist
83
bosentan adrs
Headache, flushed face, dyspepsia, liver dysfunction
84
bosentan interactions: Increased levels when used with?
Increased levels when used with ketoconazole
85
bosentan preg category
x
86
Endothelin receptor antagonists-Dental Implications
* 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
Phosphodiesterase 5 (PDE5) inhibitors 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
88
Sildenafil moa
Phosphodiesterase 5 inhibitor
89
Sildenafil ADR
Headache, flushed face, dyspepsia, rash
90
Sildenafil interactions: * Sodium Nitroprusside? * Increased levels with?
* Sodium Nitroprusside- avoid combination- severe hypotension * Increased levels with CYP 3A4 inhibition (i.e. erythromycin, clarithromycin, etc.)
91
Sildenafil Phosphodiesterase 5 (PDE5) inhibitor Dental Implications
* 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
Prostacyclin analogues 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
93
Treprostinil moa
Prostacyclin analogue
94
Treprostinil adrs
Headache, flushing, hypotension, infusion site pain * jaw pain, inhibition of platelet aggregation (increased r/o bleeding)
95
Treprostinil interactions: Other drugs that?
* Other drugs that increased r/o bleeding (i.e. NSAIDS
96
Prostacyclin analogues Dental Implications
* 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
Selexipag Mechanism of Action
* 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
Selexipag moa
IP receptor agonist
99
Selexipag adrs
* Flushing, Headache, diarrhea * Jaw pain
100
Selexipag interactions
none
101
Selexipag- Selective prostacyclin IP receptor agonist dental
* Monitor vital signs * High risk patient: Acute pulmonary hypertension could occur * Limit or avoid vasoconstrictors
102
Soluble guanylate cyclase stimulator Mechanism of Action
* 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
Riociguat moa
Soluble guanylate cyclase stimulator
104
Riociguat adrs
* Hypotension, dyspepsia, headache, edema
105
Riociguat interactions: * Avoid combination with? * Decrease effects with?
* Avoid combination with PDE5 inhibitors * Decrease effects with CYP 3A4/2C8 inducers
106
Riociguat and pregnancy
category x
107
Riociguat Soluble guanylate cyclase stimulator-Dental Implications
* 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
Jaw Pain ADR * Unique side effect to? why? * Often occurs with? * dose limiting? * Management?
* 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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