Cardiovascular Pharmacology Flashcards
(306 cards)
1
Q
How can hypertension be treated
A
Lifestyle changes (most effective), medications
2
Q
Lifestyle modifications for hypertension
A
Weight reduction and exercise Diet changes Relaxation techniques Smoking cessation Medications Encourage self monitoring
3
Q
What are antihypertensive medications
A
Diuretics, beta blocks, angiotensin receptor blockers, calcium channel blockers, ACE inhibitors
4
Q
Diuretics
A
Lower bp by reducing circulating fluid volume.
5
Q
What are the types of diuretics
A
Thiazides (hydrochlorothiazide) Loop diuretics (furosemide, ethracrynic acid) and potassium sparing diuretics (spironolactone)
6
Q
Beta blockers
A
Block sympathetic nerve impulses in the heart leading to a reduction in heart rate…decreasing cardiac output
7
Q
Examples of beta blockers
A
Atenolol
Propranolol
Metoprolol
8
Q
Angiotensin receptor blockers (ARB)
A
Specifically blocks angiotensin II from binding to vessel receptors, preventing vasoconstriction
9
Q
Examples of ARB
A
Losartan
Olmesartan
10
Q
Calcium channel blockers
A
Cause systemic vasodilation resulting in a reduced peripheral vascular resistance
11
Q
Examples of calcium channel blockers
A
Diltiazem
Verapamil
Nifedipine
12
Q
ACE inhibitors
A
Decreases the amount of angiotensin II and aldosterone in the system resulting in vasodilation and lowering circulating fluid volume. Slow progression of renal damage in patients with diabetes
13
Q
Examples of ACE inhibitors
A
Captopril
Lisinopril
Enalapril
14
Q
Nitroprusside
A
Nitrate drug with potent venodilator and vasodilator properties. It is administered via IV and is broken down in the blood into NO, which in turn increases cGMP, leading to smooth muscle relaxation . Translating into vasodilation and venodilation which is helpful in rapidly reducing the blood pressure, as this drug is rapid acting and has a short half life
15
Q
Why is nitroprusside given during malignant hypertension
A
Properties
16
Q
What is malignant hypertension
A
Severe increase in bp causing impairment of one or more organ systems
17
Q
Side effect nitroprusside
A
Cyanide toxicity
18
Q
Nitroprusside administration can lead to iatrogenic cyanide toxicity if overused.
A
Sodium nitroprusside has 5CN ligand in its molecule, and breaks down into thiocyanate. This is usually detoxified in the blood, but can reach toxic levels in the blood
19
Q
The half life of thiocyante is not as __ as nitroprusside, but is several days, and patients are at risk for toxicity and effects for longer
A
Short
20
Q
Nitroprusside MOA
A
- direct release of NO(vasodilation and venodilation)
- Increased cGMP (NO activates guanyl cyclase in SM increasing cGMP)
- CGMP inactivated myosin light chains and causes SM relaxation or arteriosus action. This drug is a potent dilator of venues and arterioles
- the drug has a half life of 1-2 min and is rapidly acting
21
Q
Indications nitroprusside
A
Malignant hypertension
22
Q
How is nitroprusside administered
A
IV
23
Q
Side effects nitroprusside
A
Cyanide toxicity
24
Q
How does nitroprusside give canine toxicity
A
Sodium nitroprusside has 5 CN ligand in its molecules and breaks down into thiocyanate. This is usually detoxified in the blood but can reach toxic levels in the blood.
25
Symptoms of cyanide toxicity
Vertigo, confusion, difficulty breathing and headaches at low doses.
26
Minoxidil (loniten, rogaine)
Vasodilator that acts primarily on arterioles
27
Although minoxidil causes more severe adverse reactions than hydralazine it also does what
More intense arteriolar vasodilation
28
Indication for minoxidil
Severe hypertensiona nd baldness
29
Side effects minoxidil
Reflex tachycardia, blood volume expansion, and pericardial effusion, excessive hair growth or a rash
30
How minimize adverse effects of minoxidil
Give with beta blockers and diuretics and diuretics
31
MOA minoxidil
Vasodilator arterioles
By dilating the resistance vessels, the medication decreases afterload and subsequently cardiac workload. This action causes cardiac output and tissue perfusion to increase.
32
Does minoxidil have venous effects
No
33
Indications for minoxidil
Severe hypertension and baldness
34
Baldness and minoxidil
Topical
35
Side effects minoxidil
Reflex tachycardia, blood volume expansion, hypertrichosis, pericardial effusion, rash
36
Reflex tachycardia and minoxidil
As baroreceptors in the aortic arch and carotid sinus sense a decrease in bp, the vasomotor center of the medulla tries to restore normal blood pressure by increasing heart rate and myocardial contractility
37
Blood volume expansion and minoxidil
Chronic use of vasodilator causes prolonged reduction of bp, which triggers adrenal glands to secrete aldosterone to promote sodium and water retention. In addition, decreasing arterial pressure leads to decreased renal blood flow and reduced GFR. Decreasingthe filtrate volume increases the kidneys ability to reabsorbed sodium and water and leads to blood volume expansion
38
Minoxidil and hypertrichosis
Vasodilator effects cause proliferation of epithelial cells at the base of the hair follicle. Hair growth begins on the face and progresses to arms, legs, and back.
