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Module 3 - CPR > 1 - Pharmacology > Flashcards

1 - Pharmacology Flashcards

1
Q

Identify the neurotransmitter present at pre- and post-ganglionic synapses in the autonomic nervous system.

A

Parasympathetic - ACh at both pre and post-ganglionic synapses
Sympathetic - ACh at pre-ganglionic, NE at post-ganglionic and EPI and systemic NE is released to blood stream from adrenal gland

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2
Q

List the major effects of the parasympathetic and sympathetic nervous system on the heart, vessels, lung, eye, GI, and sweat glangs.

A 
System	Effect				Para			Sym
heart 	HR					- - -			+ + +
		conduction velocity		- - -			+ + +
		contraction (some)		-			+ + +
Vessels						dilation		contraction
										(not sk muscle
										or liver)
lungs	bronchioles			contraction	relaxation
Eye		radial muscles			none		contraction
		sphincter muscles		contraction	none
GI		motility				+++			- 
Sweat	secretion				+			+ + +
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3
Q

Describe the mechanism of action of nicotinic ACh receptors.

A

nAChRn are act as ligand gated ion channels. When ACh binds they open and allow rapid entry of Na+ and Ca++, and in the process some K+ also leaves. This allows rapid depolarization and the Ca can initiate muscle contraction.

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4
Q

Describe the mechanism of action of muscarinic ACh receptors.

A

They are a set of 5 GCPR. M1, M3, M5 bind to Gq and increase IP3. This causes the release of Ca++ from the ER. M2, M4 bind to Gi and decrease cAMP and opening K+ channels.

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5
Q

List the steps of the synthesis and release of NE in sympathetic nerve terminals.

A

1) Tyrosine is transported into the axon where it is converted to DOPA and then dopamine
2) Dopamine is transported into vesicles, where it is converted to NE
3) An action potential causes Ca influx via voltage-gated Ca channels
4) The vesicles then fuse to the membrane and release NE
5) NE acts on the post-synaptic cell at androgenic receptors
6) NE is actively transported back into the pre-synaptic cell via NET (Norepinephrine Transporter) and stored in vescicles
7) NE also acts on a2 receptors on the pre-synaptic to inhibit further NE release
8) Any free NE in the pre-synaptic cell is digested by MAO in the Mitochondria

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6
Q

List which receptors respond to NE, EPI, Isoproterenol or Dopamine.

A

NE - a1, a2, B1
EPI - a1, a2, B1, B2, B3
Isoprotenol - B1, B2
Dopamine - D1 (low doses), B1 (high doses in heart), a1/2 (really high doses)

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7
Q

Describe (briefly) the mechanism of action for a1 and a2 receptors.

A

a1 - stimulation - bind to Gq and increase phospholipidase C –> increase IP3 –> increase Ca++
a2 - inhibitory - bind to Gi - decrease cAMP or opens K+ channels
-pre-synaptic autoregulation - bind to Go - blocks Ca channels to prevent release of NE

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8
Q

Describe (briefly) the mechanism of action of B1, B2, and B3 receptors.

A

B1 - stimulation of Heart - bind to Gs - increase cAMP, open Ca channels
B2 - relaxation of peripheral organs- bind to Gs - increase cAMP
B3 - lipolysis - bind to Gs - increase cAMP

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9
Q

Where can a1 and a2 receptors be found? What do they do?

A

a1
Blood Vessels - constriction
Iris - radial muscle contraction (dilation)
GI - sphincter contraction
Liver Met - promote gluconeogenesis, glycogenolysis

a2
pre-synaptic autoregulation
Pancrease - decreased insulin secretion

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10
Q

Where can B1, B2 and B3 receptors be found? What do they do?

A

B1
Heart - increased contraction, automaticity, and conduction velocity
Fat - lipolysis
Kidney - renin secretion (precursor to angiotensin II)

B2
Blood Vessels - dilation
GI - decreased motility
Uterus - relaxation
Liver Met - promote gluconeogenesis, glycogenolysis

B3
Fat - lipolysis

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11
Q

Describe the effects of EPI on the body.

