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Exam 5 Flashcards

1
Q

Slow Cardiac Tissues

A

SA Node
AV Node

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2
Q

Fast Cardiac Tissue

A

Atria
His Purkinje System
Ventricles

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3
Q

Na+ Channels Blocker Tissue Preference

A

Fast Tissues

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4
Q

Na+ Channels Blocker General Effects

A

Decreases Excitability
Decreases Conduction Velocity
Increases Refractory Period

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5
Q

Beta Blocker Tissue Preference

A

Slow Tissue

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6
Q

Beta Blocker General Effects

A

Decreases Excitability
Increases Refractory Period

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7
Q

K+ Channel Blocker Tissue Preference

A

Fast Tissue

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8
Q

K+ Channel Blocker General Effects

A

Increases Refractory Period

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9
Q

Ca2+ Channel Blocker Tissue Preference

A

Slow Tissue

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10
Q

Ca2+ Channel Blocker General Effects

A

Decreases Excitability
Decreases Conduction Velocity
Increases Refractory Period

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11
Q

Relationship Between Increased Available Channels and Excitability

A

Direct, more available channels means more excitable

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12
Q

Ca2+ Channel Blocker General Effects

A

Decreases Excitability
Decreases Conduction Velocity
Increases Refractory Period
ALL IN SLOW TISSUE

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13
Q

Na+ Channel Blocker General Effects

A

Decreases Excitability
Decreases Conduction Velocity
Increases Refractory Period
ALL IN FAST TISSUE

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14
Q

Use Dependent Blockade General Mechanism

A

Drug can only bind to open channels
Drug dissociates after repolarization

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15
Q

Use Dependent Blockade General Effect

A

Greater Blockade in Ischemic Tissue
Greater Blockade in Tachycardia

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16
Q

Slow Dissociating Na+ Channel Blocker General Effects

A

Decreases excitability
Decreases conduction velocity
Prolong QRS complex
CAN CAUSE ARRHYTHMIA IN DAMAGED TISSUE

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17
Q

Fast Dissociating Na+ Channel Blocker General Effects

A

Blocks Na+ channels in depolarized damaged tissue only
DOES NOT PROLONG QRS

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18
Q

K+ Channel Blocker General Effects

A

Slows repolarization
Prolongs action potential duration and refractory period

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19
Q

Na+ Channel Blocker ECG Effects

A

Longer QRS

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20
Q

K+ Channel Blocker ECG Effects

A

Longer QT

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21
Q

Arrhythmia Cellular Mechanisms

A

Altered Automaticity
Triggered Activity
Re entry

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22
Q

Abnormal Automaticity Most Common Cause

A

Ischemia causes muscle tissue to become pacemaker tissue which sends depolarization before the next SA nodal signal

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23
Q

Triggered Activity General Mechanism\

A

Two sequential action potentials in response to one depolarization event
Called “afterdepolarization”

