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Exam2Lec3Vasodilators Flashcards

1
Q

What is preload?

A
  • The passive stretching of muscle fibers in the ventricles.
  • This stretching results from blood volume in the ventricles at end of diastole.
  • The more the heart muscles stretch during diastole, the more forcefully they contract during systole
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2
Q

What is contractility

A
  • Refers to the inherent ability of the myocardium to contract normally
  • Contractility is influenced by preload
  • The greater the stretch the more forceful the contraction
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3
Q

What is afterload?

A

Refers to the pressure that the ventricular muscles must generate to overcome the higher pressure in the aorta to get the blood out of the heart

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4
Q

Why is the arterial BP regulated within a narrow range?

A

to provdie adequate perfusion of the tissues without causing damage to the vascular system, particularly the arterial intima

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5
Q

Arterial BP is directly proportional to _ _ and _ _ _

A

Arterial BP is directly proportional to cardiac output and peripheral vascular resistance

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6
Q

Cardiac output and peripheral resistance are controlled by what to two overlapping mechanisms? ⭐️

A
  • baroreflexes (symp nervous system)
  • Renin-angiotensin-aldosterone system (RAAS)
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7
Q

What do most antihypertensive drugs do to lower BP

A

by reducing cardiac output and/or decreasing peripheral resistance

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8
Q
A
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9
Q

Explain the response mediated by the sympathetic nervous system when there is a decrease in BP? (PICTURE)

A

Rapidly: incre symp activty via baroreceptors-> activate a1 (increase venous return) & B1 (incre contractility, incre CO, release renin)-> increase BP

Long term: decre in renal Blood flow-> release renin-> incr angiotensin 2-> incre aldosterone-> increase water/Na retention-> incre BV-> incre CO-> incre BP

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10
Q

Baroreceptors are fast or slow and what do they activate?

A
  • Fast
  • activate SNS
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11
Q

Is renin fast or slow and what does it do?

A
  • Slow
  • Fluid retention
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12
Q

What are the locations and nerves used for baroreceptors?

A

Location: aortic arch receptors via vagus nerve and carotid sinus receptors via carotid sinus nerve to nerve IX

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13
Q

Explain the renin-angiotensin-aldosterone sytem

A

Angiotensinogen –RENIN-> ANG1–ACE-> ANG2 (increase symp, tubular reabsorption, aldosterone and ADH increase) ALL leads to increase BP

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14
Q

Explain cardiac myocyte contraction and relaxtion

A

symp activation> release NE> binds to B1 receptor> Gs increases cAMP> incre PKA-> increase CA release extracellular> intracell Ca released from SR> binds to troponin C-> actin can bind to myosin> contraction

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15
Q

Contraction in vascular smooth muscle can be initiated by what?

A

Mechanical, electrical and chemical
* passive stretching og VSM can cause contraction that originates from VSM itself and termed a myogenic response
* Electical depolarization of VSM cell membrane elictis contraction, most likely by opening voltage dependent Ca++ channels (L-type Ca++ channels), causing an increase in the intracellular concentration of calcium
* A number of chemical stimuli such as NE, angiotension II, vasopressin, endothelin 1 and thromboxane A2 can cause contraction.

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16
Q

VSM undergoes _, _, _ contractions

A

slow, sustained, tonic

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17
Q

Explain vascular smooth muscle contractio and relaxation

A

ca->calmodulin-> MLCK->Phosph MLC->contraction

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18
Q

What type of drugs target MLC dephosphorylation?

A

Nitrate drugs

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19
Q

What is the pharmacodynamics of direct acting vasodilators? (how does it affect the heard)

A

Affects venous side with preload and affects resistance with afterload

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20
Q

What drugs are nitrates?

A

Isosorbide dinitrate
Nitroglycerine
Nitroprusside

Iso Nitro

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21
Q

What drug is a hydralazine?

A

hydralazine

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22
Q

What drug is a phophodiesterase V inhibitor?

A

Slidenafil

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23
Q

What drugs are calcium channel blockers (CCBs) (non DHP)

A
  • Diltiazem
  • Verapamil
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24
Q

What are CCBs DHP drugs?

