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Quarter 3 > Pharm Exam 2 > Flashcards

Pharm Exam 2 Flashcards

1
Q

Carbonic anhydrase inhibitors

A

Acetazolamide
Dorzolamide (opt)
Brinzolamide (opt)

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2
Q

Loop diuretics

A 
Furosemide (Lasix)
Ethacrynic Acid (Edecrin)
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3
Q

Concerning adverse effect of Loop diuretics

A

Irreversible Ototoxicity
Ethacrynic Acid is the worst

(worse when given w/ Aminoglycoside)

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4
Q

Thiazide diuretics

A

early distal tubule

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5
Q

Thiazide diuretics

A

Hydrochlorothiazide
Metolazone
Indapamide

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6
Q

Potassium Sparing diuretcs (2 subtypes)

A

Aldosterone antagonist
Direct inhibitors of Na flux

WEAK Diuretics

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7
Q

Aldosterone antagonists

A

Spironolactone

Eplerenone

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8
Q

Direct inhibitors of Na flux

A

Amiloride

Triamterene

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9
Q

Osmotic diuretics

A

Mannitol
Isosorbide
Glycerin
Urea

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10
Q

Synthetic ADH

A

“Desmopressin”

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11
Q

ADH Antagonist

A

Conivaptan
Tolvaptan

to treat SIADH

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12
Q

HF drugs with positive ionotropic effects

A

Sympathomimetics

Digitalis

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13
Q

Most HF drug classes we talk about will not have _____ effects

A

positive ionotropic

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14
Q

Diuretics

A

Decrease salt and water retention

Decrease venous pressure, edema, and cardiac size

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15
Q

Spironolactone and Eplerenone

A

additional benefits over other Diuretics bc they inhibit Aldosterone receptors

Reduced mortality rate

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16
Q

ACE-I and ARBs both inhibit

A

RAAS pathway

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17
Q

ACE-I

A

inhibit the Angiotensin Converting Enzyme (ACE) which changes Angiotensin I—-> Angiotensin II

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18
Q

ARBs block Angiotensin II from binding to

A

AT1 receptor

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19
Q

RAS-Inhibitors (ACE-I and ARBs)

A

ACE-I are DOC for HF today.

Diminish cardiac workload by:
Decrease afterload AND preload

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20
Q

Dry cough occur as adverse effect with

A

ACE-I

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21
Q

Sacubitril/Valsartan (Entresto)

A

Valsartan: ARB
Sacubitril: neprilysin inhibitor

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22
Q

What does neprolysin do?

A

Degrades bradykinin, natriuretic peptide, and other

Sacubitril inhibits Nephrolysin

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23
Q

Sacubitril/Valsartan (Entresto) Use

A

HF (better at reducing mortality in HF)

Neprolysin inhibition- decreases vasoconstriction, Na retention, and cardiac remodeling

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24
Q

Adverse effects of Sacubitril/Valsartan (Entresto)

A

Hypotension
Kyperkalemia (ARB) esp when used with K-sparing diuretic
Cough and angioedema

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25
Q

Contra to Sacubitril/Valsartan (Entresto)

A

Pregnancy (ARBs in the 2nd and 3rd trimester- Teratogenic)

Concurrent use with ACE-I (risk of angioedema)

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26
Q

B-blockers “LOL” drugs

A

Carvedilol (cardiologist’s friend), Metoprolol

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27
Q

B-blockers effects

A

Decrease mortality, decrease Renin, decrease catecholamine effects on heart, decrease HR, decrease remodeling

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28
Q

B-blockers

A

effective only in EARLY stages of HF

Dangerous in severe, end stage HF bc of the negative ionotropic effects

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29
Q

Vasodilators

A

Sodium nitroprusside, Isosorbide dinitrate, Hydralazine

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30
Q

Vasodilators

A

Reduce preload, afterload, or both

decrease damage remodeling of heart

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31
Q

Drugs with Ionotropic effects

A

Dobutamine

Dopamine

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32
Q

When is Dopamine used over Dobutamine?

A

when INCREASE IN BP is needed

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33
Q

Dobutamine and Dopamine

A

severe refractory HF

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34
Q

Digitalis

Digoxin (frm US)

A

Digitalis is cardiac glycoside isolated from plants

Inhibits Na/K ATPase

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35
Q

Digoxin

A

inhibits Na/K ATPase

binds to Na binding site- blocks its effects

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36
Q

Digoxin

A

increase Na inside cell
decrease expulsion of intracellular Ca
leading to increased Sarcoplasmic Ca Stores!
overall effect: increase crossbridge and INCREASE CONTRACTILITY

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37
Q

Digoxin indications

A

HF (last agent used) when all other benchmarks are met but pt is still feeling sluggish

Improves exercise tolerance

AND Arrhythmias (Slows HR)

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38
Q

Digoxin

A

can put put on this for longer

manage long term if pt really wants to exercise

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39
Q

Dopamine and Dobutamine

A

not a long term option

last ditchall effort
pt is about to die

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40
Q

Digoxin

A

80% excreted by kidneys- best of all glycosides

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41
Q

Digoxin adverse effects

A 
All glycosides are toxic
Narrow margin of safety
Earliest toxic signs- GI (n/v/d)
CNS effects- HA, fatigue, etc
Cardiac (MOST COMMON AND DANGEROUS)
V-fib
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42
Q

Digoxin cardiac adverse effects

A

Arrhythmia: sinus brady, ectopic ventricular beats, AV block, bigeminy (characteristic arrhythmia with Digoxin!)

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43
Q

V-fib

A

most common cause of death with Digoxin

“Sudden death”

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44
Q

Monitoring with Digoxin

A

Perform regular EKG

Measure K+ and Digoxin levels

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45
Q

How to treat Digitalis toxicity

A

Minor GI- discontinue
Arrhythmia- Oral or IV K+ along w/above
Severe OD/ life threatening arrhythmia- immunotherapy with Digitalis Immune Fab along with above (K+ and dicontinue as well)

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46
Q

Do you perform cardioversion with Digitalis toxicity?

