Coronary heart diseases and treatment strategies, Congestive heart failure and treatment strategies, Arrhythmia and treatment strategies, Hypertension and treatment strategies.
2
What is the focus of the slide?
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The focus of the slide is on outlining key topics related to heart diseases and their treatment strategies.
3
What is the leading cause of death in the United States?
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Cardiovascular disease (CVD)
4
How many US deaths are attributed to CVD each day based on 2022 data?
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2580
5
What is the percentage increase in stroke deaths in the United States between 2012 and 2022?
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28.7%
6
What is Ischemic Heart Disease?
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A condition characterized by a reduced blood supply to the heart muscle, typically due to atherosclerosis.
7
What are the main symptoms of Ischemic Heart Disease?
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Chest pain (angina), shortness of breath, and fatigue.
8
What is the definition of Coronary Artery Disease (CAD)?
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CAD is a chronic condition characterized by atherosclerotic plaque buildup in the coronary arteries, which may cause stable angina.
9
What are the three main etiologies of CAD?
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1. Reduced blood supply (e.g., narrowing of coronary arteries in atherosclerosis), 2. Increased demand of the myocardium like cardiac hypertrophy, 3. Decreased oxygen content of blood reaching the myocardium like in severe anemia.
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What is the definition of Acute Coronary Syndrome?
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Sudden, severe reduction (or block) in coronary blood flow leading to life-threatening consequences.
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What are the etiological factors of Acute Coronary Syndrome?
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Plaque rupture or thrombosis leading to sudden imbalance between myocardial demand and coronary supply.
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What are the clinical presentations of Acute Coronary Syndrome?
Calcium channel blockers (Dihydropyridines, and non-dihydropyridines), Vasodilators (Organic Nitrates)
18
What is the effect of β-blockers on the heart?
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Decrease demand
19
What is the effect of nitrates/nitrites on the heart?
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Increase oxygen supply & decrease demand
20
What is the effect of calcium channel blockers (CCBs) on the heart?
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Decrease demand
21
What are the examples of organic nitrates?
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Nitroglycerin (minitran, nitrostate) and Isosorbide dinitrate (Isordil)
22
How is nitroglycerine metabolized?
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By first-pass metabolism
23
What are the properties of nitroglycerine compared to isosorbide?
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Nitroglycerine has a faster onset of action and shorter duration compared to isosorbide.
24
What is the main mechanism of action of organic nitrates?
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Nitric oxide causes vascular smooth muscle relaxation and vasodilation.
25
How does vasodilation of the large veins affect venous return and myocardial oxygen demand?
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It reduces venous return (preload) leading to reduced myocardial oxygen demand (less workload).
26
What is the drug of choice for managing acute angina?
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Sublingual nitroglycerin
27
How should nitroglycerin be administered for acute angina?
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Place a 0.4 mg tablet under the tongue. If pain persists, a second tablet can be used, up to 3 doses.
28
What is the most common adverse effect of nitrates?
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Headache
29
What is the mechanism of action of aspirin?
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Aspirin irreversibly inhibits platelet cyclooxygenase, thus inhibiting the formation of thromboxane A2.
30
What is the role of platelet activation in thrombus formation?
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Platelet activation is an initiating factor for thrombus formation.
31
What is the clinical use of low dose aspirin?
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Low dose aspirin is used for patients with chronic CAD to prevent arterial thrombosis leading to MI, transient ischemic attack, and stroke.
32
What are the potential triggers for anginal attacks?
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Physical or emotional stress
33
What is the maximum dose of nitroglycerin tablets in 15 minutes?
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3 tablets
34
What are the cardiovascular events associated with certain NSAIDs?
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Myocardial infarctions, cardiac arrest, and stroke
35
What are HMG CoA Inhibitors commonly known as?
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Statins
36
What is the cholesterol absorption inhibitor?
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Ezetimibe
37
What are the risk factors for atherosclerosis?
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Elevated levels of low-density lipoprotein and triglycerides
38
What is the abbreviation for coenzyme A?
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CoA
39
What is the full form of LDL?
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Low-density lipoprotein
40
What is the full form of VLDL?
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Very-low-density lipoprotein
41
What are HMG CoA reductase inhibitors and what is their mechanism of action?
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HMG CoA reductase inhibitors, also known as statins, are competitive inhibitors of HMG CoA reductase in the liver. They decrease intracellular cholesterol levels by inhibiting the rate-limiting step for cholesterol synthesis.
42
What are some examples of HMG CoA reductase inhibitors and what is their suffix?