A

EPI binds to a1, a2, B1, B2, and B3 receptors
Heart - binds to B1 and increases HR, cardiac output and contractile force
Most blood vessels - a2 causes constriction
Skeletal muscle vessels - B2 receptors are more sensitive to EPI, so there is a dilation at low doses, but at higher levels, constriction is caused by a1 binding
–> overall, low doses of EPI will +HR(B1), -diastolic pressure(B2) with no change in mean BP
–> high doses of EPI will +HR(B1), + mean BP(a1)
Lungs - bronchial relaxation
Metabolic - + hyperglycemia (B2, a1), - insulin (a2), + FA (B1, B3)

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11
Q

Describe the effects of NE on the body.

A

NE stimulates a1, a2 and B1
Heart - binds to B1 and increases HR, cardiac output and contractile force (typically counteracted by vagal reflex from baroreceptors to bring pressure down again)
Vessels - contraction (a1) leading to increase mean BP and decreased flow to kidneys, stomach and skeletal muscle

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12
Q

Describe the effects of Isoproterenol on the body.

A

stimulates B1 and B2
Heart - binds to B1 and increases HR, cardiac output and contractile force
Vessels - B2 causes dilation and decrease mean BP
Smooth muscle - relaxation
Metabolic - some hyperglycemia (less than EPI)

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13
Q

What are some notable a (alpha) agonists?

A

**Phenylephrine - a1 and a2 agonist (a1>a2)
**Midodrine - a1 selective agonist
**Clonidine - a2 selective agonist
brimonidine - a2 selective (less specific than clonidine)
oxymetazoline (Afrin) - a1 and a2 agonist

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14
Q

What are some notable B (beta) agonists?

A

**Albuterol (Ventolin) - B2 selective
Riodrine (Yutopar) - B2 selective
B1 selective VERY uncommon and rather dangerous

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15
Q

What are some notable D (delta) agonists?

A
  • *Fenoldopam (Corlopam) - D1 agonist
    • works on peripheral receptors to lower BP and increase renal blood flow
    • for SHORT term management of SEVERE hypertension
    • administered via IV
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16
Q

What are some notable indirect NE agonists?

A

act by displacing NE from vesicles within the axon

    • Amphetamine - acts at peripheral a and B receptors and in the CNS. It is more powerful due to inhibition of MAO thus preventing breakdown of NE after reuptake.
  • *Ephedrine/Pseudoephedrine (Sudafed) - similar as amphetamine, but less powerful, no effect on CNS or MAO
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17
Q

What are some notable a (alpha) receptor antagonists?

A

**prazosin (Minipress) - selective a1 receptor antagonist - most common since there is less NE buildup and cardiac stimulation
-tamsulosin - is same class as prazosin but is a1A selective, which will promote urinary relaxation without cardiac effects
phenoxybenzamine (Dibenzyline) - irreversible, noncompetetive a1/a2 receptor antagonist
phenotolamine (Regitine) - reversible, competetive a1/a2 receptor antagonist

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18
Q

What are some notable B (beta) receptor antagonist (B blockers)?

A

** metoprolol (Lopressor) - relatively selective B1 blocker - decreases BP but has less bronchoconstriction
propranolol (inderal) - nonselective B blocker w/ no ISA - generally decreases BP, but can slow a diabetic recovery from hypoglycemia
pindolol (Visken) - nonselective B blocker with some intrinsic sympathomimetric activity

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18
Q

What are some notable mixed androgenic antagonist?

A

**cavedilol (Coreg) - selective a1 and nonselective B blocker with
a1 effect dominating 1:3 to 1:7 - used for hypertension and
emergencies
labetalol (Normydyne) - similar to above

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19
Q

What is a notable androgenic neuron blocking agent?