A

NO, not for digitalis-induced arrhythmias unless V-fib

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47
Q

K+ secretion

A

Distal tubule and collecting duct
Exchange of Na/K
Can be modified by Aldosterone-antagonists and K+ sparing diuretics

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48
Q

Thiazide diuretics

A

enhance Ca reabsorption

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49
Q

Loop diuretics

A

inhibit Ca reabsorption
(used to treat hypercalcemia)

Also cause body to get rid of more Mg

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50
Q

Weak acids at low pH are mostly un-ionized

A

lipid soluble

easily diffusible

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51
Q

Acidic drugs compete for uric acid excretion and can lead to

A

GOUTY attack

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52
Q

Carbonic Anyhdrase Inhibitors (CA Inhibitors)

A

Blocks bicarb production

Blocks NHE, resulting in increased Sodium and Water LOSS

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53
Q

Carbonic anhydrase

A

part of Bicarb production

Bicarb production is part of Aqueous humor and CSF production

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54
Q

CA Inhibitors use

A

Glaucoma
Alkalanize urine (drug trapping)
Alkalosis (Metabolic or Mountain sickness)

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55
Q

Metabolism of CA inhibitors

A

Short acting bc these cells are so metabolically active
H builds up naturally in cell and turns the transporters back on
“lousy” drugs bc their effects don’t last long enough

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56
Q

CA Inhibitors adverse effects

A

Hyperchloremic metabolic acidosis
Hyperuricemia
HypOkalemia
Renal stones

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57
Q

Contra to CA Inhibitors

A

Hepatic cirrhosis

Sulfa hypersensitive

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58
Q

Loop diuretics (Furosemide and Ethacrynic Acid)

A 
Mechanism:
Block NKCC2
Induce Kidney PGs
-decrease salt transport
-vasodilation
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59
Q

Loop diuretics use

A 
HF (move large volumes of water)
Pulmonary edema
Hypercalcemia
Severe peripheral edema
Work well at low GFR (best diuretic to use if pt has kidney prob)
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60
Q

Loop diuretics Adverse Effects

A

Hypokalemic metabolic acidosis
Hypocalcemia
Hypomagnesemia
Hypochloremia

Everything is hypo with Loop, besides HYPER-URICEMIA

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61
Q

Other bad side effects of Loops

A

High potency -> abnormal fluid and electrolytes

IRREVERSIBLE OTOTOXICITY

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62
Q

Which Loop is worst for Ototoxicity

A

Ethacrynic acid

worse when given w/Aminoglycosides “the 5 mycins”

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63
Q

Aminoglycosides (5)

A 
Streptomycin
Gentamycin
Tobramycin
Amikacin
Neomycin
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64
Q

Macrolides (3)

A

Erythromycin
Clarithromycin
Azithromycin

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65
Q

Contra to Loop diuretics

A 
Sulfa
Drug intxn 
-COX inhibitors
-Aminoglycosides
-Lithium
-Digoxin
Overzealous use is dangerous in
-Hepatic cirrhosis
-Borderline renal failure
-HF
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66
Q

Ethacrynic acid

A

Good thing: NOT A SULFA DRUG

bad thing: worse for ototoxicity

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67
Q

Thiazide diuretics and related compounds

A

Hydrochlorothiazide
Metolazone
Indapamide

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68
Q

Mechanism of Thiazide

A

Inhibit Na reabsorption at early distal tubule (NCC)

Dependent on Prostaglandin synthesis

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69
Q

Thiazide use

A

HTN & HF (main ones)

Also,
Nephrolithiasis
Increases ATP-dependent K channel opening
-hyper-polarization of cell membranes
-good: Vasodilation
-bad: Reduced insulin secretion from pancreatic beta cells

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70
Q

Thiazide diuretics and Diabetics

A

The hyperpolarization of pancreatic beta cells-inhibit insulin secretion- can make a pre-diabetic –> Diabetic

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71
Q

More Use of Thiazide

A

Lower systemic BP and enhance effectiveness of other HTN meds

Enhance Ca reabsorption

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72
Q

Thiazide diuretics and Gout

A

Competes with Uric Acid- caution in ppl with Gout

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73
Q

Indapamide is excreted by biliary system,

A

useful in pts with Renal insufficiency

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74
Q

Thiazide adverse effects

A

Overall well tolerated.

Hypokalemic metabolic ALKALOSIS
(not enough K –> Cramps)
Mg loss
Iodide and Bromide loss

Hyperuricemia (caution gout)
Hyperglycemia
Elevated serum lipid

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75
Q

Thiazide contra/precaution

A

Sulfa
May be inhibited by NSAIDs
Hypokalemia caused by this can contribute to DIGITALIS toxicity
Hyperglycemia and Carb intolerance in DIABETCS
Caution w/gout
Hyponatremia if water take is excessive

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76
Q

Contra for Thiazides

A

DIABETICs

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77
Q

More caution with Thiazide

A

Lithium toxicity is worsened by Thiazides

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78
Q

Metazolone (Thiazide-like)

A

Able to produce Diuresis in pts with REDUCED GFR

This is the only Thiazide that can do this, usually only Loop works at low GFR

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79
Q

Indapamide (Thiazide-like)

A

3 diff from other Thiazides

  • pronounced Vasodilation
  • does not increase Lipid levels
  • Metabolized by liver and kidney- good for a pt that has liver problems. Liver is helping out
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80
Q

K- sparing diuretics

A

Aldosterone antagonists

Direct inhibitors of Na+ flux

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81
Q

K-sparing diuretics

A

interfere with Na reabsorption at the distal exchange site- permit loss of Na and H2O
ENHANCING K conservation

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82
Q

K-sparing

A

weak diuretics compared to Loop and Thiazide

Reduce K loss and Alkalosis caused by other diuretics

Used in combo with other drugs

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83
Q

Aldosterone Antagonist- Spironolactone

A 
Competitive inhibitor of Aldosterone (promotes excretion of Na and retention of K)
Less Na channels
Hyperpolarized cell (less K excretion)
Decrease Na/K ATPase activity leading to less K secretion/excretion
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84
Q

Spironolactone use

A

Hyperaldosteronism- most effective drug for treating this
Edema
Used with Thiazide or Loop to avoid excess K loss
Hirsutism- bc this is an Androgen receptor antagonist

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85
Q

Spironolactone adverse effects

A

Occasional Hyperkalemia (too much K, makes sense)

