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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
Contra to Sacubitril/Valsartan (Entresto)
Pregnancy (ARBs in the 2nd and 3rd trimester- Teratogenic) | Concurrent use with ACE-I (risk of angioedema)
26
B-blockers "LOL" drugs
Carvedilol (cardiologist's friend), Metoprolol
27
B-blockers effects
Decrease mortality, decrease Renin, decrease catecholamine effects on heart, decrease HR, decrease remodeling
28
B-blockers
effective only in EARLY stages of HF Dangerous in severe, end stage HF bc of the negative ionotropic effects
29
Vasodilators
Sodium nitroprusside, Isosorbide dinitrate, Hydralazine
30
Vasodilators
Reduce preload, afterload, or both decrease damage remodeling of heart
31
Drugs with Ionotropic effects
Dobutamine | Dopamine
32
When is Dopamine used over Dobutamine?
when INCREASE IN BP is needed
33
Dobutamine and Dopamine
severe refractory HF
34
Digitalis | Digoxin (frm US)
Digitalis is cardiac glycoside isolated from plants Inhibits Na/K ATPase
35
Digoxin
inhibits Na/K ATPase binds to Na binding site- blocks its effects
36
Digoxin
increase Na inside cell decrease expulsion of intracellular Ca leading to increased Sarcoplasmic Ca Stores! overall effect: increase crossbridge and INCREASE CONTRACTILITY
37
Digoxin indications
HF (last agent used) when all other benchmarks are met but pt is still feeling sluggish Improves exercise tolerance AND Arrhythmias (Slows HR)
38
Digoxin
can put put on this for longer manage long term if pt really wants to exercise
39
Dopamine and Dobutamine
not a long term option last ditchall effort pt is about to die
40
Digoxin
80% excreted by kidneys- best of all glycosides
41
Digoxin adverse effects
``` 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 ```
42
Digoxin cardiac adverse effects
Arrhythmia: sinus brady, ectopic ventricular beats, AV block, bigeminy (characteristic arrhythmia with Digoxin!)
43
V-fib
most common cause of death with Digoxin | "Sudden death"
44
Monitoring with Digoxin
Perform regular EKG | Measure K+ and Digoxin levels
45
How to treat Digitalis toxicity
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)
46
Do you perform cardioversion with Digitalis toxicity?
NO, not for digitalis-induced arrhythmias unless V-fib
47
K+ secretion
Distal tubule and collecting duct Exchange of Na/K Can be modified by Aldosterone-antagonists and K+ sparing diuretics
48
Thiazide diuretics
enhance Ca reabsorption
49
Loop diuretics
inhibit Ca reabsorption (used to treat hypercalcemia) Also cause body to get rid of more Mg
50
Weak acids at low pH are mostly un-ionized
lipid soluble | easily diffusible
51
Acidic drugs compete for uric acid excretion and can lead to
GOUTY attack
52
Carbonic Anyhdrase Inhibitors (CA Inhibitors)
Blocks bicarb production | Blocks NHE, resulting in increased Sodium and Water LOSS
53
Carbonic anhydrase
part of Bicarb production | Bicarb production is part of Aqueous humor and CSF production
54
CA Inhibitors use
Glaucoma Alkalanize urine (drug trapping) Alkalosis (Metabolic or Mountain sickness)
55
Metabolism of CA inhibitors
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
56
CA Inhibitors adverse effects
Hyperchloremic metabolic acidosis Hyperuricemia HypOkalemia Renal stones
57
Contra to CA Inhibitors
Hepatic cirrhosis | Sulfa hypersensitive
58
Loop diuretics (Furosemide and Ethacrynic Acid)
``` Mechanism: Block NKCC2 Induce Kidney PGs -decrease salt transport -vasodilation ```
59
Loop diuretics use
``` 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) ```
60
Loop diuretics Adverse Effects
Hypokalemic metabolic acidosis Hypocalcemia Hypomagnesemia Hypochloremia Everything is hypo with Loop, besides HYPER-URICEMIA
61
Other bad side effects of Loops
High potency -> abnormal fluid and electrolytes | IRREVERSIBLE OTOTOXICITY
62
Which Loop is worst for Ototoxicity
Ethacrynic acid | worse when given w/Aminoglycosides "the 5 mycins"
63
Aminoglycosides (5)
``` Streptomycin Gentamycin Tobramycin Amikacin Neomycin ```
64
Macrolides (3)
Erythromycin Clarithromycin Azithromycin
65
Contra to Loop diuretics
``` Sulfa Drug intxn -COX inhibitors -Aminoglycosides -Lithium -Digoxin Overzealous use is dangerous in -Hepatic cirrhosis -Borderline renal failure -HF ```
66
Ethacrynic acid
Good thing: NOT A SULFA DRUG | bad thing: worse for ototoxicity
67
Thiazide diuretics and related compounds
Hydrochlorothiazide Metolazone Indapamide
68
Mechanism of Thiazide
Inhibit Na reabsorption at early distal tubule (NCC) Dependent on Prostaglandin synthesis
69
Thiazide use
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
70
Thiazide diuretics and Diabetics
The hyperpolarization of pancreatic beta cells-inhibit insulin secretion- can make a pre-diabetic --> Diabetic
71
More Use of Thiazide
Lower systemic BP and enhance effectiveness of other HTN meds Enhance Ca reabsorption
72
Thiazide diuretics and Gout
Competes with Uric Acid- caution in ppl with Gout
73
Indapamide is excreted by biliary system,
useful in pts with Renal insufficiency
74
Thiazide adverse effects
