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Pharmacology > Exam2Lec3Vasodilators > Flashcards

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
Q

What do nitric oxide donor cause?

A
  • Release NO when metabolized
  • Relax smooth muscle: Vascular, corpora cavernosa, short lived in others
  • Inhibit platelet aggregation
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26
Q

explain how nitric oxide donor work

A

Direct administer of NO (skips endothelial) -> Increase cGMP
○ cGMP activates MYOSIN LIGHT CHAIN PHOSPHATASE (MLCP) ->
dephosphorylation of myosin-> muscle relation

naturally: 1st step is diff: NO binds to GUANYLYL CYCLASE -> Increase cGMP etc.

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27
Q
  • 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?
A
  • Amyl Nitrate (1 NO), Isosorbide dinitrate (2 NO), nitroglycerin (3NO)
  • Metabolized in vein
  • Short hald life
  • ONLY IN VEINs
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28
Q

What is the inorganic NO donor?
Where is it metabolized?
What is a SE?
What does it target?

A
  • Nitroprusside (1NO)
  • metabolized in blood cells
  • Cyanide toxicity
  • Targets both veins and blood vessels

Cannot use a lot, only in emergency

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29
Q

Explain the pharmacodynamics of organic NO donors

A

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

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30
Q

Explain how inorganic NO donors work (pharmacodynamics)

A

Works on both
* Increase capactiance and decrease resistance to reduce preload and afterload

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31
Q

What are the factors of oxygen supply and what are the factors of oxygen demand? which do we have to increase and decrease?

A

Increase oxygen supply and decrease oxygen demand

32
Q

What happens when there is ischemia?

A
  • 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
Q

What can we give to help ischemia

A

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
Q

What are the classes of ANGINA

A

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
Q

What angina can organic NO donors work?

A

Stable angina

36
Q

What is the clinical use of isosorbide dinitrate/mononitrate?

A
  • STABLE angina
  • Heart failure
37
Q

What is nitroglycerin used for?

A
  • Acute decompensated heart failure
  • acute myocardial infaraction
  • angina
  • hypertensice emergency
  • hypotension induction
  • perioperative hypertension
  • acute pulmonary hypertension
38
Q

What is important about nitrates (nitroglycerin) and HTN?

A
  • It is only used for emergency: hypertensice emergency, hyptension induction, perioperative hypertension
  • NOT CHRONIC TXT OF HTN
39
Q

What are the short acting NO donors and what are the long acting NO donors?

A
  • Short: nitroglycerin, nitroprusside
  • Long: nitroglycerin and isosorbide dinitrate
40
Q

What is the fate and excretion of nitroprusside

A

Metabolized by intraerythrocytic reaction with hemoglobin, further metabolism in liver, metabolites excreted in urine

41
Q

Explain the Organic nitrate/nitrite tolerance

A
  • 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
Q

What are the Adverse effects, contraindications and interactions with Isosorbide dinitrate/mononitrate and nitroglycerin

A
  • AE: hypotension, dizziness, headache, flushing, syncope
  • Cont: tolerance, increased intracranial pressure, pregenacy
  • interactions: sildenafil (will kill you)
43
Q

What is the AE, contraindications of nitroprusside

A
  • AE: hypotension, dizziness, headache, flushing, syncope and cyanide toxcity
  • Cont: prolonged infusion, pregnancy
44
Q

What are phsophodiesterase V inhibitors

A
  • Slidenafil
  • Tadalafil
  • Vardenafil
45
Q

Explain the pharmacodynamics of phosphodiesterase V inhibitors

A
46
Q

What is the route of adminstration, onset of action and absorption, fate, excretion of sildenafil, tadalafil and vardenadil

A
47
Q

What is the clinical use, SE of sildenafil

A
48
Q
A

sildenafil and nitrates both increase cGMP so this would lead to severe dilation and hypotension so severe is can cause death

49
Q

What is the mechanism of action and pharmacolgy of hydralzine

A
  • 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
Q

What is the clinical use and SE/Adverse reactions of hydralazine

A
51
Q

What do we not use for angina

A

hydralazine

52
Q

What is the effects of hydralzine on Organic nitrate tolerance?
What is the drug name?

A

BiDil

53
Q

Explain why hydralzine is not used for angina?

⭐️

A

Coronary steal phenomenon
* Will vasodilate healthy vessels and less o2 will go through constricted vessel leading to angina

54
Q

What is the ROA, onset and absorption, fate and excretion of hydralazine

LY

A
55
Q

What are the effects on distinct vascular beds with nitrates, nitroprusside and hydralazine

A
56
Q

What is the MOA and pharmacology of Calcium channel blockers

A
  • Block ca channels
  • **decrease calcium influx into cell- decrease ER/SR calcium loading to cystol **
  • Effects depend on selectivity
57
Q

What are the cardiac and vascular effects of CCBs?

A
  • Cardiac: dec contracility (neg inotropy), dec HR (neg chronotropy), dec conduction velocity (neg dromptropy)
  • Vas: Smooth mus relaxation (vasodilation)
58
Q

Explain what happens when a vasoconstrictor is bound to receptor

A

No extracellular ca=no intracell ca= no constriction

59
Q

Explain the pharmacodynamics of non DHP and DHP CCBs

A
60
Q

Explain the pharmacodynamics of non DHP and DHP CCBs

A
61
Q

How do CCBs effect distinct vascular beds?

A

BOTH

62
Q

DHPS target what? non?

A

Non: both heart and vasc
DHPs: just vascular

63
Q
A

Overall: non DHP (DV) cause Vasodilation and dec HR/Contractility
DHP(DIPINE): just effect vas

64
Q

Explain the pharmacokinetics of CCBs (amlodipine and nifediphine) with onset of action and plasma half life

A
65
Q

What is the first line txt of adults with systolic/diastolic hypertension

A
66
Q

What do we do if 20 mmHg above target?

A

duel therapy, triple or quadruple therapy

67
Q

What are CCB are particularly useful for treating

A

treating hypertension in low renin producer such as african-americans and elderly patients

68
Q

What have less effect on exercise performance then B blocker and will not affect electrolytes like diuretic

A

Dihydropyridine CCBs

69
Q

Long duration of action (CCBs) provides what?

A

superior long term outcomes

70
Q

Explain the accomplish train

A
71
Q

List out all the preferred antihypertensive combo

A
72
Q

What is the first line txt of isolated systolic hypertension

A

NO ACE if just systolic HTN

73
Q

How does DHPs and Non-DHP work on oxygen supply and oxygen demand

A
74
Q

What CCBs are used for stable angina, unstable angina and variant angina

A

Stable: all CCBs
Un: Non DHP CCBs
* non DNP dec HR/contaction so will decrease O2 demand
Variant: All CCBs

75
Q

What are the AE, contractindication and interactions with CCBs

A
76
Q

What are the clinical uses of CCBs?

A

Pharmacology (26 decks)

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