Others are few
GI- n/v/cramps
Gynecomastia- androgen receptor antagonist

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86
Q

Spironolactone caution

A

caution with ACE-I or ARBs d/t elevated K levels

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87
Q

Spironolactone contra

A

Kyperkalemia (burn pts)
Chronic Renal insuff
Liver damage (acidosis may occur)

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88
Q

Eplerenone (like Spirono, but has less Androgen receptor side effects)

A

Selective aldosterone receptor antagonist (SARA)

Metabolized by CYP3A4- caution w/drug interactions

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89
Q

K-sparing diuretics that do nothing to Aldosterone, just block the ENaC channel

A

Amiloride
Triamterene

inhibit the Na/K ion exchange mechanism

leading to less K excretion

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90
Q

K-sparing diuretics use

A 
Combo with other K-losing diuretics
No hyperuricemia- good! only diuretic class that does not cause this
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91
Q

Amiloride (K sparing) is DOC for

A

Li+- induced Diabetes Insipidus

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92
Q

Adverse effects of K-sparing diuretics

A

HYPERkalemia is the only one

leading to too much K retention (often if chronic use or combined with other K sparing agents)

n/v/leg cramps/dizzy

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93
Q

Contra for K-sparing diuretics

A

Hyperkalemia- burn patients

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94
Q

Osmotic diuretics

A

Mannitol
Isosorbide
Glycerin
Urea

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95
Q

Osmotic diuretics

A

IV only
Filtered but not reabsorbed by kidney

Keeps water in tubules
Produce water diuresis (not anything to do with sodium here)

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96
Q

Osmotic diuresis use

A

Acute Renal Failure
Decrease intra-ocular pressure
Decrease intra-cranial pressure
Protect kidney

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97
Q

Adverse effects of Osmotic diuretics

A

CONTRA in HF (d/t excessive amt can cause extracellular volume expansion which affects pulmonary edema)

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98
Q

other adverse effects of Osmotic Diuretics

A

HA, n/v/chills, dizzy, polydipsia, lethargy, confusion, CP

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99
Q

ADH agonist

A

Desmopressin
synthetic ADH

Treats sx of Central Diabetes Insipidus

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100
Q

ADH agonist

A

retains water

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101
Q

ADH Antagonist

A

Conivaptan

V1a and V2 receptor antagonist

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102
Q

Conivaptan (ADH antagonist) use

A

Tx of SIADH-

euvolemic or hypervolemic Hyponatremia

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103
Q

Conivaptan (ADH antagonist)

A

increases Na concentrations and increases free water clearance

when you are too dilute

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104
Q

Conivaptan (ADH antagonist) IV only

A

Adverse effects:
Hypokalemia
Injection site rxn
Orthostatic HTN, A-fib, Hypotension

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105
Q

Contra for Conivaptan (ADH antagonist)

A

Hyponatremia associated with hypovalemia

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106
Q

Tolvaptan (ADH antagonist)

stop from retaining water

A

similar to Conivaptan, except

  • Oral
  • non-peptide V2 vasopressin antagonist
  • can be continued outpatient
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107
Q

Loop and Thiazides

A

can be combined when pt is not responding to one alone

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108
Q

Afterload is determined by:

A

Arterial resistance (Aortic impedance and vascular resistance)

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109
Q

In Heart Failure

A

Massive vasoconstriction going on:

increase in RAS
Increase in peripheral resistance via arterial constriction

Tx? AterioDILATOR drugs

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110
Q

Big problem with HF is the inability to contract strongly enough, but we dont fix this problem. Rather we treat by

A

reducing the workload that the heart has to do

B-blockers (reduce contractility)
Ionotropic drugs (last ditch effort, these ones actually do increase contractility)
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111
Q

beta blockers

A

reduce cardiac work by slowing HR

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112
Q

How to reduce preload

A

Diuretic

Venodilator

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113
Q

How to reduce afterload

A

Arteriodilator

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114
Q

How to increase contractility

A

Ionotropic drug

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115
Q

How to reduce energy expenditure

A

B-adrenergic Antagonist

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116
Q

Drugs that reduce Heart Failure Mortality

A

Aldosterone Antagonist
B-blocker
ACE-I and ARB
ARB + Nep inhibitor (ARNI)

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117
Q

Spironolactone and Eplerenone have extra benefits over other diuretics bc they

A

inhibit Aldosterone receptors

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118
Q

ACE-I

A

“prils”

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119
Q

ARBs

A

“sartans”

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120
Q

ACE-I

A

Inhibits the ACE enzyme which converts Angiontensin I –> Angiotensin II

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121
Q

ARBs

A

blocks Angiotensin II from binding to the AT1 receptor

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122
Q

ACE-I and ARBs are both considered

A

RAS pathway inhibitors

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123
Q

RAS inhibitors

A

Current DOC for Heart Failure

Reduce preload (decrease aldosterone releas) AND Reduce afterload (reduce ATII induced constriction)

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124
Q

ACE-I main side effect

A

dry cough

d/t bradykinin

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125
Q

Sacubitril/Valsartan (Entresto)

A

better at reducing mortality in HF pts compared to Enalapril alone

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126
Q

Why is Neprilysin inhibition helpful?

A

decrease vasoconstriction, decrease Na retention, decrease Cardiac remodeling*

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127
Q

Adverse effects of Sacubitril/Valsartan (Entresto)

A

Hypotension
Hyperkalemia (esp when used w K sparing diuretic)
Cough and angioedema

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128
Q

Contra to Sacubitril/Valsartan (Entresto)

A

Pregnancy! (teratogenic)

and DO NOT USE with another ACE-I (risk of angioedema)

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129
Q

ARBs contra

A

Pregnancy!

teratogenic

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130
Q

Beta blockers

A

effective only in Early stages of HF

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131
Q

Beta blockers are dangerous in severe, end stage HF because:

A

negative ionotropic effect (slow HR)

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132
Q

Vasodilators

A

Na Nitroprusside
Isosorbide Dinitrate
Hydralazine

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133
Q

HF drugs WITH ionotropic effects (few)