39
Minoxidil and pericardial effusion
Fluid retention lead to fluid accumulation underneath the pericardium and develop pericardial effusion. May compress the heart and lead to cardiac tamponade
40
Why give minoxidil with beta blocker and diuretic
Minimize reflex tachycardia, so premeditate with beta blocker to prevent sympathetic stimulation of the heart. Since blood volume increase negates the effect of vasodilation, diuretics also given to prevent fluid retention and volume expansion (if diuretic therapy inadequate will need dialysis)
41
Hydralazine
Vasodilator that helps to relax smooth muscle and decrease peripheral resistance helping to lower blood pressure and reduce afterload
42
MOA hydralazine
Increases cGMP , leading to SM relaxation, and arteriodilation with a slight amount of venodilation. So it directly relaxes arteriolar muscle
43
Indications for hydralazine
Severe hypertension and CHF
44
What is hydralazine often combined with
Methyldopa to treat hypertension in pregnancy
45
Side effects hydralazine
Drug induced lupus
With anti histone antibodies
Reflex tachycardia due to the drugs sudden pressor actions and is often co-administered with a B blocker to prevent this
46
Indications for hydralazine
Reduce afterload, severe hypertension , CHF
47
How does hydralazine reduce afterload
Relaxes SM and preferentially vasodilator arterioles,creating an afterload reduction. It is indicated in diseases where there is a cardiac failure or excess systemic resistance
48
Severe hypertension and hydralazine
Not for essential hypertension
First line of hypertension during pregnancy
49
Hydralazine is indicated for pregnancy hypertension along with ___
Methyldopa
50
MOA hydralazine
Increase cGMP which inhibits contraction in SM and leads to bv relaxation
(Grater vasodilation of arterioles than veins)
51
Side effects hydralazine
```
Drug induced lupus(have antihistone antibodies)
Reflex tachycardia (compensatory response to sudden decreased bp to maintain cardiac output.)
```
52
How prevent reflex tachycardia with hydralazine
Give with beta blocker
53
Who is hydralazine contraindicated in
Angina, CAD
It can also cause angina
54
Calcium channel blockers (verapamil and diltiazem)
Verapamil belongs to the phenylalkylamines class and diltiazem belongs to a class called the benzothiazepines
55
How are verapamil and diltiazem different from other calcium channel blockers
Have direct action on cardiac tissue at therapeutic levels
56
Verapamil and diltiazem are also classified as type IV antiarrhythmics and
Work to slow AV conduction
57
Indications calcium channel blockers (verapamil and diltiazem)
Angina pectoris, essential hypertension and arrhythmias
58
MOA calcium channel blockers
Block coltage dependent calcium channels. Since these channels are concentrated in SA and AV this drug class helps by decreasing conduction through the AV node.
59
Calcium channel blockers are contraindicated in
Heart block, espicially 2nd degree block and complete heart block
60
Indications for calcium channel blockers
Angina pectoris
Essential hypertension
Arrhythmias
61
Angina pectoris and calcium channel blockers
Calcium channels in SM or vasculature and blocking them allows blood vessels to dilate.
62
Essential hypertension and calcium channel blockers
Decrease blood pressure by dilation of the arterioles.
63
What calcium channel blocker is first line for treating chronic hypertension
Verapamil
64
Arrhythmias and calcium channel blockers
Espicially atrial tachyarrhythmias as they slow impulse conduction through the AV node
65
Side effects calcium channel blocker
```
Bradycardia
Hypotension
Constipation
Peripheral edema
Gingival hyperplasia
```
66
Calcium channel blockers bradycardia
Slow impulse conduction through the AV node to the ventricles
67
Hypotension and calcium channel blockers
Relaxing SM in vasculature, these medications can lead to the side effect of hypotension
68
Constipation and calcium channel blockers
Leads to decreased smooth muscle motility and can manifest as constipation (more so with verapamil)
69
Peripheral edema and calcium channel blockers
Arteriolar dilation leading to capillary hypertension which causes fluid extravasation into tissues
70
Gingival hyperplasia calcium channel blockers (verapamil)
Enlargement of the gums
71
Class I antiarrhythmics (Na channel blockers)
Treat tachyarrhythmias by blocking fast Na channels and there are several subcategories of drug based not heir specific effect on cardiac action potentials
72
class I antiarrhythmatics do what
Restore normal pacemaker and conduction activity and are selective for depolarized tissue, which is known as state dependent
73
MOA class I antiarrhythmics
Block Na channels to reduce rate of phase I depolarizationand prolong effective refractory period. This increases the threshold for firing within abnormal pacemaker cells.