Overall well tolerated. Hypokalemic metabolic ALKALOSIS (not enough K --> Cramps) Mg loss Iodide and Bromide loss Hyperuricemia (caution gout) Hyperglycemia Elevated serum lipid
75
Thiazide contra/precaution
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
76
Contra for Thiazides
DIABETICs
77
More caution with Thiazide
Lithium toxicity is worsened by Thiazides
78
Metazolone (Thiazide-like)
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
79
Indapamide (Thiazide-like)
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
80
K- sparing diuretics
Aldosterone antagonists | Direct inhibitors of Na+ flux
81
K-sparing diuretics
interfere with Na reabsorption at the distal exchange site- permit loss of Na and H2O ENHANCING K conservation
82
K-sparing
weak diuretics compared to Loop and Thiazide Reduce K loss and Alkalosis caused by other diuretics Used in combo with other drugs
83
Aldosterone Antagonist- Spironolactone
``` 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 ```
84
Spironolactone use
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
85
Spironolactone adverse effects
Occasional Hyperkalemia (too much K, makes sense) Others are few GI- n/v/cramps Gynecomastia- androgen receptor antagonist
86
Spironolactone caution
caution with ACE-I or ARBs d/t elevated K levels
87
Spironolactone contra
Kyperkalemia (burn pts) Chronic Renal insuff Liver damage (acidosis may occur)
88
Eplerenone (like Spirono, but has less Androgen receptor side effects)
Selective aldosterone receptor antagonist (SARA) Metabolized by CYP3A4- caution w/drug interactions
89
K-sparing diuretics that do nothing to Aldosterone, just block the ENaC channel
Amiloride Triamterene inhibit the Na/K ion exchange mechanism leading to less K excretion
90
K-sparing diuretics use
``` Combo with other K-losing diuretics No hyperuricemia- good! only diuretic class that does not cause this ```
91
Amiloride (K sparing) is DOC for
Li+- induced Diabetes Insipidus
92
Adverse effects of K-sparing diuretics
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
93
Contra for K-sparing diuretics
Hyperkalemia- burn patients
94
Osmotic diuretics
Mannitol Isosorbide Glycerin Urea
95
Osmotic diuretics
IV only Filtered but not reabsorbed by kidney Keeps water in tubules Produce water diuresis (not anything to do with sodium here)
96
Osmotic diuresis use
Acute Renal Failure Decrease intra-ocular pressure Decrease intra-cranial pressure Protect kidney
97
Adverse effects of Osmotic diuretics
CONTRA in HF (d/t excessive amt can cause extracellular volume expansion which affects pulmonary edema)
98
other adverse effects of Osmotic Diuretics
HA, n/v/chills, dizzy, polydipsia, lethargy, confusion, CP
99
ADH agonist
Desmopressin synthetic ADH Treats sx of Central Diabetes Insipidus
100
ADH agonist
retains water
101
ADH Antagonist
Conivaptan V1a and V2 receptor antagonist
102
Conivaptan (ADH antagonist) use
Tx of SIADH- euvolemic or hypervolemic Hyponatremia
103
Conivaptan (ADH antagonist)
increases Na concentrations and increases free water clearance when you are too dilute
104
Conivaptan (ADH antagonist) IV only
Adverse effects: Hypokalemia Injection site rxn Orthostatic HTN, A-fib, Hypotension
105
Contra for Conivaptan (ADH antagonist)
Hyponatremia associated with hypovalemia
106
Tolvaptan (ADH antagonist) stop from retaining water
similar to Conivaptan, except - Oral - non-peptide V2 vasopressin antagonist - can be continued outpatient
107
Loop and Thiazides
can be combined when pt is not responding to one alone
108
Afterload is determined by:
Arterial resistance (Aortic impedance and vascular resistance)
109
In Heart Failure
Massive vasoconstriction going on: increase in RAS Increase in peripheral resistance via arterial constriction Tx? AterioDILATOR drugs
110
Big problem with HF is the inability to contract strongly enough, but we dont fix this problem. Rather we treat by
reducing the workload that the heart has to do ``` B-blockers (reduce contractility) Ionotropic drugs (last ditch effort, these ones actually do increase contractility) ```
111
beta blockers
reduce cardiac work by slowing HR
112
How to reduce preload
Diuretic | Venodilator
113
How to reduce afterload
Arteriodilator
114
How to increase contractility
Ionotropic drug
115
How to reduce energy expenditure
B-adrenergic Antagonist
116
Drugs that reduce Heart Failure Mortality
Aldosterone Antagonist B-blocker ACE-I and ARB ARB + Nep inhibitor (ARNI)
117
Spironolactone and Eplerenone have extra benefits over other diuretics bc they
inhibit Aldosterone receptors
118
ACE-I
"prils"
119
ARBs
"sartans"
120
ACE-I
Inhibits the ACE enzyme which converts Angiontensin I --> Angiotensin II
121
ARBs
blocks Angiotensin II from binding to the AT1 receptor
122
ACE-I and ARBs are both considered
RAS pathway inhibitors
123
RAS inhibitors
Current DOC for Heart Failure Reduce preload (decrease aldosterone releas) AND Reduce afterload (reduce ATII induced constriction)
124
ACE-I main side effect
dry cough | d/t bradykinin
125
Sacubitril/Valsartan (Entresto)
better at reducing mortality in HF pts compared to Enalapril alone
126
Why is Neprilysin inhibition helpful?