A

Dobutamine
Dopamine

both used for severe refractory HF

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134
Q

Dobutamine

A

selevtive B1 agonist

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135
Q

Dopamine

A

3 receptors

low: renal vasodilation
med: b1 in heart, ionotropic
high: a receptor in vessels, constriction

USEFUL IF increase in BP is needed!!
Dopamine

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136
Q

Digoxin

A

inhibits Na-K ATPase

increase contractility!! positive ionotropy by increase in the intracellular Ca2+ stores

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137
Q

Digoxin use

A

Last agent used for HF
If all other meds have been tried and pt still feeling sluggish

TO IMPROVE EXERCISE INTOLERANCE

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138
Q

Digoxin use

A

HF- last agent

Arrhythmias (decreases HR)

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139
Q

Digoxin slows HR by two diff mechanisms depending on the heart health of the person

A

Normal heart: vagal stimulation, increase SA node sensitivity

Failing heart: symp tone already high, as digitalis increases contractility, symp tone is reduced and BAROREFLEX kicks in to slow HR

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140
Q

Digoxin adverse effects

A

Glycosides are toxic
Narrow margin of safety
GI toxicity- earliest sign, n/v/d

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141
Q

Digoxin more adverse SE

A

CNS-HA,fatigue, drowsy
Cardiac arrhythmia- sinus brady, ectopic beats, AV block
V-Fib

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142
Q

Digoxin maintenance

A

Regular EKG

Measure K+ and med levels

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143
Q

Digoxin toxicity tx

A

Minor Gi: stop or reduce med
Moderate (arrhythmia): Oral or IV K+ and above
Severe OD/ life threatening arrhythmia: Immunotherapy with Digitalis Immune Fab alone with Oral or IV K+ and above

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144
Q

DO NOT PERFORM CARDIOVERSION for Digoxin OD unless

A

pt is already in V-fib

(bc if theyre not, it could send them into V-fib

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145
Q

Digoxin pharm interactions

A

Increased toxicity
Thiazide or Loop- hypokalemia

Further decrease of SA/aV if on beta blockers

Decreased effectiveness of CCBs - contra in HF

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146
Q

DO NOT use Digoxin with:

if you have Heart Failure

A

CCBs

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147
Q

Nitrates and Nitrites (2)

A

Nitroglycerin
Isosorbide Dinitrate

work by increasing NO and cGMP

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148
Q

Nitrates

A

DOC for any acute Anginal attack (classic or variant)

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149
Q

primary mechanism of Nitrates

A

decrease O2 demand

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150
Q

Adverse effect of Nitrate

A

Throbbing HA
Tachycardia
Orthost hypotension

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151
Q

Adverse effect of Nitrate

A

Develop tolerance

Not suitable for long term tx

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152
Q

Ca channel blockers

“VDN”

A

better for long term tx

  • Verapamil
  • Diltiazem
  • Nifedipine
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153
Q

B-blockers

A

decrease O2 demand

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154
Q

B-blockers do not do ANYTHING for Variant angina

A

bc variant is spasm

b-blockes do not do anything for blood vessel (work indirectly via other mechanisms)

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155
Q

Ranolazine

A

only used to treat Angina as LAST DITCH EFFORT

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156
Q

Ranolazine

A

Partial fatty acid oxidation inhibitor
(PFox) Inhibitor
decrease O2 consumption in ischemic tissue

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157
Q

Sildinafeil (Viagra)

A

increase levels of cGMP and PDE5. increase relaxation and vasodilation

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158
Q

Contra to Sildenafil (viagra)

A 
Pregnant/lactating
Children or infants
Pilots
Taking Nitrate already
A-blockers
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159
Q

Other PDE5 inhibitors

A

Vardenafil (levitra)
Tadalafil (Cialis)

more selective for PDE5

160
Q

Vardenafil (levatria)

A

Onset of effects SOONER

161
Q

Tadalafil (Cialis)

A

up to 24-36 hours
Effects last waaaaaay longer
Ta-da

162
Q

ED drugs

PED5 inhibitors

A

“afil” drugs

163
Q

What determines diastolic pressure?

A

Peripheral resistance

Blood volume

164
Q

What determines systolic pressure?

A

Diastolic pressure

Pulse pressure

165
Q

What determines pulse pressure?

A 
Aortic compliance (elasticity)
Contractility
166
Q

Almost all BP drugs will decrease BP b y at least

A

10% in mild to moderate HTN

167
Q

Groups of Anti HTN meds

A

Diuretics
Symphathoplegic agents
Direct vasodilators
Angiotensin Inhibitors

168
Q

Biggest use for HTN

A

Thiazide diuretics

mild-mod HTN

169
Q

Thiazide mechanism

A

Increase sodium and water excretion
short term: decrease cardiac output
long term: hyperpolarize membrane and decrease peripheral vascular resistance

170
Q

Diuretic side effects

A 
Impotence (erectile dysfx)
Gout- hyperuricemia
Increased renin secretion
K depletion
Reduced glucose tolerance
Increased plasma lipids
171
Q

Thiazide

A

one of first recommended drugs for HTN

172
Q

Thiazide special considerations

A

Sulfa

173
Q

Thiazides are more effective in

A

African American

174
Q

Loop diuretics

A

use in severe cases for HTN

Renal insuff, HF

175
Q

K-sparing diuretics use for HTN

A

Use WITH thiazide or loop to decrease K loss

Avoid combo with other K sparing drugs

176
Q

Sympatho-lytics

A

STOPPING sympathetic effects

177
Q

Sympatho-lytic drugs

A

activate Baroreflex and cause: Sodium and Water retention

178
Q

Sympatho-lytics are best when

A

combined with Diuretic

179
Q

Clonidine and Methyldopa

A

stimulate Medullary alpha-2 adrenergic receptors –> decrease peripheral symp nerve activity

decrease transmitter release to relevant sites

180
Q

Clonidine and Methyldopa

A

Decrease BP by:

1) decrease symp outflow
2) decrease Renin secretion

181
Q

Clonidine

A

decreases HR and CO more than Methyldopa

182
Q

Methyldopa

A

recommended drug in pregnancy (compelling indication)

183
Q

Common SE with Clonidine and Methyldopa

A

Xerostomia (Dry mouth)
Sedation
ED

184
Q

Methyldopa, more side effects

A

Hemolytic anemia + coombs
Hepatotoxicity
Increased prolactin –> gynecomastia and lactation