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24
Q

Early Afterdepolarization Cause

A

Due to long action potential duration

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25
Delayed Afterdepolarization Cause
Delayed action potential
26
Drugs to Block Triggered Activity
Na+ or Ca2+ Channel Blockers
27
Early Afterdepolarization Major Pathology
Torsade de Points followed by V Fib
28
Mechanism of K+ Channel Blocker Induced Triggered Activity
Prolongs action potential which causes early Afterdepolarization
29
Mechanism of Digoxin Induced Triggered Activity
Increased intracellular Ca2+ leads to delayed Afterdepolarization
30
Re entry General Mechanism
Impulse moves in a loop If the impulse completes the loop faster than the next SA node impulse it becomes the pacemaker
31
How to Block Re entry In Fast Tissue
Decrease excitability of re entry circuit with Na+ channels blockers Increase refractory period of re entry circuit with Na+ or K+ channel blockers
32
How To Block Reentry In Slow Tissue
Decrease excitability and increase refractory period with Ca2+ channel blockers
33
How to Block Re entry in Wolff Parkinson White
Pathology involves slow AND fast tissues Use Na+, K+, OR Ca2+ channel blockers
34
Class I Antiarrhythmic Drugs
Na+ Channel Blockers Best in Fast Tissue
35
Class II Antiarrhythmic Drugs
Beta Blockers Best in Slow Tissue
36
Class III Antiarrhythmic Drugs
K+ Channel Blockers Best in Fast Tissue
37
Class IV Antiarrhythmic Drugs
Ca2+ Channel Blockers Best in Slow Tissue
38
Other Antiarrhythmic Drugs
Adenosine Best in Slow Tissue
39
Class Ia Na+ Channel Blocker Properties
Moderately slow dissociating Prolongs QRS Prolongs action potential due to partial K+ channel block Prolongs QT
40
Class Ia Adverse Effects
Torsades which can be exacerbated by low K+
41
Class Ia Quinidine Mechanisms
Na+ Channel Block Some K+ Channel Block Alpha adrenergic receptor block Muscarinic receptor block
42
Class Ia Quinidine Use
NOT a first line drug Maintain sinus rhythm in A Fib and A Flutter Treats SVT and V Tac
43
Class Ia Quinidine Adverse Effects
Torsades Long QT Exacerbated by low K+
44
Class Ia Procainamide Adverse Effects
In fast acetylators metabolized to NAPA which blocks K+ channels to cause long QT and Torsades In slow acetylators Lupus like syndrome
45
Class Ib Unique Properties
Fast dissociation which only blocks INACTIVE channels so does not increase QRS Slow dissociation in damaged tissue which reduces excitability
46
Class Ib Lidocaine Mechanism
Blocks Na+ channels Fast dissociating
47
Class Ib Lidocaine Usage
Acute ventricular arrhythmias Only given IV due to first pass metabolism
48
Class Ib Lidocaine Adverse Effects
CNS Effects Depression of Cardiac Function Generally safe and only occur with high doses, in liver disease, and in the elderly
49
Class Ic Unique Properties
VERY Slow dissociating Strong phase 0 depolarization which slows conduction velocity Widens QRS
50
Class Ic Flecainide Mechanism
Strong Na+ channel block in normal cells K+ channel block which prolongs refractory period Ca2+ and RyR channel block
51
Class Ic Flecainide Uses
Supraventricular Arrhythmias Lethal ventricular arrhythmias
52
Class Ic Flecainide Major Adverse Effect
Promote arrhythmias in damaged tissue which may increase mortality in chronic use after MI or CHF
53
Class Ic Flecainide Other Adverse Effects
Blurred Vision Worsening heart failure due to Ca2+ channel block
54
Class Ic Propafenone Unique Properties
Same as flecainide Some beta blocker activity
55
Class Ic Metabolism
CYP 2D6
56
Class II Metoprolol Mechanism
Blocks b adrenergic receptors which blocks sympathetic modulation of Ca2+ and K+ channels Decreases cardiac automaticity Reduces early Afterdepolarization and delayed Afterdepolarization Increases AV refractory period and PR interval
57
Class II Metoprolol Uses
Decreases mortality after MI WPW and AV Nodal Reentry Rate control in A Fib and A Flutter
58
Class II Metoprolol Adverse Effects
SA and AV Nodal Block Withdrawal Tachycardia Decreases ventricular function
59
Class III Amiodarone Mechanism
Blocks K+, Na+, and Ca2+ channels Beta Block Prolongs PR, QRS, and QT
60