A

guanethidine (Ismelin) - acts on post-ganglionic adrenergic nerve - transported by NET and prevents stimulation by an action potential and will eventually displace NE within vesicles –> no CNS interaction

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20
Q

What are the major side effects of sympathomimetic drugs?

A

Vascular (a1) - hypertension, headache, cerebral hemorrhage
Urinary (a1) - urinary hesitancy
Cardiac (B1) - tachycardia –> angina and arrhythmias
CNS interactions - if they cross the BBB (ie amphetamine)

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21
Q

What are some major side effects of B blockers?

A 
Bronchoconstriction
Bradycardia, cardiac arrest
Cardiac failure
Interfere with insulin treatment in diabetics
Decrease physical performance, fatigue
Increase plasma triglycerides
CNS - sedation, sleep, depression
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22
Q

What are the main therapeutic uses of sympathomimetic drugs?

A

a1 agonist - nasal decongestion, severe hypotension, dilate pupil
a2 agonist - glaucoma, hypertension
B1 agonist - tx cardiac arrest (EPI), heart failure, cardiogenic shock
B2 agonist - asthma, delay labor
D1 agonist - severe hypertension

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23
Q

What are some major theraputic uses of a (alpha) receptor antagonist?

A

Hypertension
Pheochromocytoma (catecholamine-secreting tumor)
Benign prostatic cancer
peripheral vascular disease

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24
Q

What are some major therapeutic uses of B blockers?

A 
hypertension
ischemic heart disease
cardiac arrhythmias
obstructive cardiomyopathy
CHF
tremor
prophylaxis for migraine
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25
Q

Where are muscarinic receptors found?

A

Smooth muscle
Heart
Exocrine glands - part of sympathetic pathway, but have muscarinic receptors that respond to ACh
Blood vessels - extrasynaptic receptors in arteriolar smooth muscle do not receive cholinergic innervation but dilate in response to ACh

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26
Q

What are some notable cholinergic agonists?

A

Esters
ACh - not used clinically due to fast metabolism
metacholine - more selective for muscarinic, but not used much
**bethanechol - slowly hydrolyzed and selective, most common
Alkaloids
muscarine - from mushroom - poison
**pilocarpine - topical miotic, used for glaucoma

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27
Q

What are the major therapeutic uses of muscarinic agonists?

A

relatively limited use - increase urinary motility, GI motility, iris contraction (glaucoma), increase salivary secretion (xerostomia)

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28
Q

What are some notable anticholinergics?

A 
Tertiary (can enter CNS) 
**atropine - motion sickness
** scopolamine - motion sickness
Quaternary (can't enter CNS)
ipratropium, tiotrpium - M1, M3 selective - used prophylactically for asthma
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29
Q

Describe what organs are sensitive to varying levels of atropine.

A

Hot as a hare, Dry as a bone, Red as beet, Blind as a bat, Mad as a hatter.
Low —->—–>—–>—–>—–>—–>Highest Dose
Secretory Eye/Heart GI/UT CNS
- sweating mydriasis - motility excitation
-salivation tachychardia delirium
medullary depression

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30
Q

What are the major therapeutic uses of anticholinergics?

A

Reduce secretions - pre-anestheitc medication, peptic ulcers
Reduce smooth muscle tone - mydriasis, peptic ulcers, asthma, urinary incontinence
CNS (only tertiary) - sedation, anti-motion sickness, anti-parkinsonian effects

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31
Q

What is the mechanism for nicotine addiction?

A

The rewarding effect of nicotine involves the Ventral Tegmental Area (VTA) dopamine neurons. Nicotine binds to nAChRns (a4B2) which excites dopamine neurons. It also binds presynaptic nAChRn (a7) on excitatory afferents to increase the excitatory transmission onto the VTA dopamine neurons.

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32
Q

Describe the main mechanism of nicotine toxicity.

A

Smoking as well as accidental injestion from insecticide spray and exposure to tobacco leaves.