74
Class I antiarrhythmic contraindicated
Hyperkalemia states, as excess potassium increases resisting membrane potential and can produce a sodium channel block so pronounced that asystole may result in patients taking class I
75
Arrhythmias
Refer to abnormal heart rate or regularity. They can be caused by either or regular impulse conduction or impulse generation
76
Indications class I
Arrhythmias and local anesthesia
77
MOA class I antiarrhythmics
1. Block slow conduction (block fast sodium channels. Halting conduction espicially in depolarized cells
2. block na channels to reduce rate of phase I depolarization and prolongs effective refractory period
3. raise threshold. Bc of Na channel block they increase the threshold for firing within abnormal pacemaker cells
4. State dependent -selectively depress tissue that is frequently depolarized, versus normally polarized tissue. This can include ischemic tissue
78
Contraindications for class I antiarrhythmics
Hyperkalemia
Toxicity bc k increases resting membrane potential and can produce a sodium channel blockade so pronounced that asystole may result
79
Class IA antiarrhythmics (na channel blocker)
Treat arrhythmias through blockage of na channels, prolonging action potentials and are effective for both atrial and ventricular arrhythmias
80
Indication for classI antiarrhythmias
Arrhythmias-atrial and ventricular,
| Recent rant and ectopic suprventricular and ventricular tachycardia, wolff parkinson white syndrome
81
MOA class IA
Increase PA, effective refractory period, and QT interval
82
Commonly used class IA antiarrhythmia drugs
Disopyramide, procainamide
| Quinidine
83
Shared side effects of class IA
Thrombocytopenia and torsades de pointes
84
Side effect procainamide
Drug induced lupus
85
Side effects quinidine
Cinchoism
86
Indications for class IA
Arrhythmias (vent ansupra vent)
| Recent rant and ectopic supraventricular arrhythmias, such as Wolff parkinson white syndrome
87
MOA class IA
Increase AP, ERP, and QT interval
88
Disopyramide
Similar in action to quinidine, and has the longest half life of drugs in this class. It is indicated for ventricular arrhythmias, but has pronounced anticholinergic side effects, and can possibly worsen heart block and cause severe heart failure
89
Procainamide
Similar in action to quinidine, but has less GI side effects and is safer to use intravenously
90
Side effect procainamide
Drug induced lupus , which can be catalyze by medication. Patients with drug induced lupus typically show antihistone antibodies
91
Quinidine
Indicated for supraventricular and ventricular arrhythmias and also may be used for prevention.it is a state dependent block, meaning at higher heart rates, the block increases while at lower heart rates, the block decreases
92
Side effect quinidine
Cinchonism which resents as dizziness, ringing in the ears and diarrhea
93
Shared side effects of class iA
Thrombocytopenia
| Torsades de points
94
Why may quinidine cause thrombocytopenia
Destruction of platelets by antibodies developed in response to protein quinine complexes in the circulation
95
Torsades de pointes
Quickly transform into ventricular fibrillation which may lead to sudden death. Torsades is a ventricular tachycardia which presented with shifting sinusoid waveformed on ECG. It may occur due to the increase in QT interval associated with this drug class
96
Class IB antiarrhythmics (Na channel blockers)
Class of antiarrhythmic drugs for treating ventricular arrhythmias by weakly blocking sodium channels and decreasing action potential duration. They also shorten the duration of refractory period
97
Indications for class IB
Arrhythmias (acute ventricular and digitalis-induced arrhythmias)
After MI arrhythmias
98
Class IB preferentially affect _ or _ purkinje and ventricular tissues, and act to decrease action potential duration by blocking sodium currents
Ischemic
| Depolarized
99
Commonly used IB antiarrhythmias
Mexiletine
Lidocaine
Tocainide
Phenytoin
100
Mexiletine side effect
GI upset
101
Lidocaine side effect
CNS depresssion
102
Phenytoin
Anti-epileptic drug which also has class IB antiarrhythmic properties.