decrease vasoconstriction, decrease Na retention, decrease Cardiac remodeling*
127
Adverse effects of Sacubitril/Valsartan (Entresto)
Hypotension Hyperkalemia (esp when used w K sparing diuretic) Cough and angioedema
128
Contra to Sacubitril/Valsartan (Entresto)
Pregnancy! (teratogenic) | and DO NOT USE with another ACE-I (risk of angioedema)
129
ARBs contra
Pregnancy! | teratogenic
130
Beta blockers
effective only in Early stages of HF
131
Beta blockers are dangerous in severe, end stage HF because:
negative ionotropic effect (slow HR)
132
Vasodilators
Na Nitroprusside Isosorbide Dinitrate Hydralazine
133
HF drugs WITH ionotropic effects (few)
Dobutamine Dopamine both used for severe refractory HF
134
Dobutamine
selevtive B1 agonist
135
Dopamine
3 receptors low: renal vasodilation med: b1 in heart, ionotropic high: a receptor in vessels, constriction USEFUL IF increase in BP is needed!! Dopamine
136
Digoxin
inhibits Na-K ATPase | increase contractility!! positive ionotropy by increase in the intracellular Ca2+ stores
137
Digoxin use
Last agent used for HF If all other meds have been tried and pt still feeling sluggish TO IMPROVE EXERCISE INTOLERANCE
138
Digoxin use
HF- last agent | Arrhythmias (decreases HR)
139
Digoxin slows HR by two diff mechanisms depending on the heart health of the person
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
140
Digoxin adverse effects
Glycosides are toxic Narrow margin of safety GI toxicity- earliest sign, n/v/d
141
Digoxin more adverse SE
CNS-HA,fatigue, drowsy Cardiac arrhythmia- sinus brady, ectopic beats, AV block V-Fib
142
Digoxin maintenance
Regular EKG | Measure K+ and med levels
143
Digoxin toxicity tx
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
144
DO NOT PERFORM CARDIOVERSION for Digoxin OD unless
pt is already in V-fib (bc if theyre not, it could send them into V-fib
145
Digoxin pharm interactions
Increased toxicity Thiazide or Loop- hypokalemia Further decrease of SA/aV if on beta blockers Decreased effectiveness of CCBs - contra in HF
146
DO NOT use Digoxin with: if you have Heart Failure
CCBs
147
Nitrates and Nitrites (2)
Nitroglycerin Isosorbide Dinitrate work by increasing NO and cGMP
148
Nitrates
DOC for any acute Anginal attack (classic or variant)
149
primary mechanism of Nitrates
decrease O2 demand
150
Adverse effect of Nitrate
Throbbing HA Tachycardia Orthost hypotension
151
Adverse effect of Nitrate
Develop tolerance | Not suitable for long term tx
152
Ca channel blockers "VDN"
better for long term tx - Verapamil - Diltiazem - Nifedipine
153
B-blockers
decrease O2 demand
154
B-blockers do not do ANYTHING for Variant angina
bc variant is spasm b-blockes do not do anything for blood vessel (work indirectly via other mechanisms)
155
Ranolazine
only used to treat Angina as LAST DITCH EFFORT
156
Ranolazine
Partial fatty acid oxidation inhibitor (PFox) Inhibitor decrease O2 consumption in ischemic tissue
157
Sildinafeil (Viagra)
increase levels of cGMP and PDE5. increase relaxation and vasodilation
158
Contra to Sildenafil (viagra)
``` Pregnant/lactating Children or infants Pilots Taking Nitrate already A-blockers ```
159
Other PDE5 inhibitors
Vardenafil (levitra) Tadalafil (Cialis) more selective for PDE5
160
Vardenafil (levatria)
Onset of effects SOONER
161
Tadalafil (Cialis)
up to 24-36 hours Effects last waaaaaay longer Ta-da
162
ED drugs | PED5 inhibitors
"afil" drugs
163
What determines diastolic pressure?