  1. acute toxicity (green tobacco sickness) - nausea, vomiting, weakness, headache, sweating, salivation. Death is rare.
  2. chronic toxicity - CV toxicity, hypertension, chronic obstructive pulmonary disease, low birth rate, craving, dependence, addition
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33
Q

What are the major pharmacotherapies for nicotine dependence?

A
  1. nicotine replacement therapy - gum, pathes, nasal spray (~10% success @1yr)
  2. antidepressents - buproprion - control cravings (~23% @1yr)
  3. nAChn partial agonist - varenicline - selective for a4B2 receptors on dopamine neurons in CNS - (equivalent to 1 and 2)
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34
Q

What is the mechanism of action for digoxin?

A

Digoxin increases the force and velocity of myocardial contraction by increasing intracellular Ca++.
Digoxin acts directly on the heart and is not mediated by catecholamines or the activation of adenyl cyclase. It binds to the external portion of the myocardial Na-K ATPase and inhibits its action. THis results in the increase of Na within the cell, and reduces the effect of the Na/Ca exchanger. Therefore, Ca also increases in the cell which increases contractility.

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35
Q

How does digitoxin work to treat heart failure?

A

In a patient with CHF, digoxin increases intracellular Ca and thus increases cardiac output. Increased CO improves renal perfusion, which will enhance Na excretion and reduce edema. Digoxin will also increased ejection fraction which decreases cardiac filling pressure. This decreases in venous pressure and left ventricular EDV allows the heart to return to a smaller size and relieves edema.

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36
Q

What are the major classes of anti-arrhythmic drugs? What is their mechanism of action?

A

Class I - Fast Na+ Channel Blocker
Ia - preferentially bind to Na+ in active state, but also block K+ channels –> decreased conduction velocity and increased effective refractory period
Ib - prefer Na+ in both active and inactive state, but dissociate quickly –> Na+ blockade with little effect on refractory period
Ic - strong Na+ channel binding –> strong blockage with no effect on refractory period
Class II - B blockers
non-selective - 1st generation
B1 selective - 2nd gen
B1 selective w/ vasodilation - 3rd gen
Class III - K+ Channel blockers –> lessens the K current and therefore increases the refractory period, however this can increase the possibility of Early After Depolarizations and Torsades de Pointes
Class IV - Ca++ Channel Blocker - prevents transmission of action potential, primarily at the SA and AV nodes

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37
Q

What are the notable Class I anti-arrhythmic drugs? What are some major side effects?

A

Class Ia: quinidine, procainamide - long QT, hypotension, tosades de points (TDS), lupus like syndrome
Class Ib: lidocaine - confusion, dizziness, seizures
Class Ic: flecainide

38
Q

What are the notable Class II anti-arrhythmic drugs? What are some major side effects?

A 
Class II(non-selective) - propranolol -B1/B2 blocking effects, insomnia, depression
Class II(B1 selective) - atenolol - B1 blocking effects, insomnia, depression
39
Q

What are the notable Class III anti-arrhythmic drugs? What are some major side effects?

A

amioderone - long QT, hypertension, reduced contractility, hyper or hypothyroidism, elevated activity in liver enzymes, peripheral neuropathy, headache, corneal microdeposits, testicular dysfunction, skin discoloration
sotalol
ibutilide
bretylium - increased QT, potentially leading to torsades de pointes

40
Q

What is a notable Class IV anti-arrhythmic drug? What are some major side effects?

A

verapamil - negative ionotropic effect, chest fullness dyspnea, hypotension

41
Q

What is the mechanism of action and side effects of:
Adenosine
K+ ion

A

Adenosine - binds to a specific P1 class of GPCRs and increases K+ current –> shortened AP, hyperpolarized, decreased automaticity
Side effect - headache, flushing, chest pain, bronchoconstriction with asthma, short acting
K+ Ion - proper balancing of concentration can terminate an arrythmia
side effect - either hyper or hypokalemia can lead to further arrhythmias (EAD, DAD, bradycardia)

42
Q

What is the drug of choice for the following conditions:

1) atrial fibrillation with AV conduction via accessory pathway;
2) VT with remote MI;
3) ventricular premature beats;
4) PSVT;
5) Atrial fibrillation with heart failure.

