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6902 > Pharm > Flashcards

Pharm Flashcards

1
Q

Alpha 1

A

Vasoconstricts vascular smooth muscle, GU contraction, GI relaxation, gluconeogenesis, glycogenolysis

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2
Q

Alpha 2

A

Decreased insulin secretion
Platelet aggregation
Decreased NE release
Vasoconstriction of vascular smooth muscle

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3
Q

Beta 1

A 
Increased cardiac contractility
HR
AV conduction
Increased renin secretion
Increased contractility
Arrhythmias
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4
Q

Beta 2

A 
Relaxation of vascular smooth muscle
Bronchial relaxation
GI/GU relaxation
Gluconeogenesis
Glycogenolysis
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5
Q

Dopamine 1

A

Dilation of vascular smooth muscle (renal, mesentery, coronary, renal tubules, natriuresis)
JGCs increased renin release

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6
Q

Dopamine 2

A

Inhibits NE release

May constrict renal and mesenteric smooth muscles

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7
Q

Volatile agents

A

All are cardiac depressants - amplified in diseased tissue
Affect L-type Ca+ channels located in SR of myocardial cells. This decreases contractility and prolongs isovolumetric relaxation time

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8
Q

Coronary steal

A

With volatile applied, vasodilation occurs in healthy tissues and “steals” the flow from ischemic tissue to areas with enough perfusion

  • Isoflurane most known for this
  • Sevo and Des cause coronary artery dilation
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9
Q

BP effect of volatile agent

A

All with dose-depend responses

  • With increased MAC, lower BP but maintain CO
  • Least concerning is with NO
  • At high Des flows, increase sympathetic stimulation (Rule of 24)
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10
Q

Rule of 24

A

Flows x % of gas

< 24 = sympathetic circulation less than with > 24

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11
Q

Pulmonary blood flow / effect of volatile gas

A

Halothane causes pulmonary vasoconstriction d/t catecholamine release

  • Iso and Halothane inhibit vaso-endothelial response to hypoxia through K-channel activation
  • Sevo and Des have no effect
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12
Q

Baroreceptor reflex/effect of volatile gas

A

All agents attenuate
Halothane/enflurane more than others
Suppression of reflex arc at all components - no reflex HTN

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13
Q

Under cardiac surgery/effect of volatile gas

A

Avoid Des d/t cost and length of surgery; also increased SNS stimulation which increases myocardial oxygen consumption

Avoid Nitrous d/t air bubbles I n vasculature and SNS stimulation

Volatiles better than TIVA bc protective cardiac effects to decrease size of infarct during ischemic events

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14
Q

Anesthesia pre-conditioning/effect of volatile gas

A

Dose dependent

Protective mechanism correlating with infarction, before ischemia occurs - volatiles can be protective after this “stunning” event

This works through mitochondrial K/ATPases and GCPRs

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15
Q

Propofol

A

Inhibits L-type Ca+ channels to decrease Ca+ release from SR; causing negative inotropic effects

Decreases O2 stress so better with MI (as adjunct)

Decreases SVR, vessel-autoregulation altered, and pulmonary vasculature is sensitive to catecholamines

Decreases baroreceptor reflex

CV collapse can occur in shock or trauma states - can decrease BP by 40%

Increase in lipid levels - MI risk

Decrease CBF/CMR O2 consumption and help prevent emboli transfer

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16
Q

Thiopental

A 
Decreases contractility
MAP unchanged, HR increases
Increased O2 consumption
Decreased CO
Cerebro-protective
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17
Q

Midazolam

A 
0.05-0.2 mg/kg for induction
Little variation in BP
CI stays the same
No analgesia properties - need Fentanyl (2 mcg/kg)
Long 1/2 life
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18
Q

Etomidate

A

0.3 mg/kg max
Burns with injection
Myoclonus increases O2 consumption
Adrenal/Cortisol suppression major concern
Most cardiac static induction agent
Instability can occur with high doses or with valvular issues

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19
Q

Ketamine

A

Dissociative anesthesia
Increase CI/HR/SVR/MAP through sympathetic stimulation
If catecholamine stores are low, then negative inotropic effect
Drug of choice for cardiac tamponade

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20
Q

Precedex

A

HTN with bolus dosing can occur
Increases SVR, then low BPHR
Should get loading dose to reach steady state

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21
Q

Opioids

A
  • Ischemic preconditioning
  • Endogenous opioids decrease sympathetic outflow
  • Administered with MI can improve survival outcomes by decreasing afterload and providing coronary artery dilation
  • Exogenous opioids depress the outward K+ flow, which causes bradycardia
  • Large doses prolong the QT interval.
  • All levels are decreased during CPB
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22
Q

Which opioid protects against reperfusion injury?

