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Pharmacology I > The Vascular System > Flashcards

The Vascular System Flashcards

1
Q

what is renin released by

A

the kidneys in response to perfusion

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2
Q

angiotensinogen is released by:

A

the liver

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3
Q

angiotensinogen is converted to angiotensin I by:

A

renin

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4
Q

angiotensin II causes:

A

vasoconstriction, salt retention, vascular growth

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5
Q

angiotensin II stimulates:

A

release of aldosterone

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6
Q

what is the MOA of direct renin inhibitor

A

blocks renin activity on angioteninsogen

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7
Q

what is the MOA of ACE inhibitors

A

prevents ACE from converting angiotensin I to angiotensin II

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8
Q

what is the MOA of angiotensin receptor blockers

A

blocks angiotensin II activity at the AT1 receptor

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9
Q

what is the MOA of aldosterone antagonists

A

blocks the activity of aldosterone in the kidneys and other tissues

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10
Q

what is the use for direct renin inhibitor and MOA and drug to drug interactions and ADRs

A
  • prevent conversion of angiotensinogen to angiotensin I
  • use: HTN
  • increased levels when combined with CYP3A4 inhibitors like macrolide ABs
  • ADRs: diarrhea, dyspepsia, hypotension*
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11
Q

what are the dental considerations with direct renin inhibitors

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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12
Q

what does angiotensin cause

A
  • aldosterone release
    = vasoppressin release
  • sympathetic
  • vasoconstriction
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13
Q

what else do ACE inhibitors act on

A

kininase II which inhibits bradykinin which results in cough and vasodilation

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14
Q

what are the ACE inhibitors

A
  • the “prils”
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15
Q

what is the mneumonic for adverse drug reactions to ACEi

A
  • CAPTOPRIL
  • Angioedema/agranulocytosis
  • potassium excess/proteinuria
  • taste changes
  • orthostatic hypotension
  • pregnancy - contraindication
  • renal artery stenosis- bilateral - contraindication
  • increased serum creatinine
  • leukopenia/liver toxicity
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16
Q

what is the MOA, use, ADRs, and drug-drug itneractions dor ACEi

A
  • inhibits the angiotensin converting enzyme blocking the conversion of angiotensin I to angiotensin II
  • HTN, HF, post MI, kidney disease
  • ADRs: cough, angioedema, hypotension, acute renal insufficiency, hyperkalemia, taste distrubances,
  • drug interactions: NSAIDs, alcohol, general anesthesia
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17
Q

what are the dental implications for ACEi

A
  • orthostatic hypotension
  • minotr vital signs
  • ACEi cough may make dental procedures difficult
  • if dental surgery is anticipated evaluate risk of hypotensive episode
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18
Q

what is the MOA of angiotensin II receptor blockers

A

-angiotensinogen -> angiotensin I -> angiotensin II -> works on AT1 and AT2 receptors
- AT1 receptors cause vasoconstriction and proliferative action
- AT2 receptors cause vasodilation and antiproliferative action

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19
Q

what are the drugs that are angiotensin receptor blockers

A

the “sartans”

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20
Q

what are the adverse drug reactions for angiotensin receptor blockers and how do we remember this

A
  • Halt Dangerous Hypertension
  • Headache/hypotension
  • dizziness
  • hyperkalemia
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21
Q

what is the MOA, use, ADRs, and drug interactions with angiotensin receptor blockers

A
  • MOA: blocks the AT1 receptor of angiotensin II
  • use: HTN, HF, kidney disease
  • ADRs: hypotension, dizziness and hyperkalemia
  • drug interactions: sedative meds, NSAIDs, general anesthesia
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22
Q

what are the dental implications for angiotensin receptor blockers

A
  • orthostatic hypotension
  • monitor vital signs
  • if dental surgery is anticipated evaluate risk of hypotensive episode
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23
Q

what is the MOA for angiotensin recpetor Neprilsyn inhibitor

A

Sacubitril inhibits nepryilysin resulting in evaluated levels of B-type natriuretic peptide
- valsartan blocks the angiotensin II AT1 receptor

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24
Q

what is the use, ADRs and drug interactions of Sacubritril/valsartan

A
  • USE: HF reduced ejectin fraction
  • ADRs; hypotension, hyperkalemia, angioedema
  • drug interactions: increased risk of angioedme
  • dental implications: watch to hypotension upon rising
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25
Q

what is the MOA of aldosterone antagonists

A

competitive antagonist of the aldosterone receptor (myocardium, arterial walls and kidneys)