A

1) procainamide (or DC cardioversion)
2) amiodarone, Lidocaine
3) amiodarone
4) adenosine, verapamil
5) digoxin

43
Q

Briefly describe the components of the RAAS.

A

Angiotensin –(Renin)–>Angiotensin I –(ACE Chymase)–> Angiotensin II —-> AT1 and AT2
AT1 –> Na+/fluid retention, vasoconstriction, sympathetic activation, cell growth, **aldosterone secretion
AT2 –> vasodilation, cell growth inhibition, apoptosis, antagonize AT1
Aldosterone –> MR/GPCR –> Na+&H2O reabsorption, K+ & H+ excretion

44
Q

Summarize the physiological actions of Angiotensin II.

A

ANG II act primarily on AT1 receptors which are one most tissue, but have a high concentration on vascular smooth muscle. Activation causes:
1) Fast Response (Afterload)–> vasoconstriction, up NE release, up catecholamine release
2) Slow Response (preload)–> up Na+ resorption, up aldosterone, up fluid retention
3) Other –> up cell growth, up ECM
Overall this results in increased afterload (BP), preload (volume), and hypertrophy

45
Q

What are some notable drugs that act on the RAAS?

A

Renin Inhibitor –> aliskiren
ACE Inhibitor –> captopril, enalapril
ARB (AT1)–> Losartan
MR Antagonist –> spironolactone, eplerenone

46
Q

Compare the uses of ACE inhibitors and ARBs.

A

ACE Inhibitors act on the RAAS and Bradykinin pathways, where ARBs only act within the RAAS. This means that ACE inhibitors have a vasodilator effect through Bradykinin, but this comes at the cost of increased likelihood of a persistent cough, angioedema, and hyperkalemia. ARBs are less potent that ACE, but are a good choice for those who cannot tolerate ACE inhibitors.

47
Q

What are the major effects, side effects and contraindications of Aldosterone Receptor Antagonist?

A

Spironolactone and Eplerenone are two major K+ sparing diuretics used in hypertension and CHF. Acting my in the RAAS and decreasing Aldosterone actions, these drugs decrease Na+ and fluid retention, thus decreasing BP and afterload. They also increase retention of K+. This makes them an excellent addition to management of severe CHF and hypertension. However, this also makes them contraindicated in those with hyperkalemia.
Also - decreases digitalis clearance.

48
Q

What are the mechanisms of action for organic nitrates in angina pectoris?

A

1) Organic nitrates cause vasodilation of systemic venules –> decreased diastolic pressure –> decreased preload–> greater pulse pressure –> increased coronary blood flow
2) decreased preload –> decreased cardiac muscle O2 demand
3) causes dilation of large coronary vessels, but smaller vessels are still driven by local autoregulation. This helps prevent coronary steal

49
Q

What is the proper treatment frequency to prevent nitrate tolerance?

A

Take at the start of an anginal attack, or in anticipation of exercise or stress. However, impose a 8-12 hr break each day (sleep) to prevent tolerance.

50
Q

What is the purpose and mechanism of clonidine?

A

Clonidine is a partial a2A agonist. This acts at the brainstem to reduce the sympathetic outflow from CNS. This results in a reduction in blood pressure via a reduction of NE release.

51
Q

What are some direct vasodilators of vascular smooth muscle?

A 
hydralazine - unknown mechanism
minoxidil - K+ channel opener
sodium nitroprusside - NO donor
organic nitrates (nitroglycerine) - NO donor
52
Q

What are some notable Ca++ channel blockers used for vasodilation?