103
Long term use of phenytoin
Associated with hirsuitism, but can yield many other side effects as well
104
Indications class IB
Acute ventricular and digitalis induced arrhythmias
Treat arrhythmias which arise from imporoper impulse conduction or impulse conduction or impulse generation
After MI as they preferentially affect ischemic tissue
105
MOA IB
Highly selective for ischemic or depolarized purkinje and ventricular tissue
Decrease AP duration bc of their block of sodium currents. They have fast onset/offset kinetics and have little effect on slower heart rates, but a greater effect on faster heart rates
106
Mexiletine
May cause GI upset
107
Lidocaine
IV
Treats damaged tissues and acts only on the sodium channel. It is the second line treatment for ventricular arrhythmias and has a low level of cardiotoxicity
108
Lidocaine side effect
CNS depression ==seizures in severe overdose
109
Tocainide
Orally active drug, similar to lidocaine
110
Phenytoin
Anti seizure drug that is occasionally used as an antiarrhythmic, specifically in digitalis overdose to reverse atrioventricular block. It is known to have many side effects, including drug induced lupus, gingival hyperplasia, teratogenic effects and hirsutism
111
Class IC antiarrhythmics
Treat severe ventricular tachyarrhythmias by blocking na channels and slowing conductance
112
Class IC have no effect on _ duration and are used as a last resort in ___ ___, which may become intractable or progress to ventricular fibrillation
AP
| Refractory tachyarrhythmias
113
Examples of class IC
Flecainide
| Propafenone
114
Propafenone
Acts as a b adrenergic antagonist and has the side effects of bradycardia ad CHF
115
Class IC contraindicated
In patients immediately after MI and in patients with structural abnormalities due to their propensity to increase mortality in these groups
116
Indications class IC
Last resort in refractory tachyarrhythmias
V tach which may progress to ventricular fibrillation
117
MOA class IC
No AP duration as opposed to other class I antiarrhymics
118
Examples of class CI
Propafenone
| Flecainide
119
Propafenone
Treats rapid heart beat arrhythmias such as supraventricular arrhythmias,. Similar to quinidine, and possesses b adrenergic antagonist activity. It may also represent life threatening ventricular arrhythmias,
120
Side effects propafenone
CHF, bradycardia and new arrhythmias
121
Flecainide
Class IC antiarrhythmias drug indicated for ventricular tachyarrhythmias and for maintaining sinus rhythms in cases of paroxysmal a fib or a flutter
122
Contraindications of class IC
Post MI . Has proarrhythmic activity and are contraindicated post MI and after structural heart disease due to increased mortality incidence with these diseases
123
Class III antiarrhythmics (k channel blockers)
Used when other types of antiarrhythmics fail. Work to prevent arrhythmias and re-entrant arrhythmias by increasing myocyte action potential duration, effective refractory period and Qt interval
124
Commonly used class III antiarrhythmics
Aminodarone
Ibutilide
Dofetilide
Sotalol
125
Aminodarone
Dirty drug due to its multisystemic toxicities and prescribers should heck pulmonary, liver, and thyroid function tests in patients taking this drug (causes pulmonary fibrosis, hepatotoxicity, and hypo/hyperthyroidism)
126
Ibutilide and dofetilide
Helpful in restoring a fib and flutter to normal sinus rhythm
127
Sotalol
Nonselective b blocker which has class II antiarrhythmic properties, and use of this medication can cause excessive b block in patients
128
Indications for class III
Arrhythmias
129
MOA class III
Increased AP, ERP, and QT interval
| DO NOT SLOW conduction veolcity, but rather, they prolong depolarization in atrio-ventricular myocytes
130
Amiodarone
Increases refractoriness and has a long half life. It is indicated for refractory life threatening ventricular arrhythmias, and is the first line treatment for patients not responding to CPR.
131
Why is amiodarone unique
Has class I, II, III, IV antiarrhythmic effects bc it alters the lipid membrane
132
Why do liver pulmonary and thyroid function tests when taking amiodarone
Toxicities of the drug. Can cause pulmonary fibrosis, hepatotoxicity, and hypo/jyperthyroidism
133
Why is amiodarone called a dirty drug
Can bind to several different targets or receptors and thus have a wide range of effects
134
Side effects amiodarone
CV effects (CHF, heart block, bradycardia), pulmonary fibrosis, hepatotoxicity, thyroid issues, corneal deposits, skin discolorations, neurological effects, and constipation
135
Ibutilide
Indicated for quick conversion of a flutter or a fib to a normal sinus rhythm.
136
How does ibutilide work
Give through IV infusion and works by prolonging action potential duration. A side effect is torsades de pointes
137
Side effect ibutilide
Torsades de pointes
138
Dofetilide
Indicated for converting and maintaining normal sinus rhythm in the care ofatrial flutter and atrial fibrillation
139
Sotalol
Non selective competitive b adrenergic receptor blocker , it has significant side effects, including dyspnea, dizziness, and torsades de pointes
140
Class IV antiarrhythmics (ca channel blocker)
Can be cardioselective or vasoselective, giving them a wide array of use
141
Cardioselevtive class IV
Verapamil
Diltiazem
Inhibit transport of Ca across the cell membrane during cardiac depolarization by blocking Ca channels, decreasing SA node discharge...decreasing conduction through AV leading to an increased PR interval and ERP
142
Indication for cardioselevtive class IV
Recent rant supraventricular tachycardia, also protects the ventricles from arrhythmias in atrial fluttter and fibrillation. Angina, hypertension, mostly due to SM relaxation
143
Vasoselective class VI
Nimodipine
144
MOA vasoselective class VI
Block Ca channels in SM and decrease vasoconstriction and spasm
145
Indication nimodipine
Treat subarachnoid hemorrhage due to its vasoselective properties
146
Side effects class iv
Cardiovascular (sinus node depression, AV block and CHF)
| Impaired Ca transport leads to decrease gastric signaling and decreased gut motility, causing constipation in patients
147
Indications class IV
SVT (due to AV nodal reentry), atrial fib or flutter, subarachnoid hemorrhage (nimodipine has higher effects on vascular SM than on cardiac condution)
148
MOA class VI
Ca channels in SA and AV node blocked to decrease impulse conduction and velocity through AV
Also on SM and can treat hypertension
Decrease conduction through AV leading to an increases in PR and ERP
149
Verapamil
Cardioselective Ca channel blocker, and has higher activity on slowing AV conduction than it does on vasodilation. It is indicated for use in arrhythmia prevention, hypertension, angina, and cluster headaches
150
Diltiasem
Cardioselective Ca channel blocker which has actions similar to verapamil. It is used for SVT, angina, atrial flutter, and firillation, as well as hypertension
151
Nimodipine
Vasoselective Ca channel blocker and is used to treat subarachnoid hemorrhage
152
Side effects class IV
There are numerous cardiovascular side efffects implicated with Ca channel blocker use (AV block, sinus node depression)
Constipation (esp verapamil as Ca is a 2nd messenger for gastric, which is important for gastric motility—-motility impaired)
153
Adenosine (adenocard)
A naturally occurring nucleotide in body that works by blocking cAMP induced Ca influx in cardiac myocytes.