A

Morphine

Increases post-pump contractility after CPB

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23
Q

Which opioid at large doses can lead to ventricular arrhythmias

A

Fentanyl

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24
Q

Which opioid can decrease BP? How?

A

Morphine due to histamine release. Can mitigate with administration of H1 antagonist

Sufenta can also lower BP - good with induction

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25
Q

Which opioid is exception to bradycardia rule?

A

Meperidine due to it’s similarity to atropine

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26
Q

Cardiac Bypass effects on circulation

A
  • 1.5 –2L of priming fluid in the CPB machine that mixes with pt blood
  • Pt HCT drops to 25% and increases plasma volume by 50%
  • Causing an immediate reduction in circulating free drug and proteins
  • Heparin causes release of chemicals that bind competitively to plasma proteins as well, which increases free drug concentration.
  • Acid/base changes during CPB that alter ionized vs. non-ionized forms of drugs
  • Blood flow is decreased during CPB
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27
Q

Non-pulsatile CPB is associated with . . .

A

Altered tissue perfusion and acidosis

This causes basic drugs to become trapped in acidic tissue wand will redistributed during the rewarming phase and become biologically active as pH normalizes

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28
Q

Hypothermia during CPB reduces. . .

A

hepatic and renal enzyme function

Therefore, metabolic drug clearance decreases.

Decreased perfusion to the kidneys slows renal drug excretion. GFR drops by 65% at 25 degrees C

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29
Q

Are NMB needed during CPB?

A

No. Cooling slows nerve conduction and slows cholinesterase enzyme activity. Given the protein decrease, NMB like rocuronium enjoy increased free drug levels

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30
Q

Barbiturates and Propofol during CPB

A

concentration decrease on CPB initiation

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31
Q

Benzos and CPB

A

Concentration decreases when starting CPB. They are highly-protein bound.

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32
Q

CPB and binding of drugs

A

CPB actually binds several drugs. The CPB oxygenator known to bind lipophilic drugs
(including PIA, induction agents, and opiates).

The lungs are bypassed and basic drugs can be held by the lungs and act as a reservoir for release once systemic perfusion returns.

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33
Q

Drugs used for ischemia

A

Nitrates (vasodilator)
Ca+ blockers (vasodilator and cardiac depressant)
Beta Blockers (cardiac depressant)

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34
Q

Atherosclerotic angina

A

Classic angina - 90% of cases
Associated with plaques that occlude coronary arteries
Rest usually results in relief
Precipitated by exertion

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35
Q

Vasospastic angina

A 
Rest angina
<10% of cases
Reversible spasm of coronaries
Spasm may occur during any time - even sleep
May deteriorate into unstable angina
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36
Q

Unstable angina

A

Acute Coronary Syndrome
Increase frequency and severity of attacks
Combo of plaques, platelet aggregation at plaques, vasospasm
Precursor to MI

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37
Q

Nitrate tolerance, tachyphylaxis

A

Loss of effect of a nitrate vasodilator when exposure is beyond 10-12 h

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38
Q

Intramyocardial fiber tension

A

Filling pressure Force exerted by myocardial fibers, especially ventricular fibers at any given time
(PVR, HR, EF, Venous tone, Blood volume)
A primary determinant of O2 requirements

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39
Q

Contractility is mostly controlled by

A

Sympathetic flow

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40
Q

Faster HR, diastole is . . .

A

shortened, reducing time the ventricles are filled

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41
Q

NO is produced by . . .

A

breaking down arginine by enzymes called nitric oxide synthase (NOS) into citrulline and NO. This primarily occurs by isoform of 3 of NOS, found in endothelial cells.