A

nifedipine - dihydropyridine L-type Ca++ channel blocker

verapamil - non-dihydropyridine L-type Ca++ channel blocker

52
Q

What drugs are used for hypertensive emergencies and why?

A
  • sodium nitroprusside - short acting aterial/venous dilator, but higher toxicity
  • nicardipine/clevidipine - dihydropyridine Ca++ channel blocker
  • fenoldapam - D1 agonist, increases renal purfusion
  • nitroglycerine - venous dilator, onset 2-5 min
  • phentolamine - non-selective a-adrenergic antagonist
  • esmolol - B-blocker, onset <5 min. Tx aortic dissection or postop hypertension
  • labetalol - a1/B-adrenergic antagonist, safe for patients with CAD
  • hydralazine - arteriolar dilator, good for hypertensive crises associated with eclampsia
53
Q

what are the major organic nitrates used for angina?

A

1) nitroglycerin
2) isosorbide dinitrate
3) isosorbide-5-mononitrate

53
Q

Describe the mechanisms of action of nitroglycerine.

A

1) Dilation of the systemic venules -> decrease venous return -> decrease preload -> increase coronary blood flow
2) decrease preload -> decrease heart wall tension -> decrease O2 demand of heart -> decrease ischemia
3) dilate large coronary vessels, but the smaller vessels are unaffected -> local flow determined by O2 demand, but more blood is available in coronary -> decrease in ischemia without increasing potential for coronary steal

53
Q

What are the notable Calcium channel blockers used in treatment of angina?

A
  • verapamil
  • nifedipine
  • nimodipine
  • diltiazem
53
Q

What are the major side effects of nitrate vasodilators? What are some major contraindications?

A
  • hypotension, headaches (severe at times), dizziness, weakness, reflex tachycardia
  • sildenafil (and all PDE5 inhibitors), pre-existing hypotension, obstructive hypertrophic cardiomyopathy, diastolic heart failure (amyloidosis, fibrous pericarditis, scar tissue, etc)
54
Q

What are the mechanisms of Ca Channel Blockers?

A

1) dilate arteries to reduce afterload and O2 demans
2) reduce cardiac contractility to reduce O2 demans
3) decrease HR tp reduce O2 demand
4) decrease coronary resistance to increase blood flow

55
Q

What are the major side effects of Ca Channel Blockers? What are the major contraindications?

A
  • cadiac depression, cardiac arrest, bradycardia, AV block, CHF
  • CHF!
  • non-dihydropyridinies (verapomil, diltiazem) have less of an affect on vasodilation, but have a direct impact on heart conduction and contractility (HR)
56
Q

What are the mechanisms of action for propranalol?

A

non-selective B-agrenergic antagonist

1) reduce HR -> decrease O2 demand
2) Reduce contractility -> decrease O2 demand
3) arterial vasodilation -> decrease BP(afterload) -> decrease O2 demand

57
Q

Describe the mechanism of action for Aspirin.

A
  • irreversible, non-selective inhibition of COX
  • platelets have COX1 -> stop TXA2 production -> decrease recruitment and vasoconstriction
  • platelets don’t have nuclei -> can’t synthesize new COX –> platelet inactivated for life (7-10d)
58
Q

What are the major anti-platelet drugs?

A
  • Aspirin
  • clopidogrel
  • prasugrel
  • ticagrelor
  • dipyridamole
  • cilostezol
  • abciximab
  • eptifibitide
  • tirofiban
59
Q

What are the mechanisms of the major anti-platelet drugs?

A

Oral
1) COX inhibitor (aspirin)
2) ADP receptor inhibitor, irreversible (clopidogrel, prasugrel)
3) ADP receptor inhibitor, reversibile (ticagrelor)
4) PDE3 Inhibitor (dipyridamole, cilostezol)
Parenteral
5) GPIIb/IIIa inhibitor (abciximab, eptifibatide, tirofiban)

60
Q

Describe the general mechanisms being investigated for pharmacologic treatment of bleeding disorders and trauma?