185
Q

Sudden withdrawal of Clinidine BAD

A

HTN crisis

186
Q

Tricyclic antidepressants and yohimbine

A

inhibit Clonidine’s action

187
Q

Prazosin

A

alpha-1 antagonies

dilate arteries and veins to decrease Peripheral resistance –> decrease BP

188
Q

Good thing about Prazosin

A

does not affect plasma lipids

189
Q

Compelling indication to use Prazosin

A

pt has BOTH: HTN and BPH

190
Q

Prazosin

A

First dose phenomenon (postural hypotension)
Reflex tachy
Too much water and sodium retention

191
Q

B blockers

A

young, white male

192
Q

B-blockers

A

reduce CO
reduce Renin secretion
recude symp vasomotor tone

193
Q

B-blockers are NOT recommended as Monotherapy unless compelling indication:

A

Angina
Post MI
Migraine
HF

194
Q

B-blockers decrease exercise tolerance

Other reasons to avoid b-blcokers

A 
High phys activity
African american
Asthma
Diabetes
Hypercholesterol
Periph Vasc dz
195
Q

B-blockers complete CONTRA

A 
Diabetes
End stage HF
Severe bradycardia
Heart block
Asthma
196
Q

Labetolol

A

combined a1 and b-blocker

Decrease BP in HTN emergency

197
Q

Labetolol

A

pregnancy is a compelling indication

198
Q

Carvedilol

A

combined a1 and b-blocker

HTN, HT, and post MI
“lipid neutral”

199
Q

combined a1 and b-blocker side effects

A 
Orthostatic hypotension (worse than b-blockers alone)
Bronchoconstrict: DONT USE IN ASTHMATICS
200
Q

Labetolol SE

A

Hepatotoxicity!! only use in emergency and for preggo

201
Q

Sodium nitroprusside is special bc it relaxed arterial smooth muscle AND

A

veins

202
Q

Chronic oral tx for HTN

A

Hydralazine and CCB

203
Q

Nitroprusside, Fenoldopam, and some CCB are used

A

IV for emergency

204
Q

Side effects to any vasodilators

A 
Reflex tachy and increased contraction
Increased Renin secretion
Fluid retention
HA, flushing
Palpitations, dizzy
205
Q

Drugs that act through Nitric Oxide

A

Hydralazine

Sodium Nitroprusside

206
Q

Hydralazine

A

Dilates ARTERIES but not veins

207
Q

Hydralazine use

A

Chronic tx of SEVERE HTN
Only used when other tx failed!!!
combo with others

208
Q

Hydralazine compelling indication

A

Severe HTN and or HTN emergency in PREGNANCY

209
Q

Hydralazine adverse effects

A

Systemic Lupus Eryth in “slow acetylators”

One of the “HIP” drugs of slow acetylators

210
Q

Other adverse effects of Hydralazine

A

HA, nausea, anorexia, palpitations, sweating, flushing, Angina, ischemic arrhythmia

211
Q

Sodium nitroprusside

A

IV
Emergency
dilated Arteries AND Veins
RAPIDLY LOWERS BP- in minutes

212
Q

Sodium nitroprusside pharmacokinetics

A

Metabolized by thicyanate—-> Adverse effect is Cyanide accumulation

213
Q

Cyanide accumulation in Sodium Nitroprusside administration can be extra dangerous to those who have a deficiency in Cyanide metabolsim

A

Metabolic ACIDOSIS, arrhythmia, excessive HYPOtension, death

214
Q

Fenoldopam

A

D1 receptor agonist

215
Q

Fenoldopam

A

relaxes arteriolar smooth muscle

216
Q

Fenoldopam use

A

EMERGENCY HTN

217
Q

CCB two classes

A

Dihydropyridines

Others

218
Q

Dihydropyridines (CCBs)

A

Nifedipine

Amlodipine

219
Q

Other CCBs

A

Diltiazem

Verapamil

220
Q

CCB mechanism

A

bind to L-type channels in the:

Myocardium and Vascular sm musle

221
Q

CCB effect on myocardium

A

decrease contractility, automaticity, and conduction

222
Q

CCB effect on Vascular sm.muscle

A

vasodilation

223
Q

CCBs

A

one of first choices for HTN therapy

224
Q

CCBs effects differ based on tissue selectivity, can have opposite effects on Heart Rate

A

Nifedipine has highest effect on BLOOD VESSELS and least effect on cardiac muscle

Decreases BP but INCREASES HR

225
Q

Verapamil

A

Decreases BP AND decreases HR

has highest effect on Cardiac muscle, least effect on blood vessels (therefore does not cause reflex tachy)

226
Q

Where does Nifedipine (and all “dipines”) have highest effect

A

Vascular smooth muscle (blood vessels)

227
Q

Where does Varapamil have highest effect?

A

Cardiac muscle

228
Q

CCB that is most likely to cause reflex tachycardia

A

Nifedipine

229
Q

Dihydropyridines in general have these SE more d/t their dominant effect being on Vascular Smooth Muscle

A 
Reflex tachy
HA
flushing
Dizzy
Periph edema
Gingival hyperplasia
230
Q

Verapamil side effect

A

Constipation

231
Q

CCBs that cause depressed SA and AV node fx - may cause bradycardia esp in those with SA node dysfx

A

Verapamil and Diltiazem

232
Q

Verapamil and Diltiazem Contra (CCBs)

A

already on B-blockers
SA/AV node dysfx
Heart Failure

233
Q

Dihydropyridine Contra (CCBs)

A

cautiously in pts with HF

234
Q

RAS Inhibitors (2 classes)

A

ACE-I and ARBs

235
Q

ACE-I

A

“prils”

236
Q

ARBs

A

“sartans”

237
Q

ACE-I

“prils”

A

inhibit ACE therfore ACE II cant be made

Decrease BP by:

  • reduce vasoconstriction caused by ATII
  • reduce release of Aldosterone
238
Q

ACE-I

“prils”

A

lower BP without compromising the heart, brain, or kidneys

without lipid changes

without reflex tachy

239
Q

ACE-I

“prils”