Peripheral resistance | Blood volume
164
What determines systolic pressure?
Diastolic pressure | Pulse pressure
165
What determines pulse pressure?
``` Aortic compliance (elasticity) Contractility ```
166
Almost all BP drugs will decrease BP b y at least
10% in mild to moderate HTN
167
Groups of Anti HTN meds
Diuretics Symphathoplegic agents Direct vasodilators Angiotensin Inhibitors
168
Biggest use for HTN
Thiazide diuretics | mild-mod HTN
169
Thiazide mechanism
Increase sodium and water excretion short term: decrease cardiac output long term: hyperpolarize membrane and decrease peripheral vascular resistance
170
Diuretic side effects
``` Impotence (erectile dysfx) Gout- hyperuricemia Increased renin secretion K depletion Reduced glucose tolerance Increased plasma lipids ```
171
Thiazide
one of first recommended drugs for HTN
172
Thiazide special considerations
Sulfa
173
Thiazides are more effective in
African American
174
Loop diuretics
use in severe cases for HTN | Renal insuff, HF
175
K-sparing diuretics use for HTN
Use WITH thiazide or loop to decrease K loss | Avoid combo with other K sparing drugs
176
Sympatho-lytics
STOPPING sympathetic effects
177
Sympatho-lytic drugs
activate Baroreflex and cause: Sodium and Water retention
178
Sympatho-lytics are best when
combined with Diuretic
179
Clonidine and Methyldopa
stimulate Medullary alpha-2 adrenergic receptors --> decrease peripheral symp nerve activity decrease transmitter release to relevant sites
180
Clonidine and Methyldopa
Decrease BP by: 1) decrease symp outflow 2) decrease Renin secretion
181
Clonidine
decreases HR and CO more than Methyldopa
182
Methyldopa
recommended drug in pregnancy (compelling indication)
183
Common SE with Clonidine and Methyldopa
Xerostomia (Dry mouth) Sedation ED
184
Methyldopa, more side effects
Hemolytic anemia + coombs Hepatotoxicity Increased prolactin --> gynecomastia and lactation
185
Sudden withdrawal of Clinidine BAD
HTN crisis
186
Tricyclic antidepressants and yohimbine
inhibit Clonidine's action
187
Prazosin
alpha-1 antagonies dilate arteries and veins to decrease Peripheral resistance --> decrease BP
188
Good thing about Prazosin
does not affect plasma lipids
189
Compelling indication to use Prazosin
pt has BOTH: HTN and BPH
190
Prazosin
First dose phenomenon (postural hypotension) Reflex tachy Too much water and sodium retention
191
B blockers
young, white male
192
B-blockers
reduce CO reduce Renin secretion recude symp vasomotor tone
193
B-blockers are NOT recommended as Monotherapy unless compelling indication:
Angina Post MI Migraine HF
194
B-blockers decrease exercise tolerance Other reasons to avoid b-blcokers
``` High phys activity African american Asthma Diabetes Hypercholesterol Periph Vasc dz ```
195
B-blockers complete CONTRA
``` Diabetes End stage HF Severe bradycardia Heart block Asthma ```
196
Labetolol
combined a1 and b-blocker Decrease BP in HTN emergency
197
Labetolol
pregnancy is a compelling indication
198
Carvedilol
combined a1 and b-blocker HTN, HT, and post MI "lipid neutral"
199
combined a1 and b-blocker side effects
``` Orthostatic hypotension (worse than b-blockers alone) Bronchoconstrict: DONT USE IN ASTHMATICS ```
200
Labetolol SE
Hepatotoxicity!! only use in emergency and for preggo
201
Sodium nitroprusside is special bc it relaxed arterial smooth muscle AND
veins
202
Chronic oral tx for HTN
Hydralazine and CCB
203
Nitroprusside, Fenoldopam, and some CCB are used
IV for emergency
204
Side effects to any vasodilators
``` Reflex tachy and increased contraction Increased Renin secretion Fluid retention HA, flushing Palpitations, dizzy ```
205
Drugs that act through Nitric Oxide
Hydralazine | Sodium Nitroprusside
206
Hydralazine
Dilates ARTERIES but not veins
207
Hydralazine use
Chronic tx of SEVERE HTN Only used when other tx failed!!! combo with others
208
Hydralazine compelling indication
Severe HTN and or HTN emergency in PREGNANCY
209
Hydralazine adverse effects
Systemic Lupus Eryth in "slow acetylators" One of the "HIP" drugs of slow acetylators
