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Pharm > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Autocoid

A

compounds that are released and act out locally in periphery
ex. histamine, serotonin, prostaglandins

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2
Q

What breaks down histamine?

A

MAO-B breaks histamine down into the inactive metabolite methylimidazole acetic acid which can be measured in the urine

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3
Q

Histamines function

A

PNS (autocoid) - stimulates primary afferent nerve endings: itch, pain –> H1 receptors
inflammation
CNS (NT) arousal, body temp, appetite

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4
Q

H1 receptor

A 
histamine receptors (g-coupled) 
smooth muscle cells, CNS --> increase IP3, DAG, and Ca2+ 
endothelium --> increase NO and cAMP (Gq)

the import one to know here is endothelium receptors increase NO and cAMP which causes relaxation which wins out over the contraction effect that histamine has on the smooth muscles

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5
Q

Where is histamine stored?

A

Mast cells
granules complexed with heparin/acidic protiens
protected when stored

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6
Q

H2 receptor

A

vascular smooth muscle –> increased cAMP (Gs)

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7
Q

H3/H4 receptors

A

decrease cAMP (Gi)

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8
Q

What drugs affect histamine release?

A

opioids STIMULATE release

Epi/cromolyn INHIBIT release

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9
Q

Why can’t you take antihistamines when you are in anaphylaxis?

A

most anaphylaxis sxs are NOT caused by histamines

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10
Q

How do allergic reactions differ from inflammation responses?

A 
Allergic reactions (type 1 hypersenstivity) is IgE mediated 
Inflammation is complement (C) system
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11
Q

Local Allergic Reactions

A

sxs largely due to histamines
urticaria (hives)
ALLERGIC RHINITIS (–> costs billions a year)

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12
Q

Steroids are derived from what?

A

Cholesterol

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13
Q

Where is cortisol made?

A

zona fasiculata in the adrenal cortex stimulated by ACTH (adrenocorticotropic hormone)

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14
Q

Where is aldosterone made?

A

zona glomerulosa-aldosterone in the adrenal cortex stimulated by ang 2 and K+

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15
Q

What are the 3 mechanisms of neuroendocrine control?

A

1) episodic - secretion of ACTH in response to circadian rhythm
2) stress - HPA axis responds to stress
3) feedback inhibition - by cortisol of ACTH secretion

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16
Q

CRH

A

corticotropin releasing hormone
released by hypothalamic neurons
controls ACTH release

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17
Q

Where is ACTH released from?

A

anterior pituitary

adrenocorticotropic hormone

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18
Q

What regulates glucocorticoid synthesis?

A

HPA Axis - hypothalamic - pituitary adrenal axis

negative feedback loop

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19
Q

What is the negative feedback loop to glucocorticoid synthesis?

A

Hypothalamus under stress targets neurons that release NT that stimulate the hypothalamus which releases CRH which causes ACTH release which causes cortisol release which then turns around of suppresses CRH release

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20
Q

What is the MOA of glucocorticoids?

A 
bound to protein (the steroids) d/t lipophilic 
get into cell (no GCPR needed) 
reside in cytosol 
dimerize and translocate to nucleus 
bind to GRE on DNA
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21
Q

What is the physiological actions of glucocorticoids?

A

maintain blood glucose during fasting (increase in stress)
increase glucose synthesis (in liver)
builds up glycogen (as reserve)
increase protein breakdown (osteoporosis)

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22
Q

What are the anti-inflammatory/immunosuppressive effects of glucocorticoids?

A

don’t prevent/suppress underlying disease

they suppress immune system and thus suppress inflammation

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23
Q

What are the ways to inhibit inflammatory events via glucocorticoid receptor?

A

increase annexin A1 (lipocortin 1) production
decrease COX-2 synthesis (decrease prostaglandin and luekotriene production)
decrease TNF-a synthesis (tumor necrosis factor)

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24
Q

What does annexin A1 do?

A

blocks phospholipase A2 from turning phospholipids into arachidonic acid (blocks COX pathways)

we increase this production when we are trying to inhibit inflammatory events via glucocorticoid receptor

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25
Q

What is the net effect of Epi or NE?

A

increase HR and vascular tone (BP)

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26
Q

What is the main receptor innervation of the heart?

A

Beta 1 “be my #1”

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27
Q

Who will win out if both alpha 1 and beta 2 are activated?

A

alpha 1 will win out

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28
Q

What are the 3 main examples of catecholamines?

A

Epi, NE, and dopamine

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29
Q

Where is epi released from?

A

adrenal medulla

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30
Q

What is Isoproterenol?

A

selective beta agonist that may be used to stimulate the heart

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31
Q

How is Epi synthesized?

A

Tyrosine –> DOPA –> Dopamine –> NE –> Epi

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32
Q

Presynaptically what inhibits NE release?

A

alpha 2 receptor + PGE2R on the presynaptic cell

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33
Q

What enhances NE release?

A 
Angiotensin 2 (ANG2R) 
this is because you are constricting blood vessels --giving NE a boost
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34
Q

In the terminal, what regulates NE levels?

A

MAO

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35
Q

How is released NE reaccumulated?

A

by the NET

90% of released NE is reaccumulated by the NET

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36
Q

How is circulating Epi (or any catecholamine) broken down?

A

COMT or MAO

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37
Q

How is adrenergic status measured?

A

urinary catecholamine metabolites

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38
Q

Facilitated Exchange Diffusion

A 
When NET (hotel door) allows excess NE out of the nerve terminal into the synapse 
This happens when MAO is inhibited (say by meds) and there is a buildup of NE --> this can lead to a adrenergic crisis when the NE leaves through the NET into the synapse
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39
Q

Tranylcypromine is an example of what?

A

MAO - Inhibitor

used to treat atypical depression

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40
Q

Chronic agonist use can cause?

A

desensitization and down regulation
(if you are chronically activating receptors the body will remove some and be less sensitive to the activation)

*exception: nicotinic agonists upregulate nicotine

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41
Q

Chronic antagonist use can cause?

A

supersensitization and upregulation

if you are chronically blocking receptors the body will make more in efforts to be activated

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42
Q

Beta 1 receptor prefers what drug?

A

Iso but settles for NE (NE gets the ones)

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43
Q

Beta 2 receptor prefers what drug?