NO is not stored in cells and must be made when needed

By using drugs that metabolize into NO, we can reap the benefits of NO

Inhibit platelet aggregation

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42
Q

NTG

MOA

A

Releases NO, increases cGMP and relaxes vascular smooth muscle

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43
Q

NTG

clinical application

A

Acute angina pectoris

ACS

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44
Q

NTG onset and dose

A

rapid

5-10 mcg/min is a standard starting dose.
Angina relief is typically 75-150mcg/min but may require up to 600mcg/min.

Arterial dilation at 150mcg/min

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45
Q

NTG

interactions

A

Do not use with right sided infarct bc preload dependent

Do not used with phosphodiesterase inhibitors because causes profound hypotension

Do not use as preemptive for ischemia during induction bc causes hypotension

Can cause headache, tachycardia

Arterial dilation at higher doses, causing drop in BP. While infusing intravenous NTG for ischemia, if hypotension occurs, add phenylephrine. May cause reflex in HR and contractility that can increase O2 consumption, but adding a BB can mitigate this.

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46
Q

NTG and pulmonary artery vasodilation

A

Can inhibit Hypoxic Pulmonary Vasoconstriction and Can worsen intrapulmonary shunting

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47
Q

Ca+ channel blockers

MOA

A

reduce myocardial oxygen demand by depressing contractility, HR and BP. Also dilate coronary arteries
Blocks L-type Ca+ channels in smooth muscle and heart
Decreases intracellular Ca+

Work at SA and AV nodes

Inhibit platelet aggregation

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48
Q

Ca+ Channel Blockers

clinical application

A

Angina
HTN
AV nodal arrhythmias
Migraine

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49
Q

Ca+ Channel Blockers types

A

4 classes:

  1. DHPs - nifedipine, nicardipine, amlodipine.
  2. Benzothiazepinesinclude - diltiazem.
  3. Phenylalkylamines - verapamil.
  4. Diarylaminopropylamineether - Bepridilis
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50
Q

DHPs

A

potent arterial dilator with little venodilating effects, which causes a reflexive tachycardia.

Used as anti-hypertensive

Antianginal effects come from reduced myocardial oxygen requirements from afterload reduction and coronary artery dilation.

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51
Q

What is the most potent coronary dilatory?

A

Nifedipine

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52
Q

Phenylalkylamines

A

has less potent arterial dilation and less reflex tachycardia concern.

Used for effects on conduction pathway of the heart to slow tachyarrhythmias

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53
Q

What is the least potent vasodilator CCB?

A

dilt

54
Q

CCB side effects

A 
Hypotension
dizziness
flushing
nausea
edema

Diltiazem & verapamil also cause bradycardia and myocardial depression.

55
Q

What is the most potent dilator of the DHP CCBs?

A

Nicardipine

56
Q

Verapamil side effects

A

Increase digoxin levels

When combined with BB, the risk of AV block and myocardial depression increases

Metabolized by liver

57
Q

Clevidipine

A

Metabolized by nonspecific tissue esterases and is very short acting

58
Q

Beta blockers

A

reduce oxygen consumption through lowering HR, BP, and contractility

If can’t administer NTG and BB due to BP, BB take precedence

reduce insulin release and suppress glycogenolysis and gluconeogenesis

May cause bronchospasm

59
Q

Beta blocker MOA

A

Blocks sympathetic effects on heart and BP

Reduces renin release

Reduce MI size

Chronic BB therapy causes upregulation of beta receptors, and when held cause reflex effects

60
Q

BB

clinical application

A 
Angina
HTN
Arrhythmias
Migraine
anxiety
61
Q

Mixed BB

A

Some BB –acebutolol, carteolol, penbutolol, pindololare

  • are partial agonists (meaning they don’t reach the same physiologic maximum at receptors) and also competitively antagonist.
  • There is less CO and HR reduction than seen with full antagonists.
  • Benefit in COPD patients as there is less B2 antagonism
62
Q

Lipid soluble BB

A 
produce CNS effects
metabolized by liver
propranolol
labetalol
metoprolol
63
Q