210
Other adverse effects of Hydralazine
HA, nausea, anorexia, palpitations, sweating, flushing, Angina, ischemic arrhythmia
211
Sodium nitroprusside
IV Emergency dilated Arteries AND Veins RAPIDLY LOWERS BP- in minutes
212
Sodium nitroprusside pharmacokinetics
Metabolized by thicyanate----> Adverse effect is Cyanide accumulation
213
Cyanide accumulation in Sodium Nitroprusside administration can be extra dangerous to those who have a deficiency in Cyanide metabolsim
Metabolic ACIDOSIS, arrhythmia, excessive HYPOtension, death
214
Fenoldopam
D1 receptor agonist
215
Fenoldopam
relaxes arteriolar smooth muscle
216
Fenoldopam use
EMERGENCY HTN
217
CCB two classes
Dihydropyridines | Others
218
Dihydropyridines (CCBs)
Nifedipine | Amlodipine
219
Other CCBs
Diltiazem | Verapamil
220
CCB mechanism
bind to L-type channels in the: | Myocardium and Vascular sm musle
221
CCB effect on myocardium
decrease contractility, automaticity, and conduction
222
CCB effect on Vascular sm.muscle
vasodilation
223
CCBs
one of first choices for HTN therapy
224
CCBs effects differ based on tissue selectivity, can have opposite effects on Heart Rate
Nifedipine has highest effect on BLOOD VESSELS and least effect on cardiac muscle Decreases BP but INCREASES HR
225
Verapamil
Decreases BP AND decreases HR has highest effect on Cardiac muscle, least effect on blood vessels (therefore does not cause reflex tachy)
226
Where does Nifedipine (and all "dipines") have highest effect
Vascular smooth muscle (blood vessels)
227
Where does Varapamil have highest effect?
Cardiac muscle
228
CCB that is most likely to cause reflex tachycardia
Nifedipine
229
Dihydropyridines in general have these SE more d/t their dominant effect being on Vascular Smooth Muscle
``` Reflex tachy HA flushing Dizzy Periph edema Gingival hyperplasia ```
230
Verapamil side effect
Constipation
231
CCBs that cause depressed SA and AV node fx - may cause bradycardia esp in those with SA node dysfx
Verapamil and Diltiazem
232
Verapamil and Diltiazem Contra (CCBs)
already on B-blockers SA/AV node dysfx Heart Failure
233
Dihydropyridine Contra (CCBs)
cautiously in pts with HF
234
RAS Inhibitors (2 classes)
ACE-I and ARBs
235
ACE-I
"prils"
236
ARBs
"sartans"
237
ACE-I | "prils"
inhibit ACE therfore ACE II cant be made Decrease BP by: - reduce vasoconstriction caused by ATII - reduce release of Aldosterone
238
ACE-I | "prils"
lower BP without compromising the heart, brain, or kidneys without lipid changes without reflex tachy
239
ACE-I | "prils"
most effective in young and middle aged caucasions
240
ACE-I | "prils"
one of 1st choices for HTN Definitive DOC for HTN in those with: Diabetes CKD HF w reduced EF
241
ACE-I | "prils"
particularly indicated for DIABETIC NEPHROPATHY
242
ACE-I | "prils"
Enhance antiHTN efficacy of diuretics Balance the K issue with diuretics (increase K) Decrease proteinuria and stabilize Renal fx
243
ACE-I adverse effects | "prils"
Dry, hacking COUGH!!!! and Angioneurotic EDEMA both d/t Bradykinin
244
ACE-I adverse effects | "prils"
Hyperkalemia d/t inhibited Aldosterone secretion | Acute Renal Failure (in those with bilateral renal artery stenosis)
245
Contra to ACE-I | "prils"
Pregnancy (2nd and 3rd trimester particularly)- TERATOGENIC With K-sparing agents--> hyperkalemia Combo with NSAIDs (decreases effectiveness)
246
ARBs | "sartans"
block AT1 receptors selectively
247
big diff b/w ACE-I "prils" and ARBs "sartans"
ACE-I increase Bradykinin levels which leads to side effects (dry cough and angio edema) BUT neither of those occur with ARBs
248
Classic or atherosclerotic Angina
"angina of effort" obstruction of large coronary vessels- esp w exercise
249
Classic/atherosclerotic Angina
if uncontrolled by drugs, may require stenting
250
Variant/angioSPASTIC/ Prinzmetal's angina
Spasm or constriction in atherosclerotic coronary vessel REVERSED by Nitrates or CCBs
251
Coronary blood flow is directly proportional to
Perfusion pressure | Diastole duration
252
Why are drugs that increase O2 supply ineffective?