A

Iso but settles for Epi

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44
Q

Alpha 1 receptor prefers what drug?

A

Epi but settles for NE (NE gets the ones)

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45
Q

What structural differences in adrenergic drugs determines if it can penetrate the CNS?

A

The hydroxyl groups off the ring prevent CNS penetration

non-catecholamines

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46
Q

What adrenergic drugs can enter the CNS?

A 
amphetamine 
ephedrine
phenylephrine
methoxamine 
don't have hydroxyl groups off the ring 
enter CNS --> "buzz"
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47
Q

Beta 2 activation

A

decrease in BP

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48
Q

Which receptor distribution is more restricted? Alpha 1 or beta 2?

A

Beta 2 is more restricted

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49
Q

Which receptor increases contractility?

A

beta 1

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50
Q

What do Xanthines do?

A

drugs that produce effects resembling sympathetic stimulation but are NOT binding to adrenergic receptors (theophylline + caffeine)
antagonists of adenosine receptors (these keep you awake while adenosine puts you to sleep)

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51
Q

What drugs do you use to treat variant angina?

A

CCB - to dilate smooth muscle

Beta blockers are CONTRAINDICATED

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52
Q

What is one reason why nimodipine (a CCB) would be used over any other CCB?

A

It has a high affinity for cerebral vessels and may reduce vasospasm and mortality after subarachnoid hemorrhage

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53
Q

What is CCB effect on heart cells?

A

Decrease contractility

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54
Q

What is the effect of CCB on coronary circulation?

A

Decrease coronary resistance

Increase coronary blood flow

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55
Q

What are the major differences between dihydropyridine CCB and verapamil and diltazem?

A

Nifedipine and nimodipine work better at vasodilation (esp. at lower concentrations)
Dihydropridines lower arterial resistance and BP but run the risk of reflex increase in CO (HR + contractility)
Verapamil slows AV conduction, decreases HR, contractility, and rate of recovery in Ca channels

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56
Q

What affect does nifedipine have on AV conduction and the rate of recovery of Ca channels?

A

No change

Verapamil slows AV conduction and decreases recovery rate of Ca channels

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57
Q

How does the effect of HR and Contractility differ between the two major types of CCB?

A

Dihydropyridine CCB have reflex increase in HR and contractility
Verapamil has decrease CO

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58
Q

What are the major side effects of CCB?

A 
Cardiac depression 
Cardiac arrest
Bradycardia
Peripheral edema
Constipation (esp. in verapamil) 
AV block 
CHF
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59
Q

What conditions are CCB contraindicated for?

A

HF and left ventricular dysfunction

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60
Q

Which HTN drug to use for DM pts?

A

ACE-I since it is renal protective

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61
Q

Which HTN drug to use for pregnant patients?

A

Methyldopa

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62
Q

Which HTN drug to use for MI hx?

A

Beta blocker

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63
Q

Which HTN drug to use that will regress left ventricular hypertrophy?

A

ACE-I

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64
Q

Which HTN drug to use for african americicans?

A

CCB (never an ACE-I)

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65
Q

Which HTN drug to use post subarachnoid hemorrhage?

A

Nimodipine

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66
Q

When would you use a dihydropyridine CCB?

A

If you just wanted vasodilation and did not want to affect contractility of the heart
risk of reflex tachy tho

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67
Q

MOA of HCTZ?

A

inhibit Na/Cl transporter @ DCT, increasing Na in lumen and thus reducing vascular resistance and afterload

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68
Q

What are the adverse effects of HCTZ?

A

sexual impotence

loss of K+ leading to risk of arrhythmias

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69
Q

What are the contraindications of HCTZ?

A

pts with impaired renal function

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70
Q

What are the indications for ACE-I?

A

LV hypertrophy, delay HF/MI, slow progression of renal disease in DM with HTN

1st line: DM, HF, hypertrophy
2nd line: MI (BB is 1st line for MI

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71
Q

What are the contraindications of ACE-I?

A

BILATERAL renal artery stenosis

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72
Q

BB are first line for?

A

HTN
Angina
MI
arrhythmia/fib

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73
Q

Nitrates act on the ______ while CCB act one the ______.

A

venules

arterioles

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74
Q

Prazosin is what type of drug?

A

alpha 1 antagonist (blocker)

used as a combo therapy for HTN

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75
Q

What is first dose phenomenon and with which drug do you see it?

A

orthostatic hypotension
seen with prazosin

more common in pts already on BB or diuretics

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76
Q

What is the MOA for prazosin?

A

decrease arteriole resistance and venous capacitance by inhibiting vasoconstriction induced by endogenous catecholamines

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77
Q

Prazosin SEs?

A

orthostatic hypotension
evoke Na/H2O retention

not effective as a sole HTN tx

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78
Q

What vasodilators are used to treat HTN?

A

Hydralazine
Minoxidil
Sodium Nitroprusside

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79
Q

What is the difference between Hydralazine and Minoxidil from sodium nitroprusside?

A

Hydralazine and minoxidil only relax arterioles
Sodium nitroprusside works on aterioles and some venules thus decreasing oxygen demand of the heart unlike the other two which are at risk of ischemia

plus sodium nitroprusside is IV only due to degradation in light

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80
Q

PO vasodilators for HTN are contraindicated in which patients?

A

HTN + CAD pts or ventricular hypertrophy

typically given with BB

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81
Q

Which vasodilators are used to treat CHF?

A

Hydralazine

Isosorbide dinitrate

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82
Q

MOA of most vasodilators?

A

pro-drugs metabolized to active metabolite that causes vasodilation/relaxation of arterioles

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83
Q

Which drug is safe to treat HTN in pregnancy?

A

methydopa –> alpha 2 agonist

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84
Q

What are the side effects of clonidine and methydopa?

A

dizziness, reduced libido, sedation and depression

sudden discontinuation may cause withdrawal syndrome and HTN crisis

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85
Q

Which CCB are used to treat HTN?

A

Amlodipine

Verapamil

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86
Q

Which ACE-I are used to treat HTN?

A

captopril

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87
Q

Which ARBs are used to treat HTN?

A

losartan

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88
Q

Which diuretics are used for HTN?

A

HCTZ, amioride, spironolactone (aldosterone blocker)

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89
Q

Why is alpha 2 AGONIST considered an ANTIadrenergic?