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Examples include Atorvastatin (Lipitor) and Simvastatin (Zocor). The suffix is '-statin'.
43
What are the common indications for statins in lipid-lowering therapy?
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Statins are commonly prescribed for the treatment of hypercholesterolemia and combined hyperlipidemia.
44
What are the drug interactions and contraindications of statins?
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Azole antifungals and erythromycin increase the risk of muscle adverse effects of statins, and statins can increase the anticoagulant effect of warfarin. Statins are contraindicated in pregnant females.
45
What is rhabdomyolysis?
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Rhabdomyolysis is a rare side effect characterized by rapid breakdown of skeletal muscle mass and muscle necrosis.
46
What are the adverse effects of rhabdomyolysis?
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Mild myalgia, myopathy to severe rhabdomyolysis, elevated liver enzymes, and risk of hepatotoxicity.
47
What is the primary function of HMG-CoA reductase?
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It is an enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis.
48
What are the effects of statins on oral and dental health?
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Statins have anti-inflammatory, antioxidant, antibacterial, antiviral, and fungicidal effects, as well as immunomodulatory, pleiotropic, antimicrobial, wound healing, and bone health benefits.
49
What is the mechanism of action (MOA) of Ezetimibe?
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Inhibits absorption of dietary and biliary cholesterol in the small intestine, leading to a reduction of hepatic cholesterol stores and increased cholesterol clearance.
50
What is the indication for using Ezetimibe?
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Common non-statin agent. Used as an adjunct to statin therapy or in statin-intolerant patients.
51
What are arrhythmias?
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Arrhythmias are irregularities in the heart's rhythm, which can be too fast, too slow, or irregular.
52
What is the term for an irregular heartbeat?
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The term for an irregular heartbeat is arrhythmia.
53
What is atrial fibrillation?
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Atrial fibrillation is a common arrhythmia characterized by abnormal electrical activity in the atria, leading to irregular mini-contractions and a heart rate greater than 300 bpm.
54
What are the risk factors for atrial fibrillation?
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Risk factors include older age, inflammation, stress, hypertension, and valvular diseases.
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What are the symptoms of atrial fibrillation?
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Symptoms include general fatigue, palpitations, dizziness, and shortness of breath.
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What is the primary complication of atrial fibrillation?
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Stroke
57
What does the 'A' in the ABC management of atrial fibrillation stand for?
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Anticoagulation
58
What does the 'B' in the ABC management of atrial fibrillation stand for?
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Better symptom management
59
What is ventricular fibrillation?
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An irregular, uncoordinated, rippling contraction of the ventricles leading to ineffective cardiac output.
60
What are the symptoms of ventricular fibrillation?
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Loss of consciousness that can progress to death unless effective treatment is initiated immediately.
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What are the risk factors for ventricular fibrillation?
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Myocardial infarction and prior heart attack.
62
What is the Vaughan-Williams classification system used for?
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It classifies drugs used for tachyarrhythmias into four classes based on their mechanism of action.
63
What is the therapeutic goal in the management of tachyarrhythmias?
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Restoring synchronous myocardial contraction.
64
What is the term for the cell responsible for initiating and maintaining the heartbeat?
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Pacemaker cells
65
What is the effect of β-blockers on the action potential of pacemaker cells?
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Decreases the amplitude of the action potential
66
What are the key examples of Class I Sodium channel blockers?
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Quinidine, Disopyramide (norpace), and lidocaine.
67
What is the mechanism of action for Class I Sodium channel blockers?
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They inactivate sodium channels and prevent sodium influx, slowing conduction velocity in the heart and decreasing membrane excitation of cardiomyocytes.
68
What are the adverse effects of Class I Sodium channel blockers?
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Anticholinergic 'xerostomia (sp. disopyramide)' and thrombocytopenia (gingival bleeding).
69
What are the therapeutic uses of quinidine?
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Quinidine is used for a wide variety of arrhythmias, including atrial and ventricular tachyarrhythmias.
70
What are the drug interactions with quinidine?
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Quinidine is a substrate of CYP3A4 and CYP2D6. It can be affected by enzyme inhibitors like azole antifungals (ketoconazole) or macrolide antibiotics (azithromycin), which can lead to toxicity. It also inhibits CYP2D6, affecting the metabolism of opioid analgesics.
71
What is cinchonism and what are its symptoms?
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Cinchonism is caused by quinine or quinidine overdose (toxicity). Its symptoms include blurred vision, tinnitus, disorientation, and psychosis. It can lead to permanent vision