154
Indication adenosine
Tachyarrhythmias to delay the PR interval and slow a patients heart rate to a normal sinus rhythm
Supraventricular tachyarrhythmias after other efforts like vagal maneuvers to slow the heart rate have failed.
155
Onset of adenosine
Seconds and resolves in 10 seconds. Side effects resolve in a minute
156
MOA adenosine
Slows AV conduction from the SA node through AV, which abolished tachyarrhythmias. Basically is a short term calcium channel blocker in the AV node that is induced by cAMP....causes prolonged PR
157
Indications adenosine
Supraventricular tachycardia (paroxysmal)
Must originate above AV node
158
Why does adenosine not work for a fib, a flutter, and verntricular arrhythmias
Do not typically involve AV node as part of the re-entrant circuit
159
Side effects adenosine
Bradycardia, flushing, dyspnea
160
Flushing with adenosine
Causes brief small vessel vasodilation .. could get buried hypertension, dizziness, or palpitations
161
Dyspnea adenosine
Induce bronchoconstriction
162
Caffeine and theophylline decrease effectiveness of adenosine
Caffeine increase HR.
| Methylxanthines bocks the receptors for adenosine on the heart
163
Dipyridamole may intensify effects of adenosine
It is an antiplatelet medication hat blocks the uptake and metabolism of adenosine and may intensify effects,,,may get more serious side effects
164
How is adenosine given
Rapid IV push followed by a saline fracture lush. Bc it’s Half life is only a few seconds
165
Lidocaine (xylocaine)
Sodium Channel blocker that inhibits neuronal impulses. It is indicated to treat ventricular dysrhythmias and induce local anesthesia.
166
Side effects lidocaine
Drowsiness, confusion, paresthesia, seizures, and respiratory arrest
167
Lidocaine is an __-type anesthetic and it metabolized by the liver
Amide
168
Administering lidocaine with a ___ prolongs the duration of local anesthetic effects
Vasoconstrictor
169
MOA lidocaine
Blocks na channels, preventing action potentials from creating pain perception (skin), suppresses neuronal excitability in ventricular dysrhythmias (heart) it is a class IB antiarrhythmis
170
Indications for lidocaine
Ventricular arrhythmias, anesthetic
171
Ventricular arrhythmias and lidocaine
Slows nerve conduction in heart. Slows depolarization and accelerates depolarization duration.
172
Unlike other antidysrhthmic meds, lidocaine does not cause ___ effects
Anticholinergic
173
Lidocaine anesthetic
Nonselective amide local anesthetic blocks conduction to both sensory and motor neurons.
174
In what order does lidocaine block impulses
Autonomic, somatic, sensory, somatic motor
175
Side effects lidocaine
Paresthesia
Seizure (CNS excitation(benzodiazepine may manage))
Respiratory depression (high IV doses suppress CNS)
Drowsiness 9CNS excitation is followed by depressive symptoms)
176
Giving lidocaine with a vasoconstrictor (epi)
Extends the duration of the local anesthetic. By decreasing blood flow and delaying systemic absorption of the anesthetic, epi prolongs anesthesia and decreases the risk of toxicity.
177
Magnesium sulfate
CNS depressant that inhibits release of acetylcholine at neuromuscular junctions which prevents skeletal and uterine muscle contraction.