A

because anything binding to alpha 2 acts as a negative feedback loop to stop NE release

methyldopa and clonidine

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90
Q

What is the difference between HF with REDUCED EF vs HF with PRESERVED EF?

A 
REDUCED = systolic dysfunction (volume overload = big chamber) 
PRESERVED = diastolic dysfunction (pressure overload = thick wall)
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91
Q

How do BB decrease renin?

A

block the juxtaglomerular cells from releasing renin

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92
Q

Where on the pathway of renin to Na reabsorption does spironolactone work?

A

Spironolactone is an aldosterone antagonist (as is eplerenone)
this prevents Na reabsorption as well as another pathways that protects the heart from fibrosis caused by too much aldosterone

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93
Q

What is the major adverse effect of spironolactone?

A

HYPERKALEMIA
due to it being a potassium sparing diuretic (aldosterone antagonist)
gynecomastia due to blocking progesterone and androgen receptors

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94
Q

What is the major difference between eplerenone and spironolactone?

A

both aldosterone antagonists
eplerenone is more selective for aldosterone receptors and is FDA approved for CHF following AMI
no risk of gynecomastia due to no binding to androgen receptors

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95
Q

Which diuretic is FDA approved for CHF post MI?

A

eplerenone (aldosterone antagonist)

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96
Q

treatment for variant angina

A

CCB for smooth muscle dilation

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97
Q

treatment for unstable angina

A

aspirin + statin

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98
Q

What drug has a greater decrease in mortality and morbidity than ACEI?

A

ARNI

better to give to pts with renal impairment than ACEI

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99
Q

ARNI is what kind of drug?

A

ARB + Neprilysin inhibitor

neprilysin is a vasocontrictor that also degrades ANP and BNP stimulated by CHF stress signals

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100
Q

When/why are BB used with CHF?

A

they decrease morbidity and mortality when combined with ACEI and diuretics

can only be used once pt is “stabilized” since decreasing contractility will exacerbate CHF

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101
Q

What is Ivabradine?

A

Funny channel blocker used for CHF

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102
Q

Ivabradine MOA

A

inhibits pacemaker cell funny current to decrease SA node rate and thus decrease HR

metabolized by CYP3A4

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103
Q

Indication for Ivabradine?

A

very specific

symptomatic CHF with LVEV <35% and they HAVE to have HR > 70 on BB

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104
Q

Digoxin MOA

A

increase Ca inside the cell thus increasing contractility

hyperkalmeia is sign of toxicity

indirect effects: decrease HR, decrease SA node pacemaker activity, decrease AV conduction

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105
Q

What is the drug of choice for pts with hypertriglyceremia?

A

Gemfibrozil

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106
Q

Which drug is CONTRAindicated in pts with hypertrigylceremia?

A

cholestyramine - bile acid sequestrants

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107
Q

What is the MOA for Gemfibrozil?

A

agonist for PPAR-alpha receptor (transcription factor) that then decreases TG through LPL synthesis and apoc-3 production which increases TG clearance

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108
Q

Why cant gemfibrozil be given with statins?

A

Gemfibrozil blocks OATs in the liver which is what Statins use to get into the liver cells and stop cholesterol production

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109
Q

What is the MOA, indication, and SE or Evolocumab?

A

PCSK9 inhibitor preventing the degradation of LDL receptors

indications: familial hpercholesterolemia

SE: nasopharyngitis

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110
Q

Fluticasone

A

ICS used for asthma PREVENTION
SE: oral candidiasis
controversial use in COPD

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111
Q

Fluticasone MOA

A

target and suppress inflammatory gene transcription (decrease cytokines and increase B2 receptors)

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112
Q

Methylpredinisolone

A

systemic corticosteriod for short term asthma treatment

withdrawal drug over 1-2 weeks and transfer to ICS

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113
Q

What is the most common rescue inhaler for asthma pts?

A

Albuterol (B2 agonist) SABA

if used more than 2 times per week than asthma is NOT controlled

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114
Q

What is the MOA for SABA and LABA?

A

inhibit release of mast cell mediators and increase glucocorticone nuclear transcription (LABA + ICD for asthma)
increase mucociliary transport and bind to B2 and relax airway smooth muscle

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115
Q

LABA treatment for asthma vs COPD?

A 
Asthma = ICD + LABA 
COPD = LABA monotreatment okay
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116
Q

SE for LABA/SABA

A

muscle tremor, tachycardia, hypokalemia, potential tolerance

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117
Q

Ipratropium Bromide

A

SAMA

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118
Q

Toitropium

A

LAMA (>24 h)

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119
Q

MOA for SAMA/LAMA

A

block AcH release from vagus nerve (preventing it from binding to M3 receptor)
inhibit vagally mediated airway tone
NOT an anti-inflammatory
decrease mucus secretion and smooth muscle contraction

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120
Q

What are the SE of SAMA/LAMA?

A

dry mouth

caution in older men with BPH (could prevent relaxation of prostate and preventing urination??)

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121
Q

Are muscarinic antagonists anti-inflammatory?

A

NO

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122
Q

Theophylline

A

Theo likes to cAMP (phosphdiesterase inhibitor)
increase cAMP and block adenosine receptors
decrease contraction and histamine release

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123
Q

Theophylline’s effect on COPD?

A

increase diaphragm muscle contractility (increase ventilation)

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124
Q

Montelukast in asthma vs COPD?

A 
ASTHMA ONLY (no role in COPD therapy) 
leukotriene pathway inhibitor)
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125
Q

Omalizumab

A

IgE inhibitor used for asthma
decreases frequency and severity of exacerbations

given subq
$$$

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126
Q

Explain MOA of steroids

A

get into cell –> dimerize –> translocate to nucleus –> bind to GRE on DNA

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127
Q

What are the 3 ways to inhibit inflammatory events via Glucocorticoid Receptor?

A
  • Increase Annexin A1 production (blocks phospholipase A2 from converting phospholipids into arachodonic acid
  • decrease COX2 synthesis (decreases pg and lk production)
  • decrease TNF synthesis (tumor necrosis factor –> inflammation)
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128
Q

11B-HSD2

A

turns cortisol into cortisone (inactive)

this is inhibited by glucurrhizic acid (found in licorice)

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129
Q

Cortisols affects on the kidneys

A

acts like aldosterone

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130
Q

Prolonged steroid treatment can result in…?