"Coronary steal phenomenon" arteries that are healthy and non-sclerotic will steal away the increase BF and oxygen from the calcified hardened arteries
253
HR and Cardiac contractility are decreased by
B-blockers and | some CCBs
254
Nitrates
decrease preload in veins
255
CCBs
decrease afterload in arteries
256
Nitrates
Uneven vasodilation (this is why preload is reduced more bc the big veins are markedly vasodilated more than the small veins)
257
Nitrates
Vasodilation via NO--> cGMP pathway
258
Nitrates
DOC for any ACUTE anginal attack | classic or spasm
259
Nitrates both increase and decrease cardiac workload
decrease: preload and afterload increase: decrease BP which kicks in Baroreflex which increases HR and contractility and reduces diastole time
260
Nitrates accomplish Anginal relief by
Predominant mechanism: decreasing Myocardial O2 requirement
261
Nitro (many routes!!) | sublingual, oral, transdermal
Rapid metabolization | High first pass effect
262
Sublingual Nitro is preferred bc
Avoid hepatic destruction | Rapid absorption- immediate relief
263
Adverse toxicity of Nitrates
Acute toxicity: orthost hypotension, tachycardia, HA | Repeated exposure: tolerance and reduced effects (not suitable for long term, but docs do anyway)
264
Chronic exposure to Nitrates
"monday dz"
265
CCBs
better for long term
266
CCBs
relax all smooth muscle that relies on L-type Ca channels Verapamil Diltiazem Nifedipine
267
Nifedipine has highest effects on
Vascular sm. muscle (reflex tachy!)
268
Verapamil has highest effect on
Cardiac muscle
269
Diltiazem
in the middle of the CCB sandwhich
270
Slow release Nifedipine (dominant on vascular sm.muscle) is indicated
ONLY in HTN (not angina) bc may actually cause Angina Pectoris
271
Nifedipine (and other dihyrdopyridine CCBs) harmful effects
Enhanced development of MI | rapid hypotension--> baroreflex --> increase cardiac workload --> ischemia
272
Verapamil and Diltiazem (CCBs) harmful effects
Cause serious cardiac depression that could end in cardiac arrest, AV block, or Heart Failure
273
Nifedipine and Dihydropyridine benefits
Vasodilation --> increase O2 supply and decrease afterload
274
Verapamil and Diltiazem benefits
Decrease myocardial contractility | Bradycardia caused by decreased SA/AV signalling
275
B-blockers have CV effects at 3 organs
Heart: decrease CO Kidneys: Decrease Renin CNS: decrease symp vasomotor tone
276
B-blocker Anginal relief comes from:
Decrease in symp activatoin ------> decrease heart O2 demans
277
B-blockers DO NOT WORK FOR
Variant/spasm angina!!!!
278
B-blockers adverse effects
Bronchoconstriction Increase plasma triglcyerides Decrease insulin and hypoglycemic response CNS SE
279
B-blockers DO NOT WORK FOR and can actually be HARMFUL in Variant/Spasm angina bc
Slow HR, prolong ejection time, increase L ventricular End diastolic volume, increases Oxygen requirement
280
Ranolazine unique mechanism
Partial Fatty acid oxidation inhibitor (Pfox) | Decreases oxygen consumption in ischemic tissue
281
Ranolazine
LAST CHOICE DRUG when other anti-anginal meds havent worked expensive also
282
Tx of Angina
Increase exercise tolerance | Decrease frequency and duration of myocardial ischemia
283
For Variant/spasm angina
Nitrates and CCBs preferred
284
Nitrate induced Reflex Tachy can be minimized by combining with
CCB or B-blockers
285
Common combos
B-blocker and Nitrate | B-blocker and CCBs
286
PDE5 inhibitors
Sildenafil (Viagra) Vardenafil Tadalafil
287
Sildenafil (Viagra)
selective inhibitor of cGMP specific PDE5 more vasodilation (PDE5 is specifically in the penis)
288
Sildenafil (Viagra) uses
Erectile dysfx | Pulmonary HTN
289
Sildenafil (Viagra)
Max concentration: 30-120 min Half life: 4 hr Metabolized by CYP3A4
290
Adverse effects of Sildenafil (Viagra)
Visual impairment (blue color tinge to vision), photophobia, or blurred vision bc PDE6 is found in retina
291
Adverse effects of Sildenafil (viagra)
HA, flushing, SOB, nasal congestion, UTI
292
CONTRA to Sildenafil (viagra)
Pregnant/lactating woman Infants/children With Nitrates (too much vasodilation) With A-blockers
293
CONTRA to Sildenafil (Viagra) pt 2
Inhibitors of CYP3A4 | will reduce clearance of Viagra and increase its toxic effects
294