178
Indications for magnesium sulfate
Preterm labor contractions
| Preeclampsia
179
Side effects magnesium sulfate
Warm feeling, hypotension, decreased DTR, decreased respiratory rate, decreased urine output, paralytic ileus
180
Antidote for magnesium sulfate
Gluconate
181
MOA magnesium sulfate
Muscle relaxant and depresses the CNS by stopping the release of ach resulting in decreased neuromuscular irritability and cardiac conduction. The action resolves preterm labor contractions by relaxing the uterus. In addition, by depressing the CNS, magnesium sulfate can decrease hyperreflexia and prevent the onset of seizures from eclampsia
182
Indications for magnesium sulfate
Preterm labor contractions and preeclampsia
183
Preterm labor contractions and magnesium sulfate
Relaxes the uterine muscle and resolves preterm labor contractions
184
Preeclampsia and magnesium sulfate
Muscle relaxant decreases presence of hyperreflexia and lowers risk of seizures
185
Side effects magnesium sulfate
Warm feeling, hypotension, decreased DTR, creased respiratoy rate, decreased urine output, paralytic ileus,
186
Antidote to magnesium sulfate overdose
Calcium gluconate
187
Digoxin
Cardiac glycoside extracted from the plant deigitalis
188
MOA digoxin
Direct inhibition of the Na/K ATPase pump in the membranes of myocytes. Leads to increased sodium ions int he myocytes which decreases the sodium concentration gradient. Inhibiting the Na/Ca exchanger, which depends on a constant inward sodium gradient to pump calcium out of myocytes
189
Overall effect of digoxin
Decreases sodium concentration gradient and indirectly decreases subsequent calcium outflow
190
Result of digoxin MOA
Increased calcium concentration in heart cells leading to increased contractility of the heart also called positive inotropy
191
Digoxin indication
CHF who remain symptomatic despite adequate diuretic and ACE inhibitor treatment. Also has vagal activity thereby decreasing heart rate by slowing depolarization of pacemaker cells in the AV node. Slowed conduction through AV node makes the drug commonly used in AFIB with rapid ventricular response
192
In a fib, rapid ventricular rate leads to insufficient diastolic filling time. By slowing the conduction in the AV node, digoxin can do what
Reduce ventricular rate therefore improving ventricular filling and the pumping function of the heart
193
MOA gigoxin
Direct inhibitor of Na/K ATPase
Indirect inhibition of Na Ca exchanger
Increase Ca in cell
Positive inotropy
194
Indications for digoxin
CHF
Stimulation vagus nerve
Decreased conduction at AV node
A fib
195
First line of CHF treatment
Not dogoxin
196
Digoxin and vagal nerve
Stimulate thereby decreasing heart rate by slowing depolarization of pacemaker cels in AV node
197
A fib digoxin
Slowed conduction through AV node makes this drug used for a fib with rapid ventricular response.
Digoxin can reduce ventricular rate therefore improving ventricular filling and the pumping function of the heart
198
Acute digoxin MOA
Inhibit na/k atpase pump. In heart this results in increased calcium concentration in myocytes, as well as increased vagal tone
199
Why get adverse drug reactions with dogoxin
Narrow therapeutic index
200
Side effects digoxin
Hyperkalemia
Cholinergic
Blurry yellow green vision with halo of light
Arrhythmia(bradycardia)
201
Hyperkalemia digoxin
Paralysis of Na/K ATPase pump
202
Cholinergic digoxin
Cholinergic symptoms like nausea, vomiting diarrhea and GI
203
Arrhythmia from digoxin
Increased intracellular calcium
204
Pathognomonic of dogoxin toxicity
Combo of increased atrial arrhythmias and inhibited AV conduction like paroxysmal atrial tachycardia with AV block
205
EKG changes with dogoxin
Prolonged PR interval
Decreased QT
Scooping of EKG
T wave inversion
206
Why decreased QT
Increased calcium and increasedionotropy
207
How treat digoxin toxicity
Activated charcoal and normalize k+
If that doesn’t work
Digibind (antitoxin Fab)
Rate control done with magnesium sulfate, lidocaine, and cardiac pacing
208
Digibind
First line treatment if have. A lot of digixin.
209
Beta 1 agonistdobutamine
Catecholamine that works as a beta 1 agonist, increasing inotropic activity of the heart.
210
MOA dubatamine
Cardiac stimulant used to treat heart failure, or in patients who have had cardiac surgery.
211
Side effects dobutamine
As a beta 1 sympathomimetic, it can lead to tachycardia and arrhythmias, thus, patients should be closely monitored when this medication is give.
212
What meds may increase potency of dobutamine
MAIOs and TCAs
213
MOA dobutamine
Beta 1 agonist
| Inotropic
214
Indications for dobutamine
Heart failure
Cardiac surgery or cardiogenic shock
215
Side effects dobutamine
Tachycardia, arrhythmias
216
Condiersations dobuatmine
Closed monitor patients for adverse cardiac side effects
| Other meds increase potency so be aware.
217
Norepinephrine
Ok
218
Statins
Class of medications used in clinical setting to lower patient cholesterol levels. These emdicatios work by inhibiting the HMG-CoA reductive, a rate limiting enzyme int he cholesterol synthesis pathway.
219
Effect of statins
Increase HDL and decrease LDL and triglycerides, which are proven to reduce the risk of cardiovascular events in high risk patients.