A

most effective in young and middle aged caucasions

240
Q

ACE-I

“prils”

A

one of 1st choices for HTN

Definitive DOC for HTN in those with:
Diabetes
CKD
HF w reduced EF

241
Q

ACE-I

“prils”

A

particularly indicated for DIABETIC NEPHROPATHY

242
Q

ACE-I

“prils”

A

Enhance antiHTN efficacy of diuretics
Balance the K issue with diuretics (increase K)
Decrease proteinuria and stabilize Renal fx

243
Q

ACE-I adverse effects

“prils”

A

Dry, hacking COUGH!!!! and
Angioneurotic EDEMA
both d/t Bradykinin

244
Q

ACE-I adverse effects

“prils”

A

Hyperkalemia d/t inhibited Aldosterone secretion

Acute Renal Failure (in those with bilateral renal artery stenosis)

245
Q

Contra to ACE-I

“prils”

A

Pregnancy (2nd and 3rd trimester particularly)- TERATOGENIC
With K-sparing agents–> hyperkalemia
Combo with NSAIDs (decreases effectiveness)

246
Q

ARBs

“sartans”

A

block AT1 receptors selectively

247
Q

big diff b/w ACE-I “prils” and ARBs “sartans”

A

ACE-I increase Bradykinin levels which leads to side effects (dry cough and angio edema) BUT neither of those occur with ARBs

248
Q

Classic or atherosclerotic Angina

A

“angina of effort”

obstruction of large coronary vessels- esp w exercise

249
Q

Classic/atherosclerotic Angina

A

if uncontrolled by drugs, may require stenting

250
Q

Variant/angioSPASTIC/ Prinzmetal’s angina

A

Spasm or constriction in atherosclerotic coronary vessel

REVERSED by Nitrates or CCBs

251
Q

Coronary blood flow is directly proportional to

A

Perfusion pressure

Diastole duration

252
Q

Why are drugs that increase O2 supply ineffective?

A

“Coronary steal phenomenon”

arteries that are healthy and non-sclerotic will steal away the increase BF and oxygen from the calcified hardened arteries

253
Q

HR and Cardiac contractility are decreased by

A

B-blockers and

some CCBs

254
Q

Nitrates

A

decrease preload in veins

255
Q

CCBs

A

decrease afterload in arteries

256
Q

Nitrates

A

Uneven vasodilation (this is why preload is reduced more bc the big veins are markedly vasodilated more than the small veins)

257
Q

Nitrates

A

Vasodilation via NO–> cGMP pathway

258
Q

Nitrates

A

DOC for any ACUTE anginal attack

classic or spasm

259
Q

Nitrates both increase and decrease cardiac workload

A

decrease: preload and afterload
increase: decrease BP which kicks in Baroreflex which increases HR and contractility and reduces diastole time

260
Q

Nitrates accomplish Anginal relief by

A

Predominant mechanism: decreasing Myocardial O2 requirement

261
Q

Nitro (many routes!!)

sublingual, oral, transdermal

A

Rapid metabolization

High first pass effect

262
Q

Sublingual Nitro is preferred bc

A

Avoid hepatic destruction

Rapid absorption- immediate relief

263
Q

Adverse toxicity of Nitrates

A

Acute toxicity: orthost hypotension, tachycardia, HA

Repeated exposure: tolerance and reduced effects (not suitable for long term, but docs do anyway)

264
Q

Chronic exposure to Nitrates

A

“monday dz”

265
Q

CCBs

A

better for long term

266
Q

CCBs

A

relax all smooth muscle that relies on L-type Ca channels

Verapamil
Diltiazem
Nifedipine

267
Q

Nifedipine has highest effects on

A

Vascular sm. muscle (reflex tachy!)

268
Q

Verapamil has highest effect on

A

Cardiac muscle

269
Q

Diltiazem

A

in the middle of the CCB sandwhich

270
Q

Slow release Nifedipine (dominant on vascular sm.muscle) is indicated

A

ONLY in HTN (not angina)

bc may actually cause Angina Pectoris

271
Q

Nifedipine (and other dihyrdopyridine CCBs) harmful effects

A

Enhanced development of MI

rapid hypotension–> baroreflex –> increase cardiac workload –> ischemia

272
Q

Verapamil and Diltiazem (CCBs) harmful effects

A

Cause serious cardiac depression that could end in cardiac arrest, AV block, or Heart Failure

273
Q

Nifedipine and Dihydropyridine benefits

A

Vasodilation –> increase O2 supply and decrease afterload

274
Q

Verapamil and Diltiazem benefits

A

Decrease myocardial contractility

Bradycardia caused by decreased SA/AV signalling

275
Q

B-blockers have CV effects at 3 organs

A

Heart: decrease CO
Kidneys: Decrease Renin
CNS: decrease symp vasomotor tone

276
Q

B-blocker Anginal relief comes from:

A

Decrease in symp activatoin ——> decrease heart O2 demans

277
Q

B-blockers DO NOT WORK FOR

A

Variant/spasm angina!!!!

278
Q

B-blockers adverse effects

A

Bronchoconstriction
Increase plasma triglcyerides
Decrease insulin and hypoglycemic response
CNS SE

279
Q

B-blockers DO NOT WORK FOR and can actually be HARMFUL in Variant/Spasm angina bc

A

Slow HR, prolong ejection time, increase L ventricular End diastolic volume, increases Oxygen requirement

280
Q

Ranolazine unique mechanism

A

Partial Fatty acid oxidation inhibitor (Pfox)

Decreases oxygen consumption in ischemic tissue

281
Q

Ranolazine

A

LAST CHOICE DRUG when other anti-anginal meds havent worked

expensive also

282
Q

Tx of Angina

A

Increase exercise tolerance

Decrease frequency and duration of myocardial ischemia

283
Q

For Variant/spasm angina

A

Nitrates and CCBs preferred

284
Q

Nitrate induced Reflex Tachy can be minimized by combining with

A

CCB or B-blockers

285
Q

Common combos

A

B-blocker and Nitrate

B-blocker and CCBs

286
Q

PDE5 inhibitors

A

Sildenafil (Viagra)
Vardenafil
Tadalafil

287
Q

Sildenafil (Viagra)