Class III Amiodarone Uses
Acute and chronic use for V Tac A Fib and A Flutter
61
Class III Amiodarone Adverse Effects
Pulmonary fibrosis Thyroid disfunction
62
Class III Amiodarone Unique Properties
VERY long half life Stored in the fat Inhibits P glycoprotein, CYP 3A4, and CYP 2C9
63
Class III Sotalol Mechanism
K+ Channel Block Beta Block
64
Class III Sotalol Uses
V Tac A Fib and A flutter
65
Class III Sotalol Adverse Effects
Torsades
66
Class III Ibutilide Mechanism
Near pure K+ channel block Increases action potential and refractory period
67
Class III Ibutilide Uses
Acute A Fib and A Flutter IV Use Only
68
Class III Ibutilide Adverse Effects
Torsades
69
Class IV Verapamil Mechanisms
Blocks L Type Ca2+ channels Decreases automaticity and excitability Increases refractory period Similar to beta blockers
70
Class IV Verapamil Use
Ventricular rate control in A fib and flutter Inhibits AV node and AV nodal reentry
71
Class IV Verapamil Adverse Effects
Depresses cardiac contraction that worsens CHF Constipation
72
Adenosine Mechanism
Stimulates A1 GPCR Activates IR K+ channels in SA and AV nodes Causes hyperpolarization to decrease automaticity Reduces Ca2+ current in AV node Increases AV node refractory period and PR interval
73
Adenosine Use
AV Nodal Reentry WPW Syndrome Rapid IV Bolus
74
Adenosine Drug Interactions
Caffein blocks A1 receptor so avoid before adenosine treatment
75
Digoxin Mechanism
Increases AV node refractory period
76
Digoxin Uses
CHF With A Fib Increased contractility makes it better for heart failure compared to beta blockers
77
A Fib and Flutter Acute Treatment
DC Cardioversion Class II and IV for AV nodal inhibition Digoxin if concomitant with heart failure
78
A Fib and Flutter Chronic Management
Class III and Ic if No Heart Failure Class III if Heart Failure Class Ia as a last resort
79
AV Nodal Reentry and Paroxysmal Supraventricular Tac Treatment
Acute adenosine or class II or IV Chronic class IV Class Ic or III as last resort AVOID Ic in Structural Heart Disease
80
WPW Treatment
Acute Adenosine Chronic Class I or III Accessory Path Ablation is Best
81
WPW with A Fib Treatment
Acute Procainamide or DC Cardioversion Chronic Class I or III DO NOT USE AV NODAL BLOCKERS
82
V Tac Accute Treatment
DC Cardioversion Class III Amiodarone Class Ib
83
V Tac Chronic Treatment
Implanted Defibrillator Class III Amiodarone
84
Decreased Cardiac Output Pathophysiology Steps
Sympathetic activation RAAS Activation Increase in vascular resistance Increased afterload Decreased cardiac output
85
Major Goals of CHF Therapeutics
Improve hemodynamics and symptoms Block neurohumoral activation of remodeling Prevent Arrhythmias
86
Diuretic Therapy Principles
Decreases intravascular volume Decreases preload, afterload, and edema BUT may also decrease cardiac output which is bad
87
Diuretic Effects on Mortality
No effect except aldosterone antagonists
88
Loop Diuretic Adverse Effects
Depletes K+ High and low K+ worsens CHF survival Low K+ causes arrhythmias
89
Thiazide Use in Heart Failure
Limited May potentiate loops but greater K+ depletion
90
Aldosterone Antagonist Use In Heart Failure
K+ Sparing Decrease cardiac remodeling May pathologically increase K+ especially with ACE inhibitors Monitor renal function
91
Receptor of Angiotensin II Adverse Effects
AT1
92
ACE Inhibitor Mechanism
Blocks conversion of Ang I to Ang II Blocks degradation of bradykinin
93
Ang II Escape
Ang II levels increase back to normal during long term ACE inhibitor use
94
Ang II Receptor Blocker Mechanism
Blocks AT1
95
Angiotensin Receptor Neprilysin Inhibitor Combination Therapy
Sacubitril and Valsartan
96
Angiotensin Receptor Neprilysin Inhibitor Mechanism
ACE Inhibitor effects Elevates B type natriuretic peptide Increases Na+ excretion
97
Vasodilator Combination Therapy
Hydralazine and nitrates like Isosorbide Dinitrate Reduces mortality especially in African Americans
98
Beta Blockers in CHF Therapeutic Principles
Start low go slow Too high a dose reduces cardiac function which worsens CHF
99
SGLT 2 Inhibitors
Dapagliflozin Other “gliflozin drugs”
100
SGLT 2 in CHF Therapeutic Principles
Works well whether diabetic or not