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26
Q

what is the result of aldosterone antagonists

A
  • retention of Na+ and H2O -> edema
  • exceretion K+ and Mg2+ -> arrythmias
  • collagen deposition -> fibrosis of myocardium and vessels
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27
Q

what is an example of aldosterone antagonist, use, ADRs, and drug interactions

A
  • spironolactone
  • use: HTN, HF, liver failure*, edmea, primary hyperaldosteronism
  • ADRs: hyperkalemia, renal insufficiency, gynecomastia, dry mouth
  • drug interactions: NSAIDS
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28
Q

what are the dental implications of aldosterone antagonists

A
  • monitor vital signs
  • assess salivary flow as a factor in caries, perio disease and candidiasis from dry mouth effect
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29
Q

what are the key mediators that cause vasoconstrictions

A
  • angiotensin II
  • endothelin 1
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30
Q

what are the key mediators in vasodilation

A
  • NO
  • prostaglandin
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31
Q

how do you increase contraction in vascular smooth muscle cells

A
  • increased calcium activates myosin light chain kinase through:
  • phosphorylation of myosin
  • sensitization of the myofilaments to calcium
  • inhibition of myosin phosphatase
32
Q

decreased intracellular calcium leads to ____ in SM

A

relaxation

33
Q

where is endothelin 1 produced

A

vascular tissue, smooth muscle, brain, kidney, intestines and adrenal gland

34
Q

where is endothelin 2 produced

A

kidney and intestines

35
Q

where is endothelin 3 produced

A

brain, kidney, intestine, adrenal gland

36
Q

what are the the endothelin receptor types and what do each cause

A
  • ETA: vasoconstriction, bronchoconstriction, aldosterone secretion
  • ETB: vasodilation, inhibition of platelet aggregation
37
Q

what does NO do

A

activates guanylyl cylase resulting in increase in cGMP -> reduction in calcium in cell

38
Q

what are the prostaglandins and what do each do

A
  • PGI2: prostacyline, binds to IP receptor and activates adenylyl cyclase -> cAMP leading to relaxation. also inhibits platelet aggregation
  • PGG2 and PGH2 - prostaglandin endoperoxide intermediates: have some constricting activity
39
Q

what are the direct acting vasodilators

A
  • calcium channel blockers
  • minoxidil
  • nitroprusside
  • hydralazine
  • ethanol
40
Q

what are the two types of calcium channel blockerd

A
  • dihydropyridine: end in “dipine”
  • non- dihydropyridine: eirhter dilitiazem and verapamil
41
Q

describe the dihydropryridine CCBs

A
  • more selective for calcium channels in peripheral vasculature
  • more effective for HTN
42
Q

describe the non-dihydropyridine

A

m-more selective for calcium channels in myocardium
- more effective for arrhythmias

43
Q

what is the MOA, ADRs, and drug interactions for calcium channel blockers

A
  • blocks L type channels in vascular smooth muscle
  • ADRs: edema, gingival hyperplasia
  • hypotension with sedatives, opiods, anesthetics, NSAIDs
44
Q

what are the dental implications for calcium channel blockers

A
  • gingival hyperplasia up to 10%
  • monitor vital signs
  • orthostatic hypotension
  • use vasoconstrictions and anestheics with caution
45
Q

what is the MOA of minoxidil

A
  • opening KATP channels
  • resulting in hyperpolarization of cells
  • turns off voltage dependent Ca2+ channels
  • lowering the intracellular Ca2+ concentration
  • resulting in vascular smooth muscle relaxation
46
Q

what is the use, ADRs, and drug interactions with minoxidil

A
  • use: severe resistant hypertension
    -ADRs: hair growth, edema, photosensitive
  • drug: NSAIDs, sedatives
47
Q

what are the dental implications with minoxidil

A
  • monitor vital signs
  • orthostatic hypotension - worst drug for this
  • avoid or limit vasoconstrictor
48
Q

what is the MOA for sodium nitroprusside

A

only available for IV administration
- used for acute control of hypertension

49
Q

what is the oral/topical nitrate formulation for sodium nitroprusside used for

A
  • angina
  • not effective as anti HTN agent, but may have hypotension SE
50
Q

what is the use, ADRs, drug interactions and dental implications for sodium nitroprusside

A
  • use: hypertensive crisis
  • ADRs: methemoglobinemia, hypotension, dizziness, thiocyanate toxicity
  • drug interactions: PDE-5 inhibitors
  • dental implications; none
51
Q

what is the MOA of hyrdralazine

A
  • interference with action of IP3 on calcium release from SR
52
Q

what is the use, ADRs, drug interactions for hydralazine

A
  • use:HTN, HF- acute use
  • ADRs: headache, palpitations, GI disturbances, flushed face
  • drug interactions: reduced anti-hypertensive effect with NSAIDs and sympathomimetic
53
Q

what are the dental implications of hydralazine

A
  • monitor vital signs
  • orthostatic hypotension
    avoid or limit dose of vasoconstrictor
54
Q

describe pulmonary hypertension

A
  • a rare disorder: 15-50 cases per million people
  • defined by a mean pulmonary artery pressure greater than 25mmHg at rest
55
Q

what are the groups of pulmonary hypertension and describe each

A
  • 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
  • group V: pulmonary HTN with unclear mechanism
56
Q

what are the world health organizations functional classes for pulmonary hypertension

