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pharmacology 2 > cardiovascular 1 > Flashcards

cardiovascular 1 Flashcards

1
Q

Sympatholytics are mainly used as _________

A

medication which inhibits the postganglionic functioning of the sympathetic nervous system
mainly used as AntiHTN

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2
Q

sympatholytics work on which receptors ?

A

alpha antagonist
beta antagonist
mixed alpha and beta antagonist
clonidine ( a2 agonist)

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3
Q

What do nitrates do to vascular smooth muscle?

A

vasodilate

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4
Q

This process is a part of normal endothelial function

A

NO (nitric oxide) release

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5
Q

How does Sildenafil (Viagra) work?

A

increases local availability of endogenous NO, which in turn vasodilates surrounding tissues and increases blood flow to genitals.

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6
Q

When is the best time to treat for cyanide toxicity?

A

EARLY if suspicious. Do not wait for lab results!

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7
Q

What is an early sign of cyanide toxicity?

A

Acidosis due to inactivation of cytochrome oxidase

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8
Q

What are the symptoms of cyanide toxicity?

A

Tachycardia, changed mental status, seizures, hypertension due to tachyphylaxis

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9
Q

What happens when cytochrome oxidase is inactivated during cyanide toxicity?

A
  1. Uncoupling of mitochondrial oxidative phosphorylation, inhibited cellular respiration
  2. Anaerobic metabolism and lactate formation
  3. Decreased affinity of oxygen to Hb.
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10
Q

What can be used to treat acidosis associated with cyanide toxicity?

A

NaHCO3

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11
Q

How is cyanide toxicity treated?

A
  1. STOP nitroprusside
  2. Cyanide buffers (sodium nitrate IV or amyl nitrate inhaled) followed with sodium thiosulfate IV
  3. Vitamin B12a
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12
Q

What are examples of cyanide buffers?

A

Sodium nitrate IV or Amyl nitrate inhaled

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13
Q

How do cyanide buffers work?

A

They convert ~10% of Hb to met-Hb, which sequesters the cyanide.

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14
Q

What is an indicator that there is no further need for nitrate therapy for cyanide toxicity?

A

> 10% met-Hb

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15
Q

How does sodium thiosulfate contribute to treatment for cyanide toxicity?

A

It activates the enzymatic cycle. Rhodanese enzyme converts CN to SCN- (thiocyanate) which is renally excreted.

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16
Q

What is another name for Vit B12a?

A

Hydroxocobalamin

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17
Q

How does vitamin B12a contribute to the treatment for cyanide toxicity?

A

Vit B12a chelates cyanide to form cyanocobalamin (Vit B12), which is renally excreted.

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18
Q

Where do angiotensin converting enzyme inhibitors (ACEIs) work in the renin-angiotensin-aldosterone pathway?

A

The inhibit the conversion of angiotensin I to angiotensin II in the lungs.

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19
Q

How do ACEIs differ from other anti-hypertensive agents in terms of side effects?

A

ACEIs are free from many common side effects such as depression, insomnia, sexual dysfunction, electrolyte imbalances.

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20
Q

What is used for first-line therapy for systemic hypertension and CHF?

A

ACEIs. They may reverse LV hypertrophy and decrease plasma aldosterone to reduce Na and water retention.

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21
Q

In what patient population do ACEIs improve outcomes?

A

Diabetics

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22
Q

What are examples of ACEIs?

A

Enalapril (Vasotec)
Quinapril (Accupril)
Lisinopril (Zestril)
Ramipril (Altace)

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23
Q

What are side effects of ACEIs?

A

cough, allergic-like symptoms (due to bradykinin accumulation?) possibly causing angioedema, possible hyperkalemia due to decreased aldosterone

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24
Q

What happens when ACEIs are given to patients with renal dysfunction?

A

Decreased glomerular filtration.

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25
Q

How are ACEIs excreted?

A

Renally

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26
Q

Should ACEIs be discontinued prior to surgery?

A

You should consider holding ACEIs for 24+ hours before surgery to avoid prolonged hypotension under GA.

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27
Q

If a patient is on ACEIs during general anesthesia, how do we treat any prolonged hypotension that may result?

A

Vasopressin if unresponsive to fluid bolus of sympathomimetics (Epi, NE, dopa)

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28
Q

Where do A2RBs (Angiotensin II Receptor Blockers) work in the Renin-Angiotensin-Aldosterone pathway?