101
SGLT 2 Inhibitor Mechanism
Unclear
102
Digoxin Impact on Survival
Minimal to none VERY narrow therapeutic index
103
Digoxin Mechanism
Inhibits Na+ K+ ATPase Na+ builds up inside the cell Prevents Ca2+ removal from the cell Promotes Ca2+ buildup in the cell
104
Digoxin and K+ Levels
High K+ reduces digoxin binding Low K+ promotes digoxin binding
105
Digoxin Pharmacokinetics
10% of patients have gut bacteria that eliminates digoxin Distributes to muscle so dose by lean body mass Reduced clearance in elderly
106
Digoxin Drug Interactions
Diuretics
107
Digoxin Toxicity Treatment
Withdraw digoxin Withdraw K+ wasting diuretics Lidocaine for ventricular arrhythmias Digibind
108
Ulcer and Acid Reflux Medications
Bismuth Subsalicylate and Subcitrate Aluminum or Magnesium Hydroxide Cimetidine Omeprazole Sucralfate Misoprostol
109
Gastric Acid Secretion Location
Acid canaliculi of parietal cells
110
Gastric Acid Secretion Triggers
Vagus nerve releases acetylcholine that stimulates parietal cell basolateral M3 receptors Antral G cells release gastrin that stimulates basolateral ECL cell CCK2 receptors ECL cells release histamine that stimulates parietal cell basolateral H2 receptors
111
Prostaglandin E Gastric Function
Stimulated by low pH Stimulates EP3 receptor to stop acid production via cAMP pathway
112
Two Most Common Causes of Peptic Ulcer Disease
H pylori infection Chronic NSAID Usage is a far second most common cause
113
Peptic Ulcer Disease Treatment Guidelines
If H pylori antibiotics and a proton pump inhibitor If NSAIDs switch to COX2 selective and add ulcer medication or give PPI if patient cannot switch NSAIDs
114
GERD Treatment Guidlines
Antacids, H2 blockers, and lifestyle changes for heartburn <2 times per week PPIs for heartburn >2 to 3 times per week PPIs for chronic heartburn with esophageal complications
115
GERD Treatment Guidelines in Pregnancy
Antacids and sucralfate H2 Blockers and PPIs
116
H pylori Antibiotic Treatment
At least two antibiotics Amoxicillin Clarithromycin Metronidazole Tetracycline Bismuth
117
Bismuth Subsalicylate Mechanisms
Antibacterial against H pylori Binds E. coli enterotoxins Bismuth forms protective coat on ulcers Salicylate antisecretory and anti inflammatory action DOES NOT SUPPRESS ACID SECRETION
118
Bismuth Subsalicylate Adverse Effects
Very Safe Salicylism in chronic high doses Small risk of Reye syndrome
119
Antacids Mechanism
Directly neutralize gastric acid
120
Antacids
Mg Al Hydroxide
121
Mg and Al Hydroxide Adverse Effects
High dose may alkalinize the blood
122
Antacids Use
Drug of choice for mild GERD Fast onset by short duration
123
Antacids Drug Interactions
May complex tetracyclines to render them insoluble
124
Histamine H2 Receptor Antagonists
Cimetidine
125
Histamine H2 Receptor Antagonist Mechanisms
Competitive inhibition of basolateral H2 receptors
126
Histamine H2 Receptor Antagonist Use
GERD Best for basal acid secretion thus best for relief at night Does not suppress stimulated acid secretion at mealtime Slower onset but longer duration of action
127
Histamine H2 Receptor Antagonist Adverse Effects
Mostly well tolerated Reversible gynecomastia with prolonged use CNS Effects Pneumonia B12 deficiency anemia
128
Proton Pump Inhibitors
Omeprazole
129
Proton Pump Inhibitor Mechanism
Prodrug converted to active form by stomach acid Irreversibly inhibits active H+ K+ ATPase ONLY BLOCKS ACTIVE PUMPS ONLY WORKS IF TAKEN ON CONSECUTIVE DAYS
131
Proton Pump Inhibitor Adverse Effects
Acid rebound on abrupt discontinuation C diff and other stomach infections Low K+ Low Ca2+ Low B12 Kidney disease
132
Mucosal Protective Agents
Sucralfate
133
Sucralfate Mechanism
Gels at low pH and binds to necrotic and damaged tissue to protect from acid and pepsin
134
Sucralfate Use
Oral for duodenal and stress ulcers especially in pregnancy Take on an empty stomach Does not neutralize or suppress acid
135
Sucralfate Adverse Effects
Constipation Reduces absorption of other drugs
136
Prostaglandin PGE1 Analogs
Misoprostol
137
PGE1 Analog Mechanism
Signals reduction of acid while maintaining submucosal blood flow
138
PGE1 Analog Usage