Lipid insoluble BB

A

atenolol, nadolol, acetbutolol, and sotalol

Renal excretion

64
Q

Propranolol

A

Most lipid soluble
Most CNS effects
Non-selective BB (B1 and B2)
1 mg dose

65
Q

Metoprolol

A

1st selective BB
30x affinity for B1 vs B2
1-2 mg doses

66
Q

Esmolol

A

B1
9 minute half life
Prolonged/high use can produce methanol, toxic alcohol
- loading dose of 0.5mg/kg followed by infusion of 0.05-0.3mg/kg/minute

67
Q

Labetalol

A

5-10 x > BB than Alpha 1 blocker

Partial B2 agonist

peripheral vasodilator that lacks reflex tachycardia

68
Q

Other antianginal drugs

Ranolazine

A

Blocks late Na+ current in myocardium, reduces cardiac work

Can cause QT prolongation

69
Q

Other antianginal drugs

Ivabradine

A

Blocks pacemaker Na+ current in SA node, reduces HR

70
Q

Baroreceptor reflex

A

Primary autonomic mechanism for BP homeostasis
Involves sensory input from carotid sinus and aorta to the vasomotor center and output via the parasympathetic and sympathetic motor nerves

71
Q

Catecholamine reuptake pump

A

Nerve terminal transporter responsible for recycling norepi after release into the synapse

72
Q

Catecholamine vesicle pump

A

storage vesicle transporter that pumps amine from cytoplasm into vesicle

73
Q

Essential HTN

A

HTN of unknown etiology/Primary htn

74
Q

False transmitter

A

Substance stored in vesicles and released into synaptic cleft but lacking the effect of the true transmitter - i.e. norepi

75
Q

HTN emergency

A

Accelerated form of severe HTN associated with rising BP and progressing damage to vessels and end organ180/110
Needs to be treated immediately
- Nitroprusside, nicardipine, clevidipine, fenoldopam

76
Q

Postganglionic neuron blocker

A

drug that blocks transmission by an action in the terminals of the postganglionic nerves

77
Q

Rebound HTN

A

Elevated BP resulting from loss of antihypertensive drug effect

78
Q

Reflex tachy

A

Tachy resulting from lowering of BP mediated by the baroreceptor reflex

79
Q

Sympatholytic

A

Drug that reduces effects of the sympathetic NS

80
Q

When pressures rise above 115/75 . . .

A

Double the risk for CV M & M for each 20/10 mmHg increase.

81
Q

Diuretics for HTN

A

Thiazides
loop
K+ sparing diuretics

82
Q

Thiazides

MOA

A

HCTZ, Chlorthalidone
Block Na/Cl transporter in DCT

10 mmHg decrease in BP

83
Q

Thiazide toxicities/interactions

A

Hypokalemia
Hyperglycemia
Hyperuricemia
Hyperlipidemia

84
Q

Loop diuretics

MOA

A

Furosemide, Torsemide

Block Na/K/2Cl transporter in thick ascending loop

85
Q

Loop toxicities/interactions

A

Hypokalemia
Hypokalemic metabolic acidosis
Hypovolemia
ototoxicity

86
Q

K+ sparing

MOA

A

inhibit Na+ reabsorption in Distal Collecting Duct, which indirectly increases the K+ excreted

Contraindicated in pts with hyperkalemia

87
Q

Angiotensinogen

A

Angiotensinogen is made by the liver and found in the blood. When renin is released, it cleaves angiotensinogen peptide into angiotensin I.

When angiotensin 1 comes into contact with angiotensin converting enzyme (ACE) (found in the endothelium of the vasculature), cleaved into angiotensin II.

88
Q

ACE inhibitors

A

block conversion of AT1 to AT2

Frontline drug for HTN

89
Q

ACEI toxicities/drug interactions

A
  • dry cough that bradykinin elicits.
  • angioedema not associated with dose changes (said differently, it can occur years into a stable therapy).
  • hyperkalemia/contraindicated with bilateral renal artery stenosis.
  • can produce severe hypotension in the anesthesia patient.
  • teratogens.
90
Q

ARBs MOA

A

They bind to the AT1 receptor and directly inhibit the vasoconstrictive effects of angiotensin II.