A

selective inhibitor of cGMP specific PDE5
more vasodilation
(PDE5 is specifically in the penis)

288
Q

Sildenafil (Viagra) uses

A

Erectile dysfx

Pulmonary HTN

289
Q

Sildenafil (Viagra)

A

Max concentration: 30-120 min
Half life: 4 hr
Metabolized by CYP3A4

290
Q

Adverse effects of Sildenafil (Viagra)

A

Visual impairment (blue color tinge to vision), photophobia, or blurred vision

bc PDE6 is found in retina

291
Q

Adverse effects of Sildenafil (viagra)

A

HA, flushing, SOB, nasal congestion, UTI

292
Q

CONTRA to Sildenafil (viagra)

A

Pregnant/lactating woman
Infants/children
With Nitrates (too much vasodilation)
With A-blockers

293
Q

CONTRA to Sildenafil (Viagra) pt 2

A

Inhibitors of CYP3A4

will reduce clearance of Viagra and increase its toxic effects

294
Q

Newer PDE5 inhibitors are more selective for PDE5 than PDE6 (less side effects)

A

Vardenail - very soon

Tadalafil- good for tomorrow, lasts up to 24-36 hours

295
Q

Statins

A

Lovastatin
Simvastatin (worst)
Atorvastatin (common)

296
Q

Statin mechanism

A

inhibit HMG-CoA reductase (the enzyme that makes new cholesterol in liver)

297
Q

Statin use

A 
Decrease LDL (DOC for this)
Stabilize plaques
298
Q

Atorvastatin

high intensity therapy

A

can be given in double dose, used for High Risk Atherosclerotic Cardiovascular Disease pts

299
Q

Lovastatin and Simvastatin

A

have to be activated to work- hydrolyzed

300
Q

Statins

A

high first pass, liver metabolism

301
Q

Lovastatin and Simvastatin

A

must take in evening

bc peak chol synthesis in early morning hours

302
Q

Atorvastatin

A

can be taken any time of day (longer half life)

303
Q

Statin adverse effects

A

increase serum aminotransferase- LFTs (reversible and A-sx)

may produce liver damage if alcoholic or pre-existing liver dz

304
Q

Statin adverse effects

A

Possible liver damage
Myopathy/muscle pain (increase in serum creatine kinase)
–> Rhabdomyolysis

305
Q

Hallmark adverse effect of Statins

A 
Liver
Skeletal muscle (esp Simvostatin)
306
Q

Contra to Statin

A

Pregnancy

Active hepatic dz

307
Q

Bile-Acid binding Resin

A

Cholestyramine

308
Q

Cholestyramine mechanism

A

binds bile acids to prevent their intestinal reabsorption

309
Q

Cholestyramine

A

has no effect on Homozygous familial hypercholesterolemia bc no effect on LDL receptors

may increase Triglycerides

310
Q

Cholestyramine

A

take with meals
bile acids
prevent reabsorption

311
Q

What Hyperlipidemia drug do you take if pregnant?

A

Bile Acid-Binding Resin (Cholestyramine)

312
Q

Cholestyramine (bile acid) adverse effects

A

Constipation and Bloating

313
Q

Niacin

A

Nicotinic Acid (very large amts), Vit B3 (much smaller amts)

314
Q

Niacin (nicotinic acid, vit b3)

mechanism

A

inhibit VLDL secretion which decreases both VLDL and LDL BUT most distinct effect is: INCREASING HDL

315
Q

Niacin (nicotinic acid, vit b3)

A

Increase HDL

316
Q

Niacin (nicotinic acid, vit b3) adverse effects

A

Cutaneous vasodilation* (flushing)
Hot skin
(Prostaglandin mediated- take ASA beforehand)

317
Q

Niacin (nicotinic acid, vit b3) adverse effect

A

Impair glucose tolerance

318
Q

Contra to Niacin (nicotonic acid, vit b3)

A

DIABETICS bc it impairs glucose tolerance

319
Q

Fibric Acid deriv

A

Gemfibrozil

320
Q

Gemfibrozil (fibric acid) mechanism

A

turn on genes in endothelial, adipose, muscle, increase LPL expression and other genes inv in fatty acid oxidation

321
Q

Gemfibrozil (fibric acid deriv)

USE:

A

use more fat, burn up sources

Decrease TRIGLYCERIDES

322
Q

Gemfibrozil (fibric acid deriv) adverse effect

A

Gallstones

may increase LDL

323
Q

Ezetimibe

A

blocks intestinal absorption of cholesterol and other phytosterols

324
Q

Ezetemibe

A

not very strong on its own, use WITH a Statin –> synergistic

325
Q

Ezetimibe

A

only used in combo therapy

326
Q

PCSK9 inhibitors

A

Alirocumab
Evolocumab
“cumab”

327
Q

PCSK9 inhibitors

A

stop the degrading of the LDL receptors

Now, liver has more LDL receptors to soak up LDL and reduce blood levels

328
Q

PCSK9

A

must be injected
new
do not know much
not used often

329
Q

Quinidine

A

class IA anti-arrhyth

330
Q

Quinidine

A

broad spectrum
acute or chronic
SupraVentric (Atrial) and Ventric arrhythmia

331
Q

Quinidine adverse effects

A

Low therap index (reach side effects quickly)
Cardiac toxicity: SA, AV block, V arrhythm
Block a receptors- hypotension and reflex tachy
Paradoxical tachy
Torsade de pointe***

332
Q

Quinidine adverse effects

A

Torsades de pointe

sudden death sydnrome in athletes

333
Q

Quininde adverse effects

A

Quinidine syncope
Diarrhea
Cinchonism

334
Q

Procaninamide Ia

A

same SE as Quinidine + slow acetylator - LUPUS

335
Q

Lidocaine

A

only good for Ventricular arrhythmias

1 of 2 DOC for V.arrhyth

336
Q

Lidocaine

A

IV only
Used for Acute Ventric arrhythm
(what sets Lidocaine apart from the other V.arrhyth drug)

Lidocaine is only IV

337
Q

Least toxic anti-arrhyth

A

Lidocaine

only affecting Na damaged cells

338
Q

Lidocaine adverse effect

A

Convulsions

339
Q

Class Ic- Flecainide

A

blocks all Na channel states
barely ever used
LAST DITCH EFFORT drug

effects lasts too long

340
Q

B-blocker

A

Esmolol shines as anti-arrhyth

2nd line drug for treating Paroxsymal Supraventricular Tachycardia (PSTVTs)