A

mimicing cushing syndrome (weight gain)

can also thin skin and cause osteoporosis

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131
Q

HPA axis and negative feedback mechanism

A

Hypothalamus releases CRH which acts at the anterior pituitary which releases ACTH which acts on the adrenal cortex which produces and releases cortisol from the zona fasiculata
cortisol then inhibits the hypothalamus and the anterior pituitary as the negative feedback loop

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132
Q

Aldosterone replacement therapy

A

Fludrocortisone (minteralocorticoid)

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133
Q

Which drug is used to diagnosis causes of hypercorticism?

A

dexamethasone blocks ACTH between the anterior pituitary and the adrenal cortex which would thus prevent the adrenal cortex from being stimulated to release cortisol and there would be a decrease in cortisol levels
if you give dexamethasone and it does NOT reduce cortisol levels than there might be a tumor on the adrenal gland

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134
Q

ADME for anti-histamines

A

inverse agonists (competitive antagonists)
lipid soluble
metabolized in liver/ renal excretion (except fexofenadine)
caution! elimination in breast milk!

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135
Q

1st gen vs 2nd gen antihistamines

A 
1st gen:
- cheap
-cross BBB
-anticholinergic effect --> dry up secretions 
-contraindicated in glaucoma, or BPH 
2nd gen: 
-dont cross BBB
-ionized at physiologic pH 
-little to no anticholinergic effect 
-last longer (once daily)
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136
Q

Fexofenadine

A

2nd gen anti-histamine

excreted in the bile (all others are excreted in the renal- urine)
inhibited by citric acid
transported by intestinal OATP1A2

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137
Q

What are the three 2nd gen anti-histamines?

A

Loratadine
Cetirizine
Fexofenadine

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138
Q

What are the three 1st gen antihistamines?

A

Chlorpheniramine
Diphenhydramine
Dimenhydrinate

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139
Q

Dimenhydrinate

A 
1st gen antihistamine
aka dramamine 
antiach +++
sedation +++ 
anti-motion sickness
140
Q

Diphenhydramine

A 
1st gen antihistamine 
aka Benadryl
antiach +++
sedation +++
OTC sleep aid
141
Q

Chlorpheniramine

A

1st gen antihistamine
antiach +
sedation ++
in OTC cold meds

142
Q

Cromolyn Sodium

A

anti - histamine
mast cell stabelizer
best used as prophylaxis
block release of all mediatiors at mast cell
directly inhibit mast cell degranulation (ion channel blocker)

143
Q

Which diuretic would you use as prophylaxis for acute mountain sickness?

A

Acetazolamide

144
Q

What is the MOA for CAI?

A

carbonic anhydrase inhibitor prevents the breakdown of carbonic acid to CO2 and H2O
increasing luminal Na and Bicarb which repels Cl-

145
Q

What is the end game of diuretics?

A

shift the steady state

146
Q

What is the mechanism of mannitol?

A

freely filterable, works at water permeable segments of the nephron (mainly to tDLH)

IV only d/t not GI absorbed and short half life

147
Q

What does the urine look like for a pt on mannitol?

A

increase volume
increase electrolytes
increase Mg2+ (unknown why)
decrease osmolality

148
Q

Loop diuretics

A

furosemide
ethacrynic acid
bumetanide

149
Q

MOA of furosemide

A

block Na+/K+/2Cl- at the TALH

large doses ABOLISH osmotic gradient (kidney can’t dilute urine)

150
Q

What is the first choice diuretics for HTN +CHF?

A

loop diuretics such as furosemide or ethacrynic acid

151
Q

Which diuretics are K+ wasting?

A

Loop diuretics and thiazides

152
Q

Which diuretics are K+ sparing?

A 
ENac inhibitors (amiloride) 
Aldosterone Antagonists
153
Q

HCTZ is often given with what other drug?

A

ACEI to counteract the hypokalemia –> hypovolemia

154
Q

Indications for HTCZ

A

hypercalciuria –> PREVENTS kidney stones

HTN, CHF (not first line)

155
Q

What is the MOA for HTCZ?

A

blocks Na/Cl symporter @ the DCT

156
Q

Aldosterone Antagonists

A

spironolactone

eplernone

157
Q

Spironolactone MOA

A

prevents aldosterone from binding to receptors athe the LDCT and CD –> decreasing Na+ reabsorption
canrenone the active metabolite forms inactive receptor complexes
ONLY WORKS IF ALDOSTERONE LEVELS ARE HIGH

158
Q

Side effects of spironolactone

A

GYENECOMASTIA

hypERkalemia (d/t potassium sparring)

159
Q

Amiloride MOA

A

potassium sparing ENaC diuretic
blocks ENaC channels
secreted by OCT (all others except mannitol are OAT)

rarely given alone (typically given with HCTZ or loop)

160
Q

What are the indications for Tolvaptan?

A

Talvaptan is a vasopressin antagonist (antidiuretic)

SIADH

161
Q

MOA for Tolvaptan

A

antagonist of ADH @ V2 ADH receptors (CONIVAPTAN (IV) is nonselevtive ADH receptors)
@ CD at basolateral membrane

162
Q

Adverse effects of tolvaptan?

A

hypernatremia

163
Q

Which diuretics have shown to decrease morbidity and mortality?

A

the potassium wasting ones

HCTZ and loop

164
Q

HTN tx vs HTN + CHF tx

A

HTN –> HCTZ

HTN + CHF –> Loop diuretics

165
Q

What is aldosterones effect on the CD?

A

stimulates Na/K channels to promote Na reabsorption

166
Q

Which diuretic at high doses abolishes the osmotic gradient?

A

Furosemide (loop diuretic)

167
Q

Which antiarrythmics are used as rate control for A.Fib?

A 
Class 2 (BB) 
Class 4 (CCB) 
Digoxin
168
Q

What antiarrythmics are used as rhythm control for A.Fib?

A 
Class 3 (K blocker) 
Class 1C (Na blocker)
169
Q

When to use Class 1 antiarrythmics?

A

for re-entry tach (VT) because they are selective for diseased (unpolarized) tissue

170
Q

Class 1 antiarrythmics prolong effective refractory period, order A, B, and C subclass from longest to shortest ERP.