91
Q

ARBs toxicities/interactions

A

Hyperkalemia

Teratogen

92
Q

Renin antagonist

A

Aliskiren
Renin inhibitor, reduces angiotensin I synthesis

Can cause angioedema, renal impairment

93
Q

Alpha 1 antagonists

A

competitively block NE at the post synaptic alpha 1 receptors.

  • causes vasodilation
  • Side effects are orthostatic hypotension, fluid retention, reflex tachycardia.
  • front line drug for BPH.
  • Prazosin , Doxazosin, terazosin, Tamsulosin
94
Q

Methyldopa

Sympathoplegic

A

prodrug that is converted to its active drug in the brain.

95
Q

Clonidine

Sympathoplegic

A

Agonist at alpha 2 receptor
In CNS results in decreased SANS outflow
Inhibits NE release

Sedation, dry mouth, depression

Severe rebound htn if suddenly stopped; treat with alpha 1 antagonist

96
Q

Sympathoplegic

A

reduce cardiac output, SVR.

The body compensates with salt and water retention.

97
Q

Hydralazine
MOA
Side effects

A

Causes release of Nitric acid by endothelial cells
Causes arteriolar dilation

Side effects: lupus like syndrome, tachycardia, salt and water retention

98
Q

Minoxidil

A

Prodrug, sulfate metabolite opens K+ channels, causing arteriolar smooth muscle hyperpolarization and vasodilation

Side effects: tachycardia, salter and water retention, hair growth

99
Q

Nitroprusside

A

Release NO from drug molecule

Arterial and venous dilation

Side effects: Cyanide toxicity

100
Q

Fenoldopam

A

D1 agonist
Causes arteriolar dilation

Excessive hypotension

Used for renal insufficiency

Side effects: hypotension

101
Q

Drugs used in HF

A

Positive inotropic drugs
Vasodilators
Misc

102
Q

Positive inotropic drugs

A

Glycosides - Digoxin

Beta agonists- (dobutamine, isoproterenol, dopamine, epinephrine, norepinephrine, milrinone)

Vasodilators - Nipride

Misc - Loops, ACEI, BB

103
Q

catecholamine

A

dihydroxyphenylethylamine derivative, polar molecule, that is readily metabolized

104
Q

decongestant

A

an alpha agonist drug that reduces conjunctival, nasal, or oropharyngeal mucosal vasodilation by constricting bv in mucosa

105
Q

Mydriatic

A

drug that causes dilation of the pupil; opposite of miotic

106
Q

Sympathomimetic

A

drug that mimics stimulation of the sympathetic autonomic NS

107
Q

Epinephrine

MOA and side effects

A

alpha 1
alpha 2
Beta 1, 2, 3
Agonist

Side effects: HTN, arrhythmia, MI, pulm edema

108
Q

Norepinephrine

MOA and side effects

A

Alpha 1, 2
Beta 1
Agonist

Used for profound vasodilation

Vasospasm, tissue necrosis, arrhythmias

109
Q

Dopamine

MOA and side effects

A

D1
Alpha 1, 2
Beta 1, 2, 3
Agonist

Relatively weak inotrope

Start higher if need inotropy, low doses cause vasodilation

arrhythmias

110
Q

Isoproterenol

MOA

A

B1, 2, 3
Agonist

Nebulizer in acute asthma, AV block

111
Q

Dobutamine

A

B1 agonist

Acute HF to increase Co

112
Q

Heart failure

A

HF is when the CO doesn’t meet oxygen demands of tissues.

CHF means both L and R heart failure

Comes from injury/death of heart tissue or remodeling and decline in function. The body’s response is sympathetic and activates the RAAS system, which eventually fails.

113
Q

Explain how RAAS system is activated in HF

A

Kidney juxtaglomerular cells release renin in response to decreased BP or renal perfusion. The end result is AT2 vasoconstriction, aldosterone release, and antidiuretic hormone release. The increased effects of salt and water retention increase SVR and in the later CHF causes pulmonary congestion and hemodynamic decompensation.

The RAAS system is also known to cause cardiac remodeling. AT1 receptors are thought to mediate the remodeling on the heart.