Alternative to PPIs in patients with NSAID therapy
139
PGE1 Analog Adverse Reactions
Abortifacient Diarrhea Abdominal Pain
140
Antiemetics
Ondansetron Scopolamine
141
Laxatives
Psyllium Bisacodyl Linaclotide Mg Hydroxide
142
Antidiarrheals
Loperamide Diphenoxylate
143
IBS Medication
Alosetron
144
IBD Medication
Sulfasalazine Infliximab
145
Vomiting Center Location
Medulla
146
Neurotransmitters of Emetic Response
Serotonin at the 5HT3 Receptor Dopamine at the D2 Receptors Substance P at the NK1 Receptor Vestibular Histamine at the H1 and Muscarinic M1 Receptors
147
Serotonin 5HT3 Receptor Antagonist Antiemetics
Ondansetron
148
5HT3 Receptor Antagonist Mechanism
Inhibits ligand gated ion channels on enteric motor neurons, vagal afferents, and the CNS
149
5HT3 Receptor Antagonist Pharmacokinetics
Either IV or Oral 30 min onset and long duration Cleared by CYP 3A4, 1A2, and 2D6
150
5HT3 Receptor Antagonist Uses
Chemotherapy nausea Postoperative nausea Morning sickness
151
5HT3 Receptor Antagonist Adverse Effects
Constipation and headache Long QT and serotonin syndrome
152
Scopolamine Mechanism
Blocks M1 receptors in inner ear
153
Scopolamine Usage
Transdermal patch 6 to 8 hour onset and 72 hours duration Prophylaxis of motion sickness
154
Scopolamine Side Effects
Anticholinergic
155
Laxation
Evacuation of formed fecal matter
156
Catharsis
Prompt evacuation of unformed stool from the entire bowel
157
Bulk Forming Laxatives
Psyllium
158
Bulk Forming Laxative Mechanism
Nondigestible material that swells with water to increase stool volume TAKE WITH WATER
159
Psyllium Use
Treatment for mild constipation Can be taken long term
160
Stimulant Constipation Medication
Bisacodyl
161
Bisacodyl Mechanism
Irritates the GI tract to stimulate motility
162
Bisacodyl Usage
Oral or rectal Mild to moderate constipation Slow intestinal transit
163
Bisacodyl Adverse Effects
Proctitis with habitual use
164
Osmotic Constipation Drugs
Mg Hydroxide
165
Osmotic Agent Mechanism
Non absorbable substance that pulls water into the stool
166
Osmotic Agents Adverse Effects
Dehydration and electrolyte imbalance
167
Colonic Secratory Agents
Linaclotide
168
Colonic Secretory Agent Usage
Chronic constipation Orally effective
169
Colonic Secretory Agent Mechanism
Agonist of GI epithelial guanylate cyclase C receptors Increases intracellular cGMP levels Activates CTFR
170
Colonic Secretory Agent Adverse Effects
Diarrhea DO NOT GIVE TO CHILDREN
171
Non Analgesic Opioid Antidiarrheals
Loperamide Diphenoxylate
172
Opioid Antidiarrheal Systemic Effects
Loperamide cannot cross the BBB Diphenoxylate can cross the BBB
173
IBS General Drug Therapy
Bulk forming laxatives in IBS C Secretory agents in more severe IBS C Loperamide in IBS D
174
IBS D 5HT3 Receptor Antagonist Drugs
Alosetron
175
Alosetron Usage
Approved in females only
176
Alosetron Adverse Effects
Severe Constipation Fatal ischemic colitis
177
5 ASA Based IBD Therapy
Sulfasalazine
178
Sulfasalazine Mechanism
Prodrug cleaved by intestinal bacteria into 5 ASA 5 ASA reduces intestinal inflammation directly and is not systemic
179
Anti TNF IBD Therapy
Infliximab
180
Infliximab Usage
Induce and maintain remission in Crohns
181
Infliximab Adverse Effects
Infections like TB Malignancy
182
First Line Lipid Lowering Drugs
Statins for High Cholesterol Fibric Acid Derivatives for High Triglycerides
183
Second Line Lipid Lowering Add On Drugs
Bile Acid Sequestrants Cholesterol Transport Protein Inhibitors Nicotinic Acid
184
New Lipid Lowering Drugs
PCSK9 Inhibitors MTP Inhibitors Apolipoprotein B100 Synthesis Inhibitors Adenosine Triphosphate Citrate Lyase Inhibitors
185
First Line Hyperlipidemia Treatment in Children
Meds
186
First Line Hyperlipidemia Treatment in Adults
Lifestyle and education
187
Ingested Cholesterol Structure
Esterified, so is poorly absorbed
188
Statins
Atorvastatin
189
Statin Mechanism
Competitive inhibition of HMG CoA reductase in the liver
190
Statin General Effects
Lowers LDL cholesterol by 40 to 60% Lowers triglycerides by 20% Increases HDL cholesterol by 5 to 10%
191
Statin Adverse Effects
GI irritation Headache Rash Hepatotoxicity Myopathy and Myositis Increase in fasting blood glucose