220
Side effects statins
Rhabdomyolysis and hepatotoxicity
221
Satstins __ HMG-CoA reductase
Inhibit
222
What does HMG-CoA reductase do
Cholesterol synthesis rate limiting enzyme
223
Statins decrease LDL _ times as much as they lower triglycerides
3
224
Statins increase __
HDL
225
Actor a statin (lipitor)
MNG-CoA ereductase inhibitor
226
Suffix of meds that inhibit HMG-CoA reductase
Statin
227
Indication for statins like atorvastain
Hypercholesterolemia
228
Side effect atorvastatin
Rash, hepatotoxicity, myopathy, rhabdomyolysis
229
You should monitor _ enzymes on statin
Liver
230
Why avoid grapefruit juice on statins
Contains chemicals that inhibit CPY3A4, causing levels of the. Statin to increase
231
Why give statins at bed time
Liver makes majority of cholesterol at night time
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Hepatotoxicity and statins
Liver makes cholesterol and may be harsh
| Monitor for jaundice and liver function tests
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How monitor rhabdomyolysis ons tatin
Serum CK levels
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Why is too much CK bad for kidney
Plugs the glomeruli and prevents normal glom filtration
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Vitamin B3
Niacin
| Essential vitamin used in energy reactions as a component of NAD.
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How is niacin created
From aa tryptophan and requires vitamin B6 in order to convert the aa to niacin
237
Pellet RA
Niacin defiency
238
4 Ds of pellegra defiency
Diarrhea
Dermatitis
Dementia
Death
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Niacin deficient often results from depletion of tryptophan as is seen in ___ and ___
Hartnup disease
| Serotonin syndrome
240
Niacin can also be used as a cholesterol medication
More significant side effects though
241
Niacin and NAD
Niacin is an essential component of NAD which is a coenzyme found in all living cels. It is commonly used in oxidation reduction reactions.
242
Hartnup diseases
B6 defiency
Inability ofkidney to reabsorbed aa including tryptophan. This can cause a niacin defiency bc there is no tryptophan for conversion
243
Carcinoid syndrome and niacin
From metastatic carcinoid tumor, which actively secretes serotonin.
244
How is serotonin created
Derived from tryptophan and can cause a niacin defiency due to depletion of tryptophan
245
Pellegra niacin defiency
Diarrhea
Dermatitis
Dementia
Death
246
Glossitis and niacin defiency
Tongue red? Idk
247
How can flushing from niacin therapy be treated
Aspirin
248
Niacin
B3
249
Use of B3
Decrease cholesterol
250
Effects of niacin therapy
Decrease LDL and triglycerides
| Increase HDL
251
MOA niacin
Inhibition of lipolysis in adipose tissue, as well as reduction of hepatic VLDL secretion
252
Side effect of niacin
Red, flushed face
253
Why get flushing with niacin
Prostaglandin activation
254
How can we reduce flushing from niacin
Asprin by blocking the prostaglandin mediated pathway
255
Side effect niacin therapy
Hyperglycemia and hyperuricemia
256
MOA niacin B3
1. Inhibits lipolysis in adipose tissue (cant make vldl and ldl)
2. Reduces hepatic vldl secretion—->decrease in FFA also suppresses hepatic expression of apolipoprotein C3 and leads to a reduced VLDL
257
Indications for niacin
Want to decrease triglycerides, LDL and increase HDL
258
What is a triglyceride
Esters derived from glycerol and three fatty acids—->high levels can lead to atherosclerosis so use statins
259
Side effects niacin
Flushing-give asprin
Hyperglycemia
Hyperuricemia(may exacerbate gout)
260
Why may niacin exacerbate gout
May cause hyperuricemia
261
Fibrates
Carboxylic acid medications indicated for use in hyperlipidemia and other dyslipidemias
262
Action of fibrates
Decrease triglycerides, increase HDL (slight), decrease LDL (slight)
263
MOA fibrates
Upregulate LPL, allowing accessibility to triglyceride-rich lipoproteins for lipolysis
Increasing hepatic uptake of fatty acids and decreasing hepatic production of triglycerides, decreasing their overall levels
264
What causes a slight increase in HDL with fibrates
Increased amounts of apoporoteins A-1 and A-II which allow more efficient reverse cholesterol transport
265
Why get slight decrease of LDL with fibrates
Formation of LDL with a higher affinity for its receptor, allowing it to be catabolized quicker
266
Side effects of fibrates
Hepatotoxicity and increase LFT values as well as cholesterol gallstones, which is due to increased cholesterol content in bile. Also myagias, increased CPK and resulting acute kidney injury
267
Indications for fibrates
Hyperlipidemia
268
MOA fibrates
Upregulated LPL(metabolizes triglyceride)
Decrease triglycerides
Slight increase in HDL
Slight decrease in LDL
269
Side effect fibrates
Hepatotoxicity
| Cholesterol gallstones
270
Why get cholesterol gallstones with fibrates
Increase the cholesterol content of bile
271
Ezetimibe
Lowers the plasma cholesterol in patients with hyperlipidemia by preventing cholesterol reabsorption at the small intestine brush border
272
With ezetimibe, what happens when cholesterol reabsorption at brush border is inhibited
LDL receptors are upregulated , causing increased LDL uptake into cells. Thus there is a lower LDL value in circulating blood
273
Side effect ezetimibe
Diarrhea-from large amounts of cholesterol being trapped in the gut lumen
Also increased LFT values
274
Indications for ezetimibe
Hyperlipidemia
275
MOA ezetimibe
```
Cholesterol absorption blockers at brush border
Decreases LDL (but upregulation of LDL receptors so increased LDL uptake into cells and decreased levels in bloos)
```
276
What is ezetimibe often combined with
Statins
277
Why is upregulating LDL receptors good with ezetimibe
Increase uptake into shell
278
Side effects ezetimibe
Diarrhea and increased LFT values
279
Bile acid resins
Sequester bile acids and disrupt enterohepatic circulation of bile
280
Indication for bile acid resin
Hyperlipidemia
281
MOA bile acid resins
Bind to bile acids and represent their reabsorption in the GI system, leaving them to be excreted. Circulating cholesterol is then utilized to replace the lost bile, decreasing blood levels of cholesterol.