114
Q

Why are ACEI first line treatment in HF?

A

They are vasodilators.
They increase the amount of NO, bradykinin and prostacyclin circulating, all of which are vasodilators in addition to reducing the amount of the vasoconstrictor angiotensin II.

They decrease the amount of aldosterone and ADH.

They attenuate angiotensin II induced remodeling.

115
Q

Aldosterone levels remain high in HF pts despite use of ACEI and ARBS. . .

A

thought to come from hypomagnesemia. Low magnesium stimulates aldosterone secretion.

Spironolactone and eplerenone. Eplerenone is better tolerated with less hyperkalemia.

116
Q

Why are BB indicated in HF?

A
  • improve systolic function
  • help reverse remodeling
  • Lower heart rate and therefore myocardial O2 consumption.
  • Beta blockers are cardiac depressants.
  • Clinical benefit of BB in HF patients takes 3 months
  • Third generation BB have efficacy in HF patients and include labetalol and carvedilol.

-The ACC/AHA and European Society of Cardiology recommend BB use in all HF patients with reduced EFS (<40%) who are on ACEI or ARBs.

117
Q

Carvedilol and HF

A

Carvedilol is a first line drug that increases insulin sensitivity, has antioxidant effects, and have Beta3 activity.

118
Q

Hydralazine in HF

A

Hydralazine combined with isosorbide dinitrate reduced preload, afterload, improves regurgitant valves, improves exercise capacity and prolongs survival in HF patients.

It also interferes with remodeling.
-most impactful on African Americans

119
Q

HF pts with symptomatic fluid overload should . . .

A

be optimized with diuretics before beginning BB

120
Q

What is the only positive inotropic drug approved for HF and how does it work?

A

Digoxin

acts by inhibiting myocardial sarcolemmal Na/K-ATPase and thereby increasing intracellular Na+. This indirectly inhibits the Na/Ca exchanger to retain Na at the expense of extruding Ca, making contractions more efficacious from increase calcium retention.

Digoxin slows AV nodal conduction rates and can also be used in Afib.

It has a narrow therapeutic index and toxicity occurs from increased intracellular calcium. PVCs warning sign of toxicity

121
Q

HF pts at risk for thromboembletic events. why?

A

Stasis in the hypokinetic heart.

also associated with afib

122
Q

What antihypertensive is NOT used in HF pts?

A

Ca+ channel blockers

123
Q

Acute CHF pt

A

Vasodilators (like morphine, NTG) reduce ventricular filling pressures and SVR while increasing SV and CO. They work especially well when afterload is the issue (post MI HTN).

Nesiritide is an analogous to BNP and serves as a negative feedback mechanism for AT2, NE, and endothelin. It acts by increasing cGMP levels causing arterial and venous dilation. It is very renal toxic and short-term use only

Inotropes including dobutamine or milrinone can also be used in the acute HF. These are phosphodiesterase inhibitors and increase cAMP

124
Q

Group 1 A antiarrhythmic

A

Na+ channel blocker

Slow conduction velocity and PM activity

*Prolong AP

Use for atrial and ventricular arrhythmias

Procainamide

125
Q

Group 2 antiarrhythmic

A

BB - block sympathetic activation

Slow PM activity

Slow phase 4 depolarization by reducing cAMP (decreased Na/Ca conductance) and PR prolongation
Esmolol
Propanolol

126
Q

Group 3 antiarrhythmic

A

K+ channel blockers

Amiodarone

127
Q

Group 4 antiarrhythmic

A

Misc

adenosine

128
Q

Group 1 B antiarrhythmic

A

Highly selective use

Na blockade
*Shorten AP risk for R on T torsade’s

Minimal effect in normal tissue

-Ventricular arrhythmias and digitalis induced arrhythmias

Lidocaine

129
Q

Group 1 c antiarrhythmic

A

Selective use of Na channel blockade

Slowed conduction velocity and PM activity
*Unchanged AP

WPW syndrome

Used in refractory arrhythmias

130
Q

Vasoplegic syndrome

A

vasopressin and methylene blue can be given

NE and phenylephrine will increase RH afterload from pulmonary vascular constriction

6902 (4 decks)

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