192
Statin Genetic Concerns
CYP 2D6 is absent in 7% of whites and blacks This deficiency is rare in Asians
193
Statin Drug Interactions
Any drug also metabolized by CYP 3A4 and 2C9 Pravastatin avoids this issue
194
Statin Cautions
Liver disease
195
Fibric Acids
Fenofibrate
196
Fibric Acid General Mechanisms
Increase expression of proteins that oxidize fatty acids Increase proteins that catabolize VLDL Reduces expression of ApoC III to enhance clearance of VLDL Increases expression of ApoA I and II which increases HDL
197
Fibric Acid General Effects
Lower triglycerides by 55% Increase HDL by 5% alone and 20% with statins
198
Fibric Acid Uses
Reduction in cardiovascular events in patients with triglycerides over 400mg/dL
199
Fibric Acid Adverse Effects
GI Issues Rash Hair Loss Muscle pain Fatigue and headaches
200
Fibric Acid Drug Interactions
Enhances warfarin effects Enhances statin myopathy
201
Bile Acid Binding Resins
Colesevelam
202
Bile Acid Binding Resin Mechanism
Bind bile in the intestines to inhibit reabsorption Decrease feedback inhibition of enzyme that converts cholesterol to bile acids Increases LDL receptors
203
Bile Acid Binding Resins General Effects
Lower LDL by 20% with statins 5% rise in HDL levels
204
Bile Acid Binding Resin Adverse Effects
Bloating and constipation Mild steatorrhea
205
Bile Acid Binding Resin Drug Interactions
Prevents absorption of many drugs Take other meds 1 hour before or 3 to 4 hours after
206
Cholesterol Absorption Inhibitor
Ezetimibe
207
Cholesterol Absorption Inhibitor Mechanism
Inhibits cholesterol transport protein Niemann Pick C1 Like 1
208
Cholesterol Transport Inhibitor General Effects
Lowers LDL 25%
209
Cholesterol Transport Inhibitor Adverse Effects
Diarrhea Increases prothrombin time with Warfarin
210
Nicotinic Acid Mechanism
Inhibits lipolysis of triglycerides which decreases hepatic triglyceride synthesis
211
Niacin General Effects
Lowers LDL 25% Increases HDL 20 to 30% ONLY DRUG TO DO THIS
212
Niacin Adverse Effects
Intense flushing and pruritus GI Issues Hepatic toxicity Ulcer Hyperglycemia Gout
213
Niacin Drug Interactions
Myopathy when given with statins
214
PCSK9 Inhibitors
Evolocumab Inclisiran
215
PCSK9 Inhibitor General Effects
Reduces LDL C dose dependent by 70% when used alone Reduces LDL C by 60% with statins
216
PCSK9 Inhibitor Mechanism
Enables more LDL receptors to become available on liver cells Best in patients that become statin sensitive
217
PCSK9 Inhibitor Adverse Effects
Small risk of cognitive deficit Nasopharyngitis UTIs and URIs Injection site reaction NO RISK OF MYOPATHIES
218
Inclisiran Mechanism
Small interferin RNA molecules of RNA
219
MTP Inhibitors
Lomitapide
220
MTP Inhibitor Mechanism
Inhibits accretion of triglycerides to VLDL in liver and to chylomicrons in intestine
221
MTP Inhibitor General Effects
Reduces LDL 50% Use with max dose of statins
222
MTP Inhibitor Adverse Effects
GI Issues Hepatotoxicity and fatty liver Embryotoxic
223
Apolipoprotein B100 Synthesis Inhibitors
Mipomersen
224
Mipomersen Mechanism
Binds and inhibits ApoB 100 mRNA
225
Mipomersen General Effects
Lower LDL 30 to 50%
226
Mipomersen Adverse Effects
Injection site reaction Flu like symptoms Hepatotoxicity
227
Adenosine Triphosphate Citrate Lyase Inhibitors
Bempedoic Acid
228
Adenosine Triphosphate Citrate Lyase Inhibitor Mechanism
Inhibits conversion of Citrate CoA to Acetyl CoA, which inhibits cholesterol synthesis
229
Adenosine Triphosphate Citrate Lyase Inhibitor General Effects
Lowers LDL over 20% when taken alone Lowers LDL by 35 to 40% when taken with statins Lowers LDL by 35 to 40% when taken with ezetimibe and statin Lowers HDL by 6%
230
Adenosine Triphosphate Citrate Lyase Inhibitor Adverse Effects
OAT 2 Inhibition can cause gout Bloody urine and difficult urination Productive cough Difficulty breathing Ear congestion
231
Influenza Antivirals
Amantadine Oseltamivir Zanamivir
232
Herpes Antivirals
Acyclovir Valacyclovir Ganciclovir Foscarnet Docosanol
233
Viral Hepatitis Antivirals
Ribavirin Simeprevir Sofosbuvir Entecavir
234
Enveloped Virus Structure
Viral genome surrounded by lipid bilayer