A
  • Recombinant factors of the coagulation cascade
  • specific factor depends of form or Hemophilia (A=XIII, B=IX, C=XI)
  • factor VIIa is indicated in trauma (potential)
61
Q

What test are used to monitor anticoagulation therapy dosage?

A

aPPT and PT
activated Partial Thromboplastin Time -> intrinsic pathway (~20-40s)
Prothrombin Time -> extrinsic pathway (~10-14s)

62
Q

Describe the mechanism of action for heparin, low molecular weight heparin, and fondaparinux.

A

1) Heparin - irreversibly binds to the Antithrombin III and increase its affinity for thrombin (IIa), Xa, IXa, XIa, XIIa and kallekrein. This GREATLY increases the rate of break down of these factors –> decrease coagulation
2) LMWH - binds to ATIII and increases its affinity for ONLY factor Xa. This decreases rate of coagulation, but not to the extent of heparin, which lessens the risk of bleeding.
3) fondaparinux - smaller, synthetic fraction of heparin that also only increases the affinity for Xa

63
Q

What is the mechanism of action for warfarin?

A

Warfarin interrupts the reduction of Vitamin K. This depletes the supply of Vitamin K reductase, which is required for the activation of several coagulation factors (II, VII, IX, X). This decreases coagulation activity.

63
Q

What are some major drug interactions with warfarin?

A

Warfarin’s affect is driven by inhibition of Vitamin K and is cleared through metabolism in the liver/kidneys, and excreted in urine. Anything that affects these paths will change warfarin.
Increase effect:
Aspirin - decreased clotting directly
Amiodarone - inhibit metabolism
3G cephalasporin - eliminate bacteria in gut that make vitamin K
Decrease effect
barbituates - increase metabolism in liver
Vitamin K foods

64
Q

What are some potential alternatives to warfarin?

A

dabigatran - direct thrombin inhibitor
rivaroaban - direct Xa inhibitor
apixaban - direct Xa inhibitor

65
Q

What is the purpose and mechanism of thrombolytics?

A

Used parenterally to break down a clot. They stimulate the conversion of plasminogen to plasmin, which will then dissolve the fibrin in the clot.

  • urokinase
  • streptokinase
  • tissue plasminogen activator (t-PA)
66
Q

What are two natural compounds that can increase HDL?

A 
Fish oil (omega-3)
estrogen
67
Q

What is the mechanism of action of bile acid-binding resins?

A

lower cholesterol by binding bile acids in the intestine, which allows them to be cleared. This is sensed by the liver, and it upregulates cholesterol receptors, which helps to replace the bile acids. This decreases internal concentration.

68
Q

What are some notable HMG-CoA reductase inhibitors?

A
  • lovastatin
  • simvastatin
  • fluvastatin
  • atorvastatin
  • rosuvastatin
69
Q

What is the mechanism of action for statins?

A

competitively inhibit HMG-CoA reductase, which is a key enzyme in cholesterol synthesis.
Decrease in hepatic cholesterol -> upregulate cholesterol receptors on liver -> increased clearance of VLDL, IDL and LDL

70
Q

What are some major side effects and drug interactions with statins?

A

-mild hepatotoxicity, myopathy, rhabdomyolysis
NEVER give during pregnancy
Increase effect - grapefruit juice, verapamil

71
Q

What are some notable drugs that lower triglycerides?

A
  • niacin
  • fenofibrate
  • fish oil
72
Q

What are some notable drug combinations used to tx hyperlipidemia?

A

niacin + fibrate -> increase in rhabdomyolysis
niacin + statin
niacin + neomycin

Used when the tolerable dose of one drug is not adequate to lower lipids.