282
Bile acids: by promoting apoprotein A1 synthesis, HDL levels __ __
Slightly increase
283
Bile acids: by activating phosphatidic acid phosphatase, triglyceride synthesis is promoted slightly ____ ___
Raining triglycerides
284
These drugs lead to upregulation of __ receptors in hepatocytes
LDL. So it is taken intracellular lh, decreasing plasma LDL cholesterol levels
285
Common bile acids
Colestipol, cholestyramine, which can be used for diarrhea treatment and toxin absorption and colesevalam
286
Side bile acid resins
Complaint of bad taste and GI disturbances that accompany their use. These medications lead to decreased absorption of fat soluble vitamins and cholesterol gallstones aw well.
287
Indications for bile acid resins
Hyperlipidemia -
| Familial hyperlipidemia type IIa
288
What is familial hyperlipidemia type IIa
An inherited disease where patients display xanthelasmas, arcus senilis, and tendon xanthomas
289
MOA bile acid resins
Bile acid reabsorption prevented (bind to bile acids in GI and makes insoluble so excreted in poop)
Slight increase HDL/Triglycerides
Activate phosphatidic acid phosphatase (which promotes hepatic TG synthesis and slightly raises their levels)
Decrease LDL...upregulation of hmg coa reductase and LD reductase restulting in increase uptake of LDL particles by hepatocytes and reduction in plasma LDL
290
Colestipol
Bile acid resin
| Can bind to other medications and decrease their absorption/MOA such as digoxin, lasix and tetracycline
291
Cholestyramine
Bile acid resin
Used for crohns who had ileal resection to prevent diarrhea
Can also be used to absorb toxins during C diff infection
292
Colesevelam
Bile acid resin
| Also used to improve glycemic control in TIID
293
Side effects bile acid resins
Cholesterol gallstones
Decreased absorption of fat soluble vitamins
Patients hate it(taste bad and lead to GI discomfort)
294
Nitroglycerin
I rate medication used to treat angina and pulmonary edema . Fast acting and a potent vasodilator
295
Low doses of nitroglycerin
Angina and pulmonary edema, as it vendor lates on a larger scale than it vasodilator, causing it to decrease cardiac preload
296
High doses nitroglycerin
Vasodilator more than venodilates and can be sued as an antihypertensive agent
297
Nitroglycerin is broken down in the blood stream into __ which does what
NO
| Activates guanyl cyclase and a resulting increase in cGMP. This acts to relax SM, decreasing venous pressure
298
Side effects nitroglycerin
Directly related to vasodilator effects
| -hypotension, reflex tachycardia, flushing and Monday disease(industrial workers mainly)
299
Contraindication nitroglycerin
In combination with viagra (sildenafil) as it can lead to unsafe , rapid decreases in blood pressure
300
Nitroglycerin indications
```
Pulmonary edema (quick potent vasodilator to reduce preload—>>decreases amount of blood flowing into heart and decreasing edematous in lungs)
Angina
```
301
MOA nitroglycerin
Decreases preload->potent vasodilator and at low doses venodilates more than vasodilates. (High doses opposite and decreases afterload to be used as an antihypertensive agent)
Releases NO in blood-activated guanyl cyclase in smooth muscle, leading to an increase in cGMP, which acts to relax muscle contraction and leads to vasodilation
302
Side effects nitroglycerin
Hypotension, reflex tachycardia, flushing, Monday disease
303
Why get reflex tachycardia with nitroglycerin
Compensatory mechanism for maintaining cardiac output as bp drops
304
Why get flushing with nitroglycerin
Vasodilator effects-common face ad neck
305
Monday disease and nitroglycerin
Usually industrial workers exposed to nitroglycerin.
Cerebral vasodilation and terrible headaches. Workers develop tolerance to nitroglycerin and feel fine throughout week. After weekend when not exposed they return to work and feel the effects of nitroglycerin on Monday
306
Contraindications for nitroglycerin
Viagara
| Both drugs potential cGMP and venodilates. This combination is unsafe due to huge drops in bp