235
Antiviral Therapy General Mechanism
Virustatic Host immune system ultimately clears infection
236
Antiviral Drug General Structure
Mimic nucleotides like guanine All are prodrugs that require phosphorylation
237
Non retroviral Viral Replication Cycle
Attaching, uncoating, and entry Transcription Maturation Assembly and release
238
Influenza Viral Type
RNA Virus Subdivided into flu A and B Most infections caused by flu A Further divided by hemagglutinin and neuraminidase surface antigens
239
When to Treat Flu
Limit to severe disease or those at high risk for severe disease Most effective in first 24 to 28 hours
240
Amantadine Mechanism
Blocks flu a M2 ion channel which reduces influx of protons into virus Prevents viral uncoating into host cell
241
Amantadine Use
100% resistance in US Can also treat Parkinson’s
242
Amantadine Adverse Effects
CNS Effects Teratogenic
243
Neuraminidase Inhibitors
Oseltamivir
244
Oseltamivir Mechanism
Competitive inhibitor of viral neuraminidase Virus cannot release from infected cells
245
Oseltamivir Pharmacokinetics
Orally available prodrug Metabolized to active carboxylate form by liver Carboxylate excreted by kidneys
246
Zanamivir Use
Used when Oseltamivir resistant flu is suspected Administered as an inhaled powder
247
Zanamivir Adverse Effects
Bronchospasm and impaired lung function
248
Herpesvirus Classes
HSV causes cold scores, genital infection, and meninges and brain infection VZV causes varicella chicken pox and herpes zoster shingles CMV opportunistic infection of retina, lungs, and GI tract
249
Herpesvirus General Properties
DNA Virus Latency and reactivation Latent virus not eradicated by antivirals
250
Acyclovir Structure
Acyclic guanine nucleoside prodrug that lacks 3’ OH group
251
Acyclovir Mechanism
Converted to acycloGMP by VIRAL thymidine kinase in cytosol of infected cells Inserted into viral DNA to terminate chain elongation Competitive inhibition of VIRAL DNA polymerase
252
Acyclovir Resistance Mechanism
Viral thymidine kinase deficiency
253
Acyclovir Pharmacokinetics
Orally available LOW Bioavailability Short half life Must be given IV to treat severe infections Widely distributed and eliminated unchanged by the kidneys
254
Valacyclovir Structure
Added valine to increase bioavailability Converted to acyclovir by first pass metabolism
255
Acyclovir HSV Therapy
Shortens symptoms, reduced recurrence, and reduces viral shedding in genital herpes Cold sores Prophylaxis in immunosuppressed patients IV for HSV encephalitis
256
Acyclovir VZV Therapy
Active infections in children and adults Elderly with oral infection Immunocompromised patients
257
Acyclovir Adverse Effects
Well tolerated Crystalline nephropathy from IV use in dehydrated patients
258
Docosanol Structure
Long chain alcohol
259
Docosanol Mechanism
Coats virus to prevent viral entry
260
Docosanol Usage
Topical prophylaxis and active treatment DOES NOT KILL VIRUS
261
Ganciclovir Structure
Acyclovir with a 3’ like OH group
262
Ganciclovir Mechanism
Metabolized to monophosphate by CMV UL97 kinase Further metabolized to di and tri phosphates Triphosphate inhibits viral DNA polymerase
263
Ganciclovir Pharmacokinetics
Analogous to acyclovir
264
Gancyclovir Uses
Treatment of CMV retinitis in immunocompromised patients CMV prophylaxis in transplant patients
265
Gancyclovir Adverse Effects
Myelosuppression CNS effects Carcinogenic Teratogenic
266
Foscarnet Structure
Non nucleoside analogue Phosphorylated formic acid
267
Foscarnet Mechanism
Inhibits viral DNA polymerase Not a prodrug
268
Proton Pump Inhibitor Use
Must be taken about 30 minutes before a meal Taken for about 8 weeks
269
Foscarnet Use
Resistant CMV retinitis Resistant HSV and VZV
270
Hepatitis C Viral Structure
RNA virus that does not integrate into human genome 7 genotypes Type 1 is most common in the US and most resistant to treatment
271
Hepatitis C Virus Treatment
24 to 48 weeks of interferon alpha and ribavirin Goal is absence of viral RNA 24 weeks after conclusion of therapy
272
Ribavirin Structure
Purine nucleoside prodrug Phosphorylated by host kinases
273
Ribavirin Mechanism