A

1C (longest ERP) > 1A > 1B

171
Q

The difference between Class 1A and 1B in regards to potassium and action potential duration (ARD)

A

1A decreases K and increases APD

1B increases K and decreases APD

172
Q

How does Amphetamine work?

A

it is a substrate for the NET since it looks like NE
it blocks MAO metabolism so when it replaces NE in the vesicles and send NE into the synapse there is an increase in BP and HR
it doesnt have a hydroxyl group allowing it to enter the CNS and get that “buzz”

good for narcolepsy and weight reduction

173
Q

How does Tyramine work?

A

typically ingested by cheeses, wine, beer, and fava beans
gt metabolized in GI via MOA
if tyramine escapes MOA or pt is on MOAI then the tyramine uses NET and kicks out NE similar to reserpine

if on MOAI then NE can’t get metabolized –> HTN crisis

174
Q

What do Cocaine, Imipramine, and Atomoxetine have in common?

A

All block NET and cause HTN crisis because that 90% of NE can’t be brought back into the presynaptic neuron

175
Q

Norepinephrine is an agonist to what receptors?

A

it likes the 1s
B1 and Alpha 1
thus Increase HR(B1) and BP(alpha)

176
Q

What are the indications for norepinephrine?

A

ER for shock

177
Q

Which receptors does epi like?

A

Its promiscuous
at low doses - betas
high doses - alpha

178
Q

What is phenylephrine?

A

alpha agonist

it does not have hydroxyl groups so it enters the CNS and causes that “buzz”

179
Q

What receptors does dopamine like?

A

at high doses, everything

decrease BP d/t DA and B2 but increase BP at high doses due to alpha 1

180
Q

Does dopamine cross into the BBB?

A

no

181
Q

What are the side effects of dopamine?

A

CTZ, chemotrigger zone –> N/V

tachy, angina, arrythymias

182
Q

What receptors does dobutamine like?

A

low doses: betas

high doses: also alpha 1

183
Q

What does dobutamine do?

A

Contractility&raquo_space;»>rate
increases contracctility
at high doses will also increase BP due to alpha 1

184
Q

What are the indications of dobutamine?

A

HF associated with open heart surgery or acute cardiac infarction

185
Q

Does dobutamine cross the BBB?

A

no

186
Q

What are the side effects of dobutamine?

A

arrythmias

187
Q

What is isoproterenol?

A

synthetic catecholamine designed to stimulate the heart

it likes the betas! B1 (4+) B2 (4+)

188
Q

What are the effects of isoproterenol?

A

increase HR and decrease BP (B2)

bronchodilation (B2)

189
Q

What are the indications for isoproterenol?

A

emergency heart block (stimulate the heart!)

or in preparation for pacemaker surgery

190
Q

What are the side effects of isoproterenol?

A

fatal arrhythmias, tachycardia, palpitations, angina

191
Q

Ephedrine

A

Weak alpha and beta agonist
enters CNS –> “buzz”
causes increase in BP (pressor agent), dilates pupils, eye drops (gets the red out by vasoconstriction)
nasal decongestant ( bronchodilation, relaxation of preg. uterus

192
Q

What are the side effects of ephedrine?

A

excessive alpha 1 —> increase BP

excessive dose can activate B1 and effect the heart

193
Q

Terbutaline

A

same as albuterol
bronchial dilation in asthma pts
these are considered b2 selective but nothing is really selective, especially at high doses

194
Q

What are the functions of Beta 2?

A

Dilate the blood vessels
Bronchodilation
Decrease motility in the GI
relax uterus

195
Q

Besides for asthma, albuterol and terbutaline can be used for what?

A

Remember that they are Beta 2 “selective”

so they will relax the pregnant uterus

196
Q

What are the functions of Beta 1?

A

increase renin release

increase HR, CO, contractility, and decrease efficacy of the heart

197
Q

What are the functions of Alpha 1?

A 
constrict vessels 
decrease secretions
contract sphincters in both bladder and GI
ejecaculation 
contracts uterus
198
Q

Which type of G protein receptor is Alpha 2?

A

Gi –> inhibit

199
Q

What type of G protein receptor is alpha 1?

A

Gq –> PIP –> IP3 + DAG

200
Q

What type of G protein receptor are the betas?

A

Gs

201
Q

How does Caffeine work?

A

Xanthines
drugs that produce effects resembling sympathetic stimulation but are NOT binding to adrenergic receptors

adenosine antagonists –> keeps you awake (adenosine puts you to sleep)

increases HR, contractility, dilates blood vessels, decrease TRP (

202
Q

Theophylline

A

Xanthines
MOA: phosphodiesterase inhibitor which increase cAMP (Theo likes to camp) which pushes the system towards bronch and vasodilation
also an adenosine antagonist so it keeps you awake

203
Q

Phentolamine

A

alpha blocker (non-selective)

think about what alpha 1 and 2 does
decrease HR (due to alpha 1) ???
alpha 2 will prevent NE release (negative feedback)
GREATER TACHY REFLEX

204
Q

Phenoxybenzamine

A

IRREVERSIBLE alpha blocker

a1 > a2

205
Q

What are the indications of phenoxybenzoamine?

A

BPH

pheochromocytoma when given with phetolamine

206
Q

Prazosin

A

alpha 1 blocker (reversible)
used in HTN and BPH (relax and allow for urination)

decrease BP (because you are preventing vasoconstriction) 
REFLEX TACHY
207
Q

Carvedilol

A

mixed alpha and beta blocker
used in HTN and CHF (mainly for its beta blockingness)
B:A 10:1

208
Q

Labetalol

A

mixed alpha and beta blocker
B:A 4:1
used in HTN (chronic and acute secondary to increased catecholamines)

209
Q

Esmolol

A

Beta 1 blocker “selective”

good for EMERGENCY BP management

210
Q

Atenolol

A

Beta 1 selective blocker

211
Q

Timolol

A

non-selective beta blocker
used for its effects on the eye –> decrease aqueous humor production
indications: glaucoma

SE: think about blocking betas —> bonchospasm (b2), decrease HR, CO

212
Q

Guanethidine

A

works presynaptically
gets in via the NET and concentrates in vesicles depleting NE overtime
historyically used for HTN

213
Q

Reserpine

A

lipid soluble, doesnt need to use the NET

blocks VMAT from letting NE into the vesicles so you end up with empty vesicles

214
Q

What is the difference between guanethidine and amphetamine?