73
Q

a-adrenergic agonists

A 
Epi (1,2)
Ne (1,2)
Clodipine (2)
midodrine (1)
brimonidine (2)
phenylephrine (1,2)
oxymetazoline (1,2)
Dopamine (1 at high doses)
indirect effect by displacing NE: amphetamine, ephedrine
74
Q

B-adrenergic agonists

A 
Epi (1,2)
NE(1)
isoproterenol (1,2)
dobutamine (1)
Dopamine (weak 1 at low doses)
albuterol (2)
indirect effect via displacing NE: amphetamine, ephedrine
74
Q

dopamine agonist, antagonist

A 
Agonist:
Dopamine (D1, B1 @low doses)
fenoldapam (1)
Antagonist:
buproprion (nicotine dependence therapy)
75
Q

a-adrenergic antagonist

A 
phenoxybenzamine (1,2)
phentolamine (1,2)
prazosin(1)
terazosin(1)
tamsulosin (1)
Mixed w/ B1/2:
carvedilol(1)
labetalol (1)
76
Q

B-adrenergic antagonist

A 
propanolol (1,2)
metoprolol (1)
atenolol (1)
sotalol (1,2)
esmolol (1)
pindolol(1,2 w/ partial agonist)
Mixed w/ a1: 
cladivilol (1,2)
labetalol (1,2)
77
Q

cholinergic

A

ACh
bethanechol
muscarine
pilocurpine

78
Q

anticholinergic/antimuscarinic

A 
atropine 
scopolamine
ipratropium
tiotropium (M1,3)
pirenzepine (M1)
79
Q

ganglionic agonists, antagonists

A 
all for nAChN
Agonist:
nicotine
Antagonist:
hexamethonium
varenicline
80
Q

class I anti-arrhythmic

A 
Class I - Na channel blockade
Ia - procainamide
Ib - lidocaine
Ic - flecainide
amiodarone -> class I-IV action
81
Q

class III anti-arrhythmic

A

class III -> K+ channel blockade
ibutilide
bretylium (also decrease NE)
amiodarone -> class I-IV action

82
Q

Ca++ channel blocker

A 
Ca++ blocker = class IV anti-arrhythmic 
verapamil
diltiazem
adenosine (also increases K+)
nifedipine
nicarpidine
clevidipine
nimodipine
83
Q

RAAS

A 
aliskiren (renin inhibitor)
captopril (ACE i)
enalapril (ACE i)
losartan (ARB)
spirinolactone (aldosterone i)
eplerenone (aldosterone i)
84
Q

direct vasoldilator

A 
hydralazine
minoxidil (K+ donor)
NO donors
85
Q

NO donors

A

nitroglycerine
sodium nitroprusside
isosorbide dinitrate
isosorbide-5-mononitrate

86
Q

anti-thrombolitic

A 
aspirin(COX i)
clopidigrel (ADP receptor i)
prasurgrel (ADP receptor i)
ticagrelor (ADP receptor i)
dipyridamol (PDE i)
cilastazol (PDE i)
abiximab (direct GPIIb/IIIa i -> Fab)
eptifibatide (direct GPIIb/IIIa i)
tirofiban (direct GPIIb/IIIa i)
87
Q

anticoagulant

A 
heparine (II, Xa, IXa, XIa)
LMWH (Xa)
fondaparinux (Xa)
warfarin (II, VII, X, IX)
lepirudin (II)
bivalirudin (II)
dabigatram(II)
rivaroxaban (Xa)
88
Q

thrombolytic

A

promote plasminogen->plasmin –> fibrinolysis
urokinase
streptokinase
tissue plasminogenic factor (t-PA)

89
Q

hyoplipidimic

A 
Decrease cholesterol:
colestipol (bile salt)
cholestyramine (bile salt)
colesevelam (bile salt)
lovastatin (HMG-CoA)
simvostatin  (HMG-CoA)
pravastatin  (HMG-CoA)
atorvastatin (HMG-CoA)
rosuvastatin (HMG-CoA)
ezetimibe (chol receptor i)
Decrease TG:
niacin (-VLDL synthesis)
fenofibrate (+VLDL metabolism)

Module 3 - CPR (10 decks)

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