341
Q

Class III: Amiodarone

A

blocks K channel

“the jack of all antiarrhythmics”

342
Q

Class III: Amiodarone

A

jack of all antiarrhythmics bc it blocks everything

covers all bases

343
Q

DOC for ventricular Arrhyth

A

Amiodarone

then, Lidocaine

344
Q

Sotalol adverse effect

A

Torsade de pointes

345
Q

Verapamil

A

constipation

346
Q

Verapamil and Diltiazem

A

do not give with B-blockers

347
Q

Adenosine

A

stops heart for 10 seconds

Acute PSVT and WPW synd

348
Q

PSVT tx order

A

Adenosine
Esmolol
CCBs (IV)

349
Q

Chronic tx of PSVT

A

B-blockers (safe)

CCBs

350
Q

DOC for Torsade de pointes

A

Magnesium

351
Q

Potassium

A

to stabilize membrane and prevent arrhythmias

352
Q

Heparin

A

mix of sulfated mucopolysaccharides (action of a unique pentasaccharide)

353
Q

Heparin mechanism

A

Activates Antithrombin III
-mainly affects 10a and Thrombin
1,000fold

354
Q

Heparin antidote

A

Protamine sulfate (has + charge and wants to bind to Heparin)

355
Q

Therapeutic target for Heparin- must measure with

A

PTT

356
Q

Heparin indications

A

Operations (always heparinized b4 surgery)
IV catheters
Prophylaxis for DVT/PE
Bridging therapy if pt is on Warfarin and needs to get off of it b4 surgery

357
Q

Heparin adverse effects

A

Hemorrhage
Allergic rxn
Mild decrease in platelets
HIT- Hep induced thrombocytopenia

358
Q

Contra to Heparin

A

Actively bleeding
Hemophilia (or other blood clotting disorder)
Hypersensitive
During/after surgery of BRAIN, SPINAL CORD, EYE

359
Q

Caution with Heparin in:

A

Liver or Kidney dysfx

dose adjustment needed

360
Q

LMWH

A

Enoxaprin
Fondaparinux

similar to HMW except a shorter chain
BETTER SUBcutaneous delivery

361
Q

LMWH

A

preferred for subcutaneous injections (shorter pieces)

outpatient instances

362
Q

LMWH Use:

A

Pregnant
Outpatient bridging
1/day dose

363
Q

LMWH

A

main inhibitory action on factor 10a

364
Q

Benefit of LMWH

A

Lower incidence of HIT

BUT less help with Protamine Sulfate

365
Q

Dabigatran (Pradaxa)

A

Oral direct inhibitor or Thrombin

366
Q

Dabigatran (Pradaxa) use

A

Prevention of stroke in pts with non-valvular A-Fib

367
Q

Dabigatran (pradaxa) contra

A

mechanical heart valves

368
Q

BLACK BOX WARNING for Dabigatran (Pradaxa)

A

Avoid abrupt discontinuation without alternate med–> inc risk of clot

369
Q

All oral anticoagulants

A

predictable effects

do not need to monitor

370
Q

Antidote for Dabigatran (Pradaxa)

A

Idarucizumab (Praxbind)

371
Q

Factor 10a Direct inhibitors

A

replacing Warfarin

372
Q

“Xaband”

A

Direct inhibitor of Xa

Prophylaxis for ANY CLOTS

373
Q

Ribaroxaban (Xarelto) and Apixaban (Eliquis)

A

direct 10a inhibitors

374
Q

Antidote for Xarelto and Eliquis “Xaban”

A

Andexxa

375
Q

Warfarin/ coumadin

A

interrupts the reduction of Vitamin K

Inhibit synthesis of many clotting factors

376
Q

Warfarin/ coumdain

A

lasts 4-5 days

Peak effect: 48 hrs

377
Q

Warfarin/coumadin downfalls

A

Many drug intxns

Needs to be monitored by INR

378
Q

Warfarin/coumdain

A

Oral
Prophylaxis
Chronic use
Start slowly over a week (need to give Heparin in this bridge time)

379
Q

Why is bridge therapy (heparin) needed for 5 days with start of Warfarin/coumadin

A

Protein C disappears first which actually promotes clot formation
(cutaneous necrosis and infarction)

380
Q

Warfarin contra

A

Pregnant

Category X

381
Q

Warfarin precaution

A

Drug interactions

382
Q

Fibrinolytics

A

break down existing clots

plasmin degrades the fibrin threads of clot

383
Q

t-PA

A

convert Plasminogen –> Plasmin which then degrates fibrin thread

384
Q

t-PA

A 
"Tissue plasminogen activator"
Lysis of clots (MI)
Severe PE
DVT
Arterial thrombosis
385
Q

Antidote for t-PA

A

aminocaproic acid

386
Q

Antifibrinolytics

A

used for bleeding disorders

Reverse fibrinolytic therapy

387
Q

Anitplatelet

A

ASA

inhibitor of thrombogenesis

388
Q

ASA use

A

Secondary prevention of CVD events if pt has established CVD

389
Q

ASA

A

irreversible inhibition of COX enzyme

decrease thromboxane A2

390
Q

ADP receptor inhibitors

A

Clopidogrel (plavix)

Ticagrelor (Brilinta)

391
Q

ADP receptor inhibitor (Clopidogrel and Ticagrelor)

A

if pt can’t tolerate ASA

Following stent placement to prevent clot

392
Q

Abciximab (ReoPro)

A

inhibit GP IIb/IIIa receptor from binding fibrinogen

Inhibits platelet aggregation

393
Q

Clopidogrel

A

Genotype for CYP2C19 before giving bc pt needs this enzyme in order to be able to convert this drug to its active form

394
Q

Clopidogrel contra

A

do NOT take with Omeprazole (bc Omep will inhibit CYP2C19 function and now allow Clopidogrel to be converted to its active form)

395
Q

Abciximab

A

given DURING stent placement with heparin to prevent clot

Given IV

Quarter 3 (17 decks)

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