Inhibits IMP dehydrogenase to deplete guanine nucleotide pool Interferes with capping of 5’ end of viral mRNA
274
Ribavirin Pharmacokinetics
Oral Long half life Eliminated by hepatic metabolism and renal excretion
275
Ribavirin Use
Refractory or chronic hepatitis C virus CANNOT BE GIVEN ALONE
276
Ribavirin Adverse Effects
Teratogenic Hemolytic anemia Respiratory deterioration in children
277
Direct Acting Hepatitis C Antiviral Classes
Inhibitors of NS3 4A serine protease that cleaves viral poly proteins into mature forms Inhibitors of NS5B RNA polymerase responsible for replicating viral RNA Inhibitors of NS5A critical viral replication and assembly protein
278
NS3 4A Inhibitor
Simeprevir
279
Simeprivir Adverse Effects
Photosensitivity rash Teratogenic CYP 3A4 inhibition
280
NS5B Inhibitor
Sofosbuvir Other “buvir” drugs
281
Sofosbuvir Structure
NUCLEOTIDE prodrug
282
Sofosbuvir Pharmacokinetics
Oral once per day P gp Substrate
283
Sofosbuvir Adverse Effects
Well tolerated Headache Fatigue
284
Hepatitis B Viral Structure
DNA virus that integrates into host genome
285
Hepatitis B Treatment
Interferon and Ribavirin Entecavir
286
Entecavir Mechanism
Converted to Triphosphate by host kinases Inhibits viral DNA polymerase and HIV reverse transcriptase Acts as a chain terminator
287
Entecavir Adverse Effects
May cause resistance to NRTIs in concomitant HIV infection Lactic Acidosis Steatosis
288
HIV Viral Structure
Enveloped single stranded RNA virus
289
HIV Viral Lifecycle
Must dock to TWO host cell membrane receptors Injects ssRNA into host cell SsRNA converted to ssDNA by reverse transcriptase SsDNA integrated into host cell genome Viral components translated and virion buds off Virion converted to active form by HIV protease
290
HIV 3 Drug Minimum
2 NRTIs and a third agent
291
HIV Drug Resistance and Viral Load
Greater viral load is proportional to greater risk of resistance
292
HIV Therapy General Long Term Adverse Effects
HIV Lipodystrophy Syndrome Increased risk of MI
293
HIV Therapy Drug Classes
Prevention of fusion and entry Reverse Transcriptase Inhibitors Integrase Inhibitors Assembly and maturation inhibitors
294
NRTI Drugs
Abacavir
295
Abacavir Mechanism
Phosphorylated three times by host cell kinase Inhibits reverse transcriptase Causes retroviral DNA chain termination
296
Abacavir Resistance Mechanisms
Decreased binding of reverse transcriptase Increased removal of NRTI from cells
297
Abacavir Adverse Effects
Lactic acidosis Liver disease Lipodystrophy syndrome Exacerbation of hep B HLA B 5701 Allele carriers can get severe rash
298
Tenofovir Structure and Mechanism
NucleoTIDE reverse transcriptase inhibitor
299
Tenofovir Use
Given in combination for PrEP and PEP
300
NNRTI Dugs
Efavirenz
301
Efavirenz Mechanism
Non competitive inhibition of reverse transcriptase
302
Efavirenz Pharmacokinetics
Orally effective Daily Cleared by CYP 2B6 and 3A4 Induces CYP 3A4
303
Efavirenz Adverse Effects
CNS Effects Vivid Dreams Rash
304
HIV Protease Inhibitors
Lopinavir
305
Lopinavir Pharmacokinetics
Orally available Extensively metabolized by CYP 3A4 Must be administered with BOOSTER DRUGS
306
Booster Drugs
Ritonavir Cobicistat CYP 3A4 Inhibitor
307
Lopinavir Adverse Effects
GI Issues Lipodystrophy
308
Fusion Inhibitors
Efuvirtide Maraviroc
309
Efuvirtide Mechanism
Binds to HIV gp41 protein to prevent fusion with host cell
310
Efuvirtide Use
Must be given parenterally Added to existing regiments with refractory HIV
311
Efuvirtide Adverse Effects
Injection site reaction Bacterial pneumonia
312
Entry Inhibitor
Maraviroc
313
Maraviroc Mechanism
CCR5 Co receptor blocker ONLY ARV TO TARGET HOST PROTEIN
314
Maraviroc Use
Only used in CCR5 tropic HIV infection
315
Maraviroc Adverse Effects
Hepatotoxicity
316
Integrase Inhibitors
Raltegravir
317
Raltegravir Mechanism
Inhibits HIV integrase Stops HIV replication
318
Raltegravir Pharmacokinetics
Orally available Cleared by hepatic glucuronidation
319
Raltegravir Use
Given with 2 NRTis Good for patients with abnormal lipid profiles
320
Foscarnet Adverse Effects
Nephrotoxicity Severe Electrolyte disturbance

PHARM (7 decks)

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