A
  • Amlodipine
  • Nifedipine
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25
What do nitric oxide donor cause?
* Release NO when metabolized * Relax smooth muscle: Vascular, corpora cavernosa, short lived in others * Inhibit platelet aggregation
26
explain how nitric oxide donor work
Direct administer of NO (skips endothelial) -> Increase cGMP ○ cGMP activates MYOSIN LIGHT CHAIN PHOSPHATASE (MLCP) -> dephosphorylation of myosin-> muscle relation ## Footnote naturally: 1st step is diff: NO binds to GUANYLYL CYCLASE -> Increase cGMP etc.
27
* What are the organic nitrites and nirtates (+ how many NO they have)? * Where do they metabolize? * How long it their half life? * What does it target?
* Amyl Nitrate (1 NO), Isosorbide dinitrate (2 NO), nitroglycerin (3NO) * Metabolized in vein * Short hald life * ONLY IN VEINs
28
What is the inorganic NO donor? Where is it metabolized? What is a SE? What does it target?
* Nitroprusside (1NO) * metabolized in blood cells * Cyanide toxicity * Targets both veins and blood vessels | Cannot use a lot, only in emergency
29
Explain the pharmacodynamics of organic NO donors
Target is the vein so increase capcitance vanules to decrease preload so the heart doesnt have to work as hard * increase oxygen demand, improved collateral flow * Increase blood flow to coronary arteries to suppy heart * less blood in heart to pump, more blood supplying heart
30
Explain how inorganic NO donors work (pharmacodynamics)
Works on both * Increase capactiance and decrease resistance to reduce preload and afterload
31
What are the factors of oxygen supply and what are the factors of oxygen demand? which do we have to increase and decrease?
Increase oxygen supply and decrease oxygen demand
32
What happens when there is ischemia?
* heart isnt getting enought blood which can cause angina (no O2 to heart so pain) * If left too long will lead to MI * More oxygen demand than oxygen supply
33
What can we give to help ischemia
Give organic NO donor * Can increase coronary BF and give heart more O2 * Reduce Preload=Less O2 demand * Increase O2 supply, decrease oxygen demand
34
What are the classes of ANGINA
stable anigna-exertion * When you work hard and have heart pain unstable angina - plaque * severe athertoscelerosis-> coronary is blocked by platelet Variant angina-Spasm * Contracts and blocks blood flow
35
What angina can organic NO donors work?
Stable angina
36
What is the clinical use of isosorbide dinitrate/mononitrate?
* STABLE angina * Heart failure
37
What is nitroglycerin used for?
* Acute decompensated heart failure * acute myocardial infaraction * **angina** * **hypertensice emergency** * **hypotension induction** * **perioperative hypertension** * acute pulmonary hypertension
38
What is important about nitrates (nitroglycerin) and HTN?
* It is only used for emergency: hypertensice emergency, hyptension induction, perioperative hypertension * NOT CHRONIC TXT OF HTN
39
What are the short acting NO donors and what are the long acting NO donors?
* Short: nitroglycerin, nitroprusside * Long: nitroglycerin and isosorbide dinitrate
40
What is the fate and excretion of nitroprusside
Metabolized by intraerythrocytic reaction with hemoglobin, further metabolism in liver, metabolites excreted in urine
41
Explain the Organic nitrate/nitrite tolerance
* Cont. 24 hour plasma levels of organic nitrates results in insurmontable tolerance (tachyphylaxis) * Nitrate-free period of more than 10 hours is needed to prevent or attenuate tolerance * NO TOLERANCE IS NOT DEVELOPED TO NITROPRUSSIDE
42
What are the Adverse effects, contraindications and interactions with Isosorbide dinitrate/mononitrate and nitroglycerin
* AE: hypotension, dizziness, headache, flushing, syncope * Cont: tolerance, increased intracranial pressure, pregenacy * interactions: sildenafil (will kill you)
43
What is the AE, contraindications of nitroprusside
* AE: hypotension, dizziness, headache, flushing, syncope and **cyanide toxcity** * Cont: prolonged infusion, pregnancy
44
What are phsophodiesterase V inhibitors
* Slidenafil * Tadalafil * Vardenafil
45
Explain the pharmacodynamics of phosphodiesterase V inhibitors
46
What is the route of adminstration, onset of action and absorption, fate, excretion of sildenafil, tadalafil and vardenadil
47
What is the clinical use, SE of sildenafil
48
sildenafil and nitrates both increase cGMP so this would lead to severe dilation and hypotension so severe is can cause death
49
What is the mechanism of action and pharmacolgy of hydralzine
* MOA is unknown * Required NO from the endotheium so if endothelial is not working the drug will not work * targets arteries and decrease resistiance to decrease afterload
50
What is the clinical use and SE/Adverse reactions of hydralazine
51
What do we not use for angina
hydralazine
52
What is the effects of hydralzine on Organic nitrate tolerance? What is the drug name?
BiDil
53
Explain why hydralzine is not used for angina? | ⭐️
Coronary steal phenomenon * Will vasodilate healthy vessels and less o2 will go through constricted vessel leading to angina
54
What is the ROA, onset and absorption, fate and excretion of hydralazine | LY
55
What are the effects on distinct vascular beds with nitrates, nitroprusside and hydralazine
56
What is the MOA and pharmacology of Calcium channel blockers
* Block ca channels * **decrease calcium influx into cell- decrease ER/SR calcium loading to cystol ** * Effects depend on selectivity
57
What are the cardiac and vascular effects of CCBs?
* Cardiac: dec contracility (neg inotropy), dec HR (neg chronotropy), dec conduction velocity (neg dromptropy) * Vas: Smooth mus relaxation (vasodilation)
58
Explain what happens when a vasoconstrictor is bound to receptor
No extracellular ca=no intracell ca= no constriction
59
Explain the pharmacodynamics of non DHP and DHP CCBs
60
Explain the pharmacodynamics of non DHP and DHP CCBs
61
How do CCBs effect distinct vascular beds?
BOTH
62
DHPS target what? non?
Non: both heart and vasc DHPs: just vascular
63
Overall: non DHP (DV) cause Vasodilation and dec HR/Contractility DHP(DIPINE): just effect vas
64
Explain the pharmacokinetics of CCBs (amlodipine and nifediphine) with onset of action and plasma half life
65
What is the first line txt of adults with systolic/diastolic hypertension
66
What do we do if 20 mmHg above target?
duel therapy, triple or quadruple therapy
67
What are CCB are particularly useful for treating
treating hypertension in low renin producer such as african-americans and elderly patients
68
What have less effect on exercise performance then B blocker and will not affect electrolytes like diuretic
Dihydropyridine CCBs
69
Long duration of action (CCBs) provides what?
superior long term outcomes
70
Explain the accomplish train
71
List out all the preferred antihypertensive combo
72
What is the first line txt of isolated systolic hypertension
NO ACE if just systolic HTN
73
How does DHPs and Non-DHP work on oxygen supply and oxygen demand
74
What CCBs are used for stable angina, unstable angina and variant angina
Stable: all CCBs Un: Non DHP CCBs * non DNP dec HR/contaction so will decrease O2 demand Variant: All CCBs
75
What are the AE, contractindication and interactions with CCBs
76
What are the clinical uses of CCBs?

Pharmacology (26 decks)

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