Newer PDE5 inhibitors are more selective for PDE5 than PDE6 (less side effects)
Vardenail - very soon Tadalafil- good for tomorrow, lasts up to 24-36 hours
295
Statins
Lovastatin Simvastatin (worst) Atorvastatin (common)
296
Statin mechanism
inhibit HMG-CoA reductase (the enzyme that makes new cholesterol in liver)
297
Statin use
``` Decrease LDL (DOC for this) Stabilize plaques ```
298
Atorvastatin | high intensity therapy
can be given in double dose, used for High Risk Atherosclerotic Cardiovascular Disease pts
299
Lovastatin and Simvastatin
have to be activated to work- hydrolyzed
300
Statins
high first pass, liver metabolism
301
Lovastatin and Simvastatin
must take in evening | bc peak chol synthesis in early morning hours
302
Atorvastatin
can be taken any time of day (longer half life)
303
Statin adverse effects
increase serum aminotransferase- LFTs (reversible and A-sx) may produce liver damage if alcoholic or pre-existing liver dz
304
Statin adverse effects
Possible liver damage Myopathy/muscle pain (increase in serum creatine kinase) --> Rhabdomyolysis
305
Hallmark adverse effect of Statins
``` Liver Skeletal muscle (esp Simvostatin) ```
306
Contra to Statin
Pregnancy | Active hepatic dz
307
Bile-Acid binding Resin
Cholestyramine
308
Cholestyramine mechanism
binds bile acids to prevent their intestinal reabsorption
309
Cholestyramine
has no effect on Homozygous familial hypercholesterolemia bc no effect on LDL receptors may increase Triglycerides
310
Cholestyramine
take with meals bile acids prevent reabsorption
311
What Hyperlipidemia drug do you take if pregnant?
Bile Acid-Binding Resin (Cholestyramine)
312
Cholestyramine (bile acid) adverse effects
Constipation and Bloating
313
Niacin
Nicotinic Acid (very large amts), Vit B3 (much smaller amts)
314
Niacin (nicotinic acid, vit b3) | mechanism
inhibit VLDL secretion which decreases both VLDL and LDL BUT most distinct effect is: INCREASING HDL
315
Niacin (nicotinic acid, vit b3)
Increase HDL
316
Niacin (nicotinic acid, vit b3) adverse effects
Cutaneous vasodilation* (flushing) Hot skin (Prostaglandin mediated- take ASA beforehand)
317
Niacin (nicotinic acid, vit b3) adverse effect
Impair glucose tolerance
318
Contra to Niacin (nicotonic acid, vit b3)
DIABETICS bc it impairs glucose tolerance
319
Fibric Acid deriv
Gemfibrozil
320
Gemfibrozil (fibric acid) mechanism
turn on genes in endothelial, adipose, muscle, increase LPL expression and other genes inv in fatty acid oxidation
321
Gemfibrozil (fibric acid deriv) | USE:
use more fat, burn up sources | Decrease TRIGLYCERIDES
322
Gemfibrozil (fibric acid deriv) adverse effect
Gallstones | may increase LDL
323
Ezetimibe
blocks intestinal absorption of cholesterol and other phytosterols
324
Ezetemibe
not very strong on its own, use WITH a Statin --> synergistic
325
Ezetimibe
only used in combo therapy
326
PCSK9 inhibitors
Alirocumab Evolocumab "cumab"
327
PCSK9 inhibitors
stop the degrading of the LDL receptors Now, liver has more LDL receptors to soak up LDL and reduce blood levels
328
PCSK9
must be injected new do not know much not used often
329
Quinidine
class IA anti-arrhyth
330
Quinidine
broad spectrum acute or chronic SupraVentric (Atrial) and Ventric arrhythmia
331
Quinidine adverse effects
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
Quinidine adverse effects
Torsades de pointe | sudden death sydnrome in athletes
333
Quininde adverse effects
Quinidine syncope Diarrhea Cinchonism
334
Procaninamide Ia
same SE as Quinidine + slow acetylator - LUPUS
335
Lidocaine
only good for Ventricular arrhythmias | 1 of 2 DOC for V.arrhyth
336
Lidocaine
IV only Used for Acute Ventric arrhythm (what sets Lidocaine apart from the other V.arrhyth drug) Lidocaine is only IV
337
Least toxic anti-arrhyth
Lidocaine only affecting Na damaged cells
338
Lidocaine adverse effect
Convulsions
339
Class Ic- Flecainide
blocks all Na channel states barely ever used LAST DITCH EFFORT drug effects lasts too long
340
B-blocker
Esmolol shines as anti-arrhyth 2nd line drug for treating Paroxsymal Supraventricular Tachycardia (PSTVTs)
341
Class III: Amiodarone
blocks K channel | "the jack of all antiarrhythmics"
342
Class III: Amiodarone
jack of all antiarrhythmics bc it blocks everything covers all bases