A
  • class 1: no limitation
  • class II: slight limitation
  • class III: marked limitation of physical activity
  • class IV: inability to carry out any physical activity without symptoms
57
Q

what are the oral medications for PAH

A
  • endothelin receptor antagonists
  • PDE5 inhibitors
  • prostacyclin analogue
  • soluble guanylate cyclase stimulator
  • selective prostacyclin IP receptor agonist
58
Q

what are the parenteral medications for PAH

A
  • inhaled options: ilprost, treprostinil
  • IV options: treprostinil, epoprostenol
  • subcutaneous options: treprostinil
59
Q

what is the MOA of endothelin recepotr antagonist

A
  • block the ETA receptor
  • decreasing the formation of IP3
  • lowering the intracellular Ca2+ concentration
  • resulting in vascular smooth muscle relaxation
60
Q

most ERAs block both _______ but have a high affinity for ______

A

ETA and ETB; ETA

61
Q

what is an exampleo of ERA, use, ADRs, drug interactions

A
  • bosentan
  • use: PAH WHO FC III and IV
  • ADRs: headache, flushed face, dyspepsia, liver dysfunction*
  • drug interactions: increased levels when used with ketoconazole
  • pregnancy category X
62
Q

what are the dental implications for bosentan

A
  • monitor vital signs
  • high risk pts- acute pulmonary HTN could occur
  • bleeding gums
  • limit or avoid vasoconstrictors
  • low risk for orthostatic hypotension
63
Q

what is the MOA of PDE5 inhibitors

A
  • inhibit action of PDE5
  • increase intracellular cGMP concentration
  • lowering the intracellular Ca2+ concentration
  • resulting in vascular smooth muscle relaxation
64
Q

PDE5 inhibitors are also used to treat:

A

erectile dysfunction

65
Q

what is an example of PDE5 inhibitors, use, ADRs, drug to drug interactions

A
  • sildenafil
  • use: PAH, erectile dysfunction and BPH
  • ADRs: headache, flushed face, dyspepsia, rash
  • drug interactions: sodium nitroprusside- avoid combo bc severe hypotension. increased levels with CYP 3A4 inhibition
66
Q

what are the dental implications with sildenafil

A
  • monitor vital signs
  • high risk pateint if using for PAH
  • limit or avoid vasoconstrictors
  • avoid use of nitroglycerin of nitroprusside
  • low risk of orthostatic hypotension
67
Q

what i the MOA for prostacylcin analogues

A
  • bind to prostacyclin receptor (IP)
  • stimulate activity of adenylate cyclase
  • increase intracellular cyclic AMP levels
  • lowering the intracellular Ca2+ concentration
  • resulting in vascular smooth muscle relaxation
68
Q

what is the example, use, ADRs and drug interactions of prostacyclin analogue

A
  • treprostinil
  • use: PAH
  • ADRs: headache, flushing, hypotension, infusion site pain, jaw pain, inhibition of platelelt aggregation
  • drug interactions; other drugs that increase risk of bleeding
69
Q

describe jaw pain as a SE of prostacyclin therapy, the cause and management

A
  • prostacyclin is a mediator in inflammation and pain - may produce hyperalgesia
  • often occurs with 1st bite of meal
  • not dose limiting
  • management: taking slow bites, sucking on a saltine cracker or hard candy or chewing gum before eating
70
Q

what are the dental implications of prostacyclin analogues

A
  • monitor vital signs
  • limit or avoid vasoconstrictors
  • high risk pt- acute PAH could occur, continuous infusion could be interrupted
  • increased risk of bleeding because it inhibitrs platelet aggregation
71
Q

what is the MOA of selexipag

A
  • selective prostacylin IP receptor agonist
  • stimulate activity of adenylate cyclase
  • increase intracellular cyclic AMP levels
  • lowering the intracellular Calcium concentration
  • resulting in vascular smooth muscle relaxation
72
Q

what is the example, use, ADR and drug interaction of selective prostacyclin IP receptor agonist

A
  • selexipag
  • use: PAH group I
  • ADRs: flushing, headache (65%), diarrhea (42%) and jaw pain (26%)
  • drug interactions: none
73
Q

what are the dental implications of selexipag

A
  • monitor vital sings
  • high risk pt: acute PAH can occur
  • limit or avoid vasoconstrictors
74
Q

what is the MOA of soluble guanylate cyclase stimulator

A
  • sensitizes guanylyl cyclase to NO but also directly activates guanylyl cyclase
  • increase intracellular cGMP concentration
  • lowering the intracellular Caclium concentration
  • resulting in vascular smooth muscle relaxation
75
Q

what is the example, use, ADRs, drug interactions of soluble guanylate cyclase stimulator

A
  • riociguat
  • use: PAH group 1 and 4
  • ADRs: hypotension, dyspepsai, headahce, edema
  • drug interactions: pregnancy category X, avoid PDE5 inhibitors, decrease effects with CYP3A4/2C8 inducers
76
Q

what are the dental implications of riociguat

A
  • monitor vital signs
  • High risk pt- acute PAH can occur
  • avoid or limit vasoconstrictors
  • increased risk of bleeding
77
Q
A

Pharmacology I (12 decks)

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