A

Later in the pathway, at the Angiotensin II receptors within the body to inhibit the hypertensive effect of Angiotensin II.

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29
Q

What is an example of an A2RBs?

A

Losartan (Cozaar)

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30
Q

How are A2RBs metabolized?

A

Hepatic metabolism – with active metabolites!

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31
Q

Do you want to discontinue A2RBs prior to major surgery?

A

Consider to prevent resulting prolonged hypotension during GA.

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32
Q

Which shows less incidence of cough: ACEIs or A2RBs?

A

A2RBs

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33
Q

What is a side effect of A2RBs?

A

Hyperkalemia, especially when used with K-sparing diuretics

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34
Q

what type of drug are Phentolamine, phenoxybenzamine and prazosin

A

alpha antagonist

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35
Q

what drugs are used for management of pheochromocytoma ?

A

phentolamine, phenoxybenzamine, prazosin

blocks action of catecholamines

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36
Q

a2 receptor blockade will ______ NE release and ______heart rate

A

a2 receptor blockade will Enhance NE release and Increase HR

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37
Q

side effects of A2 receptor blockade are

A

reflex tachycardia, orthostatic hypotension, cholinomimetic side effects , unrecognized volume depletion

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38
Q

what are cholinomimetic side effects?

A

hyperperistalsis , abdominal pain, diarrhea

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39
Q

how do you treat cholinomimetic side effects?

A

atropine and glycopyrrolate

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40
Q

alpha antagonist may lead to hypotension because…

A

unopposed stimulation of beta receptors .

beta stimulation decreases diastolic pressure

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41
Q

what drug is a non selective Beta antagonist

A

propranolol

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42
Q

what are side effects of propranolol or non selective Beta antagonist

A

bronchospasm and CHF

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43
Q

what are the B1 selective antagonist

A

metoprolol , atenolol, esmolol

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44
Q

which drug (metoprolol, atenolol, esmolol) is the shortest acting

A

esmolol

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45
Q

what are side effects of Beta 1 Antagonist

A

bradycardia
av heart block
hypotension

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46
Q

why do you get HoTN from Beta Antagonist

A

due to decreased myocardial contractility / decreased HR / decreased renin release

47
Q

Beta Antagonist is good for pt with coronary artery disease because

A

it decreases the reduced myocardial O2 demand

48
Q

which drug is a mixed alpha and beta antagonist ?

A

labetalol ( a:b = 1:7 )

49
Q

cardedilol is a _______________ antagonist and a1______

A

cardedilol is a non selective B antagonist and an A1 antagonist

50
Q

what is the advantage of using Labetalol ?

A

no reflex tachycardia as with pure alpha antagonists, and less bradycardia than with pure beta antagonists

a- activity decreases peripheral vascular resistance and decrease renin

51
Q

what is the result of cardedilol?

A

drops BP

52
Q

which drug is a a centrally-acting a2 agonist

A

Clonidine

53
Q

clonidine is a centrally acting a2 ________

A

agonist

54
Q

clonidine decreases CNS sympathetic output at __________ a2 receptor

A

pre-synaptic

55
Q

nitric oxide release inhibits…

A

platelet aggregation, activation, and adhesion

56
Q

NO is rapidly inactivated by?

A

hemoglobin

57
Q

inhaled nitric oxide can be used as a

A

selective pulmonary vasodilator, bronchodilator, and can improve V/Q mismatch

58
Q

inhaled nitric oxide can be used to treat:

A

pulmonary hypertension, persistent pulmonary HTN of newborn, adult respiratory distress syndrome/acute lung injury

59
Q

nitric oxide combines with Hgb to make…

A

met-Hgb

60
Q

Isosorbide Mononitrates (Imdur) is used in the prevention of

A

angina pectoris

61
Q

Isosorbide Dinitrates (Isordil) is used in the prevention of _______ and the treatment of ______

A

angina pectoris; CHF

62
Q

What are side effects of oral nitrates?

A

headache, orthostatic hypotension

63
Q

Nitroglycerin is a long acting or short acting drug?

A

short acting

64
Q

Nitroglycerin mainly causes

A

venous dilation

65
Q

NO is released through what pathway?