343
DOC for ventricular Arrhyth
Amiodarone then, Lidocaine
344
Sotalol adverse effect
Torsade de pointes
345
Verapamil
constipation
346
Verapamil and Diltiazem
do not give with B-blockers
347
Adenosine
stops heart for 10 seconds Acute PSVT and WPW synd
348
PSVT tx order
Adenosine Esmolol CCBs (IV)
349
Chronic tx of PSVT
B-blockers (safe) | CCBs
350
DOC for Torsade de pointes
Magnesium
351
Potassium
to stabilize membrane and prevent arrhythmias
352
Heparin
mix of sulfated mucopolysaccharides (action of a unique pentasaccharide)
353
Heparin mechanism
Activates Antithrombin III -mainly affects 10a and Thrombin 1,000fold
354
Heparin antidote
Protamine sulfate (has + charge and wants to bind to Heparin)
355
Therapeutic target for Heparin- must measure with
PTT
356
Heparin indications
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
Heparin adverse effects
Hemorrhage Allergic rxn Mild decrease in platelets HIT- Hep induced thrombocytopenia
358
Contra to Heparin
Actively bleeding Hemophilia (or other blood clotting disorder) Hypersensitive During/after surgery of BRAIN, SPINAL CORD, EYE
359
Caution with Heparin in:
Liver or Kidney dysfx | dose adjustment needed
360
LMWH
Enoxaprin Fondaparinux similar to HMW except a shorter chain BETTER SUBcutaneous delivery
361
LMWH
preferred for subcutaneous injections (shorter pieces) | outpatient instances
362
LMWH Use:
Pregnant Outpatient bridging 1/day dose
363
LMWH
main inhibitory action on factor 10a
364
Benefit of LMWH
Lower incidence of HIT | BUT less help with Protamine Sulfate
365
Dabigatran (Pradaxa)
Oral direct inhibitor or Thrombin
366
Dabigatran (Pradaxa) use
Prevention of stroke in pts with non-valvular A-Fib
367
Dabigatran (pradaxa) contra
mechanical heart valves
368
BLACK BOX WARNING for Dabigatran (Pradaxa)
Avoid abrupt discontinuation without alternate med--> inc risk of clot
369
All oral anticoagulants
predictable effects | do not need to monitor
370
Antidote for Dabigatran (Pradaxa)
Idarucizumab (Praxbind)
371
Factor 10a Direct inhibitors
replacing Warfarin
372
"Xaband"
Direct inhibitor of Xa | Prophylaxis for ANY CLOTS
373
Ribaroxaban (Xarelto) and Apixaban (Eliquis)
direct 10a inhibitors
374
Antidote for Xarelto and Eliquis "Xaban"
Andexxa
375
Warfarin/ coumadin
interrupts the reduction of Vitamin K Inhibit synthesis of many clotting factors
376
Warfarin/ coumdain
lasts 4-5 days | Peak effect: 48 hrs
377
Warfarin/coumadin downfalls
Many drug intxns | Needs to be monitored by INR
378
Warfarin/coumdain
Oral Prophylaxis Chronic use Start slowly over a week (need to give Heparin in this bridge time)
379
Why is bridge therapy (heparin) needed for 5 days with start of Warfarin/coumadin
Protein C disappears first which actually promotes clot formation (cutaneous necrosis and infarction)
380
Warfarin contra
Pregnant | Category X
381
Warfarin precaution
Drug interactions
382
Fibrinolytics
break down existing clots | plasmin degrades the fibrin threads of clot
383
t-PA
convert Plasminogen --> Plasmin which then degrates fibrin thread
384
t-PA
``` "Tissue plasminogen activator" Lysis of clots (MI) Severe PE DVT Arterial thrombosis ```
385
Antidote for t-PA
aminocaproic acid
386
Antifibrinolytics
used for bleeding disorders | Reverse fibrinolytic therapy
387
Anitplatelet
ASA | inhibitor of thrombogenesis
388
ASA use
Secondary prevention of CVD events if pt has established CVD
389
ASA
irreversible inhibition of COX enzyme decrease thromboxane A2
390
ADP receptor inhibitors
Clopidogrel (plavix) | Ticagrelor (Brilinta)
391
ADP receptor inhibitor (Clopidogrel and Ticagrelor)
if pt can't tolerate ASA | Following stent placement to prevent clot
392
Abciximab (ReoPro)
inhibit GP IIb/IIIa receptor from binding fibrinogen | Inhibits platelet aggregation
393
Clopidogrel
Genotype for CYP2C19 before giving bc pt needs this enzyme in order to be able to convert this drug to its active form
394
Clopidogrel contra
do NOT take with Omeprazole (bc Omep will inhibit CYP2C19 function and now allow Clopidogrel to be converted to its active form)
395
Abciximab
given DURING stent placement with heparin to prevent clot | Given IV

Quarter 3 (17 decks)

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