A

both use NET to get in and concentrate in the vesicles, replacing and ultimately depleting NE
amphetamine just does it much FASTER so the MAO can’t keep up and you end up with an increase in BP which is the opposite effect of guanethidine

215
Q

Clonidine

A

alpha 2 agonist –> antiadrenergic

prevents NE release

216
Q

What are the indications for Clonidine?

A

essential HTN, ADHA, opioid withdrawal sxs

217
Q

What are the side effects of clonidine?

A

dry mouth, sedation, dizziness, depression,

HTN crisis if abruptly stopped

218
Q

Methyldopa

A

alpha 2 agonist (antiandrenergic)
used for HTN in pregnancy

SE: dry mouth, sedation, increase autoimmune response (+COOMBS test)

219
Q

What is the overall effect of alpha 1 blocker?

A 
decrease TPR (d/t decreasing vasconstriction) 
reflex tachy because of the increase in NE released (alpha 2 compensates slightly with the negative feedback and decreases the NE released)
220
Q

What is the overall effect of nonselective alpha blockers?

A

decrease in TPR
MUCH GREATER REFLEX TACHY because NE is released but there is no feedback loop when alpha 2 is blocked so even more NE is released

221
Q

Lidocaine

A 
Class 1B (B = BEST for post MI) 
MOA: block Na channels, primarily in the depolarized (sick) cells 
increase ERP and Potassium out --> decrease AP duration
222
Q

Class 1B drugs

A

Lidocaine and Mexiletine

223
Q

What are the adverse effects of Lidocaine?

A

respiratory arrest, convulsions d/t blockade of inhibitory transmission in brain

224
Q

When to use Class 1B drugs and what do they target?

A

best post MI and the target Na+ channels in phase 0 of the AP

225
Q

Flecainide

A 
Class 1C (strongest) 
targets Na+ in phase 0
226
Q

What are the contraindications for class 1C?

A

post MI (B is best for post MI, C is contraindicated)

227
Q

What is the MOA of flecainide?

A

block Na+ channels in the depolarized cells, increasing ERP but not effecting K+
normal AP duration

228
Q

Side effects of flecainide?

A

ataxia

229
Q

What are the Class 1A drugs?

A

Quinidine and procainamide

230
Q

What is the MOA for class 1A drugs?

A

block Na+ channels more in the depolarized cells, increasing ERP
blocking TEAK type K+ channels thus increasing AP duration

231
Q

What are the adverse effects of class 1A drugs?

A

Quinidine and proainamide
Torsades de pointes
long QT syndrome –never give with HCTZ or loop diuretic due to risk of torsades–> AF

232
Q

What are the contraindications for Class 1A drugs?

A

AV blocks because excessive Na+ channel blocks could lead to asystole

233
Q

What is the MOA for Class 3 drugs?

A

Block K+ efflux during phase 3, increasing APD

234
Q

What are the Class 3 drugs?

A

Amiodarone and sotalol

235
Q

Rank the Class 1 drugs from longest to shortest prolongation of the ERP.

A

1c > 1a > 1b

236
Q

What are the indications for amiodarone?

A

low dose - rhythm control for A.Fib
high dose - VTs in structurally abnormal hearts
especially VT post MI, post electroversion for Vfib

237
Q

What are the adverse effects of amiodarone?

A

long QT —> torsades
pulmonary fibrosis
rhabo when given with simvastatin

toxicity is a BITCH 
B - bradycardia/blue man 
I - intersitial lung disease 
T - thryoid 
C - corneal/cutaneous 
H - hepatic/hypotension with IV
238
Q

What toxicity is a BITCH?

A 
Amiodarone toxicity 
B - bradycardia/blue man 
I - interstitial lung disease 
T - thyroid 
C - corneal/cutaneous 
H - hepatic/ hypotension when IV
239
Q

What is the MOA for Sotalol?

A

Class 3

blocks K+ efflux during phase 3, increase APD

240
Q

What are the indications for Sotalol?

A

SVT, VT, pts with ICD

241
Q

What are the adverse effects of Sotalol?

A

long QT –> torsades de pointes

242
Q

What drugs are class 4?

A

CCB

Diltiazem and verapamil

243
Q

What is the MOA for class 4 drugs?

A

block Ca+ channel (L-type) in phase 2, decreasing conduction in SA/AV nodes (rate control) and decreasing automaticity

244
Q

What are the indications for class 4 drugs?

A

SVT (fib or flutter)

245
Q

What are the contraindications for class 4 drugs?

A

use EXTREME CAUTION with CHF pts d/t decrease contractility

246
Q

What are the side effects for class 4 drugs?

A

constipation (worse in verapamil)

247
Q

What drugs are class 2?

A

Beta Blockers

Metoprolol

248
Q

What are the indications of class 2 drugs?

A

SVTs (v.tach with structural heart disease)

249
Q

What is the MOA for class 2 drugs?

A

block beta adrenergic receptors –> sympatholytic
decreasing AV node conduction (rate control)
decrease excitability (ectopic pacemakers)
decrease SA node rate
decrease contractility
will suppress sympathetic drive arrhythmias

250
Q

Which drug do you use to suppress sympathetic driven arrythmias?

A

Beta Blockers - metoprolol
its the only one working on adrenergic receptors
all the other classes work on calcium, sodium, or potassium channels

251
Q

What are the indications for digoxin?

A

CHF + A.fib

252
Q

What is the MOA for digoxin?

A

directly increase Na+ in the cell and thus increase contractility
it does this by blocking the Na/K ATPase
increases vagal activity which increases ERP and decreases AV node conduction

253
Q

Adenosine indications

A

IV
AV node dependent tachy (narrow QRS)
dx + tx termination of SVT

254
Q

What is the MOA for adenosine?

A

acts @ adenosine receptor in the heart
increase K+ which hyperpolarizes and decreases Ca+ in
thus decreasing SA/AV conduction and automaticity

255
Q

What are the adverse effects of adenosine?

A

dyspnea, flushing, hypotension

256
Q

What drugs cause long QT syndrome?

A 
Quinidine 
Procainamide 
Amiodarone 
Sotalol 
Chlorpromazine (antipsych) 
Droperidol (sedation) 
Erythromycin (ABX) 
Methadone (opioid agonist)
257
Q

What is Amiodarones half life?

A

WEEKS

much be given with loading dose

258
Q

What is the first line treatment for V.Tach post MI?

A

Amiodarone

followed by lidocaine (2nd line)

259
Q

What is the first line treatment for V.tach with structural heart dx?

A

Acute:
Beta blockers
verapamil
adenosine

Chronic:
verapamil
beta blockers

260
Q

What is the first line treatment for A. fib?

A

defibrillation
amiodarone
lidocaine

261
Q

What channels are found in the AV node?

A

Calcium channels only (no sodium)

262
Q

What antiarrythmia drugs are CONTRAindicated in pts with WPW?

A

rate control drugs taht decrease AV conduction velocity

can lead to AVRT

263
Q

What is the first line drug for A.fib?

A

Control ventricular rate:
CCB
BB
Digoxin

restore sinus rhythm:
defib

264
Q

What is the first line drug for A.flutter?

A

CCB
BB

Chronic: ablation

265
Q

What is the first line drug for A.tach?

A

CCB

BB

266
Q

CNS depressants include…

A

EtOH
Benzos
Barbituates

267
Q

What is the MOA for Barbituates?

A

same as for all depressants:

enhance GABA binding to GABA-A receptor causing CNS depression

268
Q

What are the adverse effects of CNS depressants?

A

respiratory depression (not in benzos)

269
Q

What tolerance/withdrawal sxs are seen in CNS depressants?

A

seizures

270
Q

How is EtOH MOA different than other CNS depressants?

A

in addition to the GABA binding to GABA-A i also prevents glutamate from binding to NMDA receptor

271
Q

What are the withdrawal sxs of EtOH?

A

tremors, sweaty, tachy, HTN

272
Q

What are the withdrawal sxs of Benzos?

A

seizures, anxiety, paresthesia, sleep disturbance

273
Q

Opioid drugs include…

A

heroin, morphine

addiction + dependence

274
Q

What is the CNS/reward pathway for opioids?

A

activation of mu opioid receptors in medullary respiratory center, spinal and supraspinal sites
mediating analgesia, enteric nerves!

275
Q

What are the effects of opioids?

A

histamine release –> vasodilation, bronchoconstriciton, hypotension, respiratory depression

effects are also the toxicities

276
Q

What are the withdrawal sxs of opioids?

A

NOT life-threatening

hyperalgesia, diarrhea, DILATED pupils, HTN, sweating, dysphoria, craving

277
Q

What is addiction?

A 
a BEHVARIORAL syndrome 
1-4 = impaired control 
5-7 = social impairment 
8-9 = risk use 
10-11 = pharmochological criteria
278
Q

What is dependence?

A

physiological dependence measured by withdrawal sxs

279
Q

Nicotine MOA

A

activation of central/peripheral nicotinic acetylcholine receptors –> reward pathway

280
Q

What is the effect of nicotine?

A 
increase arousal + concentration (stimulant) 
decreased anxiety (depressant)
281
Q

What are the withdrawal sxs of nicotine?

A

irritability, anxiety, dysphoria (depressed mood), difficulty concentrating, restlessness, increase appetite

addiction + dependence

282
Q

What is the MOA/effect of cannabinoids?

A 
activation of cannabinoid receptors in brain and spinal cord --> reward pathway 
effect: 
depressant like: relaxation
psychedelic like 
sympathomimetic effects 
increased appetite

less prominent addiction + dependence

283
Q

Tolerance and withdrawal of cannabinoids?

A

Tolerance develops rapidly

withdrawal: mild: restlessness, irritability, depression, insomnia

284
Q

CNS stimulants

A

ampethamine + methamphetamine

285
Q

What is the MOA and effect of amphetamine?

A

enhance release of DA and NE (DA -> reward)
effect:
arousal, alertness, euphoria (increase HR and BP)

chronic use: hallucinations, violent behavior, psychosis

addiction PROFOUND, dependence less so

286
Q

What are the OD risk of meth?

A

arrhythmias, MI, stroke, seizures

287
Q

Tolerance and withdrawal to CNS stimulants?

A

Tolerance to euphoria develops quickly

withdrawal: mild: dysphoria, sleepiness, brady, craving, depression

cocaine, meth, etc.
addiction PROFOUND, dependence less so

288
Q

What is cocaines MOA?

A

stimulant
blocks DA, NE, and 5HT reuptake
reward = DA reuptake block keeping DA in synapse longer

289
Q

What is the effect of cocaine?

A

CNS arousal, alertness, euphoria (increase HR and BP)

290
Q

What are psychedelic drugs?

A

LSD, MDMA, psilocybin

291
Q

What are dissociative drugs?

A

PCP and ketamine

292
Q

What is the MOA for LSD?

A

the same as psilocybin

related to 5HT - agonist @ 5HT and DA

reward = weak

293
Q

What is the MOA for MDMA?

A

related to DA and amphetamine - induce 5HT and DA release and agonist for 5HT and DA

294
Q

What is the MOA for dissociative drugs?

A

inhibit NMDA receptors

295
Q

What is the effects of LSD and MDMA?

A

sympathomimetic, altered perception, hallucinations, altered mood

296
Q

What are the withdrawal for psychedelics?

A

craving, confusion, anxiety, depression

addiction/dependence minimal

297
Q

What are the withdrawal and toxicities for dissociative drugs?

A

PCP and ketamine

toxicities: hallucinations, delusions, psychosis, violent behavior, seizure, coma, death
withdrawal: craving, confusion, depression

298
Q

What is disulfiram used for?

A

EtOH aversion therapy

preventing relapse

299
Q

What is the MOA for disulfiram?

A

inhibits acetaldehyde dehydrogenase (ALDH), leading to accumulation of acetaldehyde, upon EtOH consumption causing facial flushing, N/V, HA, hypotension

300
Q

What are the adverse reactions of disulfiram?

A

hepatotoxic @ high doses
can lead to marked respiratory depression
CV collapse, convulsion (MONITOR THESE PTS)

301
Q

What is acamprosate?

A

FDA approved anti-craving for EtOH

302
Q

What is topiramate?

A

FDA approved anti-craving for EtOH

303
Q

What is the MOA for acamprosate and topiramate?

A

unknown
known to increase GABA-A receptors + inhibit NMDA receptor activity

not used to treat EtOH withdrawal

304
Q

What is the best combo drug for EtOH anti-craving?

A

acomprosate + disulfiram

305
Q

What is Naloxone?

A

narcan!
narcan test
opioid OD

306
Q

What is the Narcan test?

A

suspect recovering alcoholics are abusing opioids perform the narcan test prior to tx with naltrexone

307
Q

What is the MOA for naloxone?

A

inhibit mu opioid receptors in VTA

short acting antagonist

308
Q

What are the adverse effects of naloxone?

A

arrhythmias, hepatotoxic, pulmonary edema, opioid withdrawal

309
Q

What is naltrexone used for?

A

1) anti-craving EtOH; prevent relapse

2) limited success in opioid dependence tx (doesnt alleviate craving, but prevents the “high”)

310
Q

What is the MOA for natrexone?

A

inhibits mu opioid receptors in VTA (same as naloxone)

311
Q

What are the adverse effects of natrexone?

A

hepatotoxic at high doses (same as disulfiram)

312
Q

What is methadone used for?

A

both drug maintenance therapy and detox of opioid addiction (strong opioid analgesic)

313
Q

What is the MOA for methadone?

A

high efficacy agonist @ mu opioid receptor

decrease craving/withdrawal d/t slow absorption and long half life leading to stable plasma opioid levels

314
Q

What are the adverse effects of methadone?

A

cardiac arrest, arrhythmia –> QT prolongation

respiratory arrest, constipation, nausea, risk of death with combined with other CNS depressants

315
Q

What special dosing rules do you need to know for methadone?

A

it needs to be administered daily

significant abuse liability

316
Q

What is LAAM used for?

A

maintenance therapy and detox of opioid addiction

317
Q

What is the MOA for LAAM?

A

Similar to methadone but longer acting

318
Q

what are the adverse effects of LAAM?

A

AT prolongation, ECG monitoring recommended

319
Q

How often are you administering LAAM?

A

2-3 times/week

320
Q

What is buprenorphine?

A

drug maintenance and detox of opioid addiction

321
Q

What is the MOA for buprenorphine?

A

partial agonist @ mu opioid receptor + antagonist @ kapp opioid receptor
long acting

322
Q

What is the adverse effects of buprenorphine?

A

respiratory depression, hypotension, dizziness, sedation, brady/tachy arrhythmias

323
Q

OD is less likely in …

A

partial agonists

324
Q

What is the MOA in NRT?

A

nicotine replacement therapy

different kinetics from smoking; slower absorption and longer nicotine plasma levels (less rewarding)

325
Q

What is bupropion for?

A

smoking cessation aid
reduces craving
prevents withdrawal
(same as varenicline)

326
Q

What is the MOA for burpropion?

A

antidepressant (unrelated)
MOA unknown
non-competative antagonist of nicotinic acetylcholine receptors
weak inhibitor of DA, NE, 5HT reuptake

327
Q

What are the adverse effects of bupropion?

A

BBW: suicidal thoughts, aggressive behavior, exacerbation of underlying psych illness

328
Q

What is varenicline?

A

smoking cessation aid, reduces craving, precents withdrawal (like burpropion)

329
Q

What is the MOA for varenicline?

A

partial agonist @ alpha 4 beta 2 nicotinic receptor (nAChRs) in VTA and nucleus accumbens
inhibits nicotine full agonists @ nAChRs

330
Q

What are the adverse effects for varenicline?

A

BBW - suicidal thoughts, aggressive behavior, exacerbation of underlying psych disorders (same as bupropion)

331
Q

What is fibers overall effect on the body?

A

Decrease LDL

Absorbs choelsterol and bile acids —> slows absorption of cholesterol

332
Q

PUFAs

A

Omega 3 fatty acids
EPA and DHA
Increase clearance of TGs (decrease TG and VLDL)
Anti-inflammatory

333
Q

How do statins work?

A

Structural analog of HMGCoA
Inhibits HMGCoA reductase
This decreases cholesterol synthesis

334
Q

What are the adverse effects of statins?

A

Myopathy and myaglgia

Risk of DM

335
Q

When and how do administer statins?

A

Generally administered at night (except atorvastan)

Decrease absorption with food

336
Q

What are the biggest differences between atorvastatin and provastatin?

A

Atorvastatin are high intensity
Flourinated and have a long half life so they don’t need to be admistered at night
Metabolized by CYP3A4
Crosses the BBB

Pravastatin is low intensity 
Metabolized by suflation 
Excreted unchanged in the urine (not protein bound) 
Does not cross the BBB 
More hepatoselective
337
Q

Ezetimibe

A

Cholesterol absorption blocker

Works best with statins at decreasing LDL

338
Q

What is the MOA for eztimibe?

A

Block the NPC1L1 which blocks cholesterol absoprtion in intestinal tract and thus decreasing cholesterol to liver and the liver increases LDL recptors and increase LDL clearance

339
Q

What is special about ezetimibe half life?

A

Long half life

Active drug and active metabolite so it just keeps on going

340
Q

Cholestyramine

A

Bile acid sequestrants
Used as a combo drug with statin
Increase HDL, VLDL, and TGs

341
Q

What are the contraindications of cholestrymaine?

A

Hypertriglycerdemia (due to increase in TG)

Diverticulitis (due to increase in GI SE)

342
Q

Niacin

A

Active form of vitamin B3
Increase HDL, decrease LDL and TG
Inhibits lipolysis

343
Q

What are the contraindications and SE of Niacin?

A

Contraindicated in pregnancy
Cutaneous flushing
Hepatotoxicity
GI discomfot

344
Q

Evolcumab

A

PCSK9 inhibitor
Prevents degredation of LDL receptors
$$$$

345
Q

What are the indications and SE of evolcumab?

A

Indications: familial hypercholesterolemia

SE: nasopharygnitis

346
Q

Gemfibrozil

A

Fibrate
Derived from fibric acid
Drug of choice for patients with hypertriglyceremia
Agonists for PPAR-alpha receptor
Increase LPL synthesis which increases TG clearance
Decrease production of apoC3

347
Q

What are the indications for gemfibrozil?

A

Pts with hyperTG

Better absorbed with food (which is the opposite of statins)

Contraindicationed in pregnancy and hepatic/renal dysfunction

Pharm (1 decks)

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