A

glutathione-dependent

66
Q

nitroglycerin causes cerebral vasodilation which in turn increases…

A

ICP and CBF, which can cause headaches

67
Q

NTG is less potent than

A

SNP (sodium nitroprusside)

68
Q

NTG can be used for

A

controlled hypotension, uterine relaxation

69
Q

the risk of metHgb-emia is rare with the use of NTG because

A

of rapid hepatic metabolism

70
Q

NTG can be given

A

sublingually, transmucosally, and transdermally, IV

71
Q

What is the benefit of giving NTG sulingually or transmucosally

A

avoids 1st pass effect and goes right into the superior vena cava

72
Q

dosing for sublingual NTG in treatment of angina pectoris

A

0.3 mg

73
Q

dosing for NTG ointment for treatment of angine pectoris

A

2%

74
Q

NTG increases coronary perfusion to what layer of the heart?

A

ischemic subendocardium

75
Q

IV dosing for NTG

A

10-100 mcg IV

76
Q

infusion rate of NTG

A

0.5-2 mcg/kg/min

77
Q

tolerance for nTG develops with how many hours of sustained treatment?

A

24 hours

78
Q

SNP causes direct

A

arterial and venous vasodilation

79
Q

What is Fe-(CN)5(NO)

A

SNP

80
Q

SNP is used for

A

controlled hypotension, hypertensive emergencies, cardiac disease

81
Q

SNP can cause

A

reflex tachycardia

82
Q

Does SNP increase or decrease cerebral blood flow?

A

increase

83
Q

SNP ___________ (increases or decreases) hypoxic pulmonary vasoconstriction

A

decreases (attenuates)

84
Q

What is the concentration of SNP?

A

50 mg per 250 ml = 200 mcg/ml

85
Q

What is the starting dose of SNP?

A

0.3-0.5 mcg/kg/min = ~10 mL/hr

86
Q

What is the onset of SNP?

A

almost instant

87
Q

What is the duration of SNP?

A

1-10 minutes

88
Q

Titrate SNP up by what increment?

A

0.2-0.5mcg/kg/min

89
Q

Common dose of SNP?

A

~3 mcg/kg/min

90
Q

What is the max dose of SNP for less than 10 minutes?

A

10 mcg/kg/min

91
Q

What is the max dose of SNP for long term purposes?

A

2 mcg/kg/min

92
Q

Why dose SNP need to be wrapped in foil or black plastic?

A

it breaks down in light

93
Q

continuous arterial BP monitoring is necessary for what drug?

A

SNP

94
Q

what happens at 10 mcg/kg/min of SNP?

A

CN toxicity

95
Q

in nitroprusside mtabolism, what percentage of Hgb is naturally met-Hgb?

A

1%

96
Q

CN + et-Hgb =

A

cyanmet-Hgb

97
Q

the rhodanese enzyme converts CN to ________ in the liver/kidney

A

thiocyanate

98
Q

what happens to the remaining CN that is not converted by the rhodanese enzyme?

A

causes toxicity

99
Q

what should be a concern if you discontinue the use of clonidine?

A

rebound hypertension

100
Q

how do you treat rebound hypertension cause by discontinuation of clonidine ?

A

treat with vasodilator

101
Q

what are other use of clonidine?

A

analgesia, pre- anesthetic medication, regional anesthesia, treatment of opioid, withdrawal syndrome , post operative shivering

102
Q

methyldopa ( he said he wont test over this)

A

a parkinson drug that treats HTN, especially in pregnancy induced HTN

inhibits DOPA dedcarboxylase which converts dopa into dopamine > NE > epi

thus low catocholaines&raquo_space; lowers BP

metabolize into a2 agonist ( similar to clonidine)

103
Q

hydralazine directly cause ______________ relaxation

A

vascular smooth muscle ( arterioles > veins )

104
Q

hydralazine has its largest effect in which part of the body

A

coronary , cerebral, renal, splanchnic circulation

105
Q

hydralazine decrease _____ more than _____

A

hydralazine decreases DBP more than SBP

106
Q

what is the dose of hydralazine

A

2.5-10 mg IV

107
Q

effect of hydralazine starts in ______ minutes

A

10-20 min. not a fast acting drug

108
Q

how is hydralazine metabolized and excreted ?

A

liver metabolism and renal excretion

109
Q

what is an side effect of hydralazine ?

A

reflex tachycardia

110
Q

what is an oral medication with action like hydralazine?

A

minoxidil

111
Q

when do you use minoxidil?

A

used for the most severe forms of hypertension

112
Q

what are the effects of minoxidil?

A

fluid retention, edema, pericardial effusion

113
Q

what is hypertricchosis

A

hair growth

114
Q

minoxidil is also known as

A

rogaine

pharmacology 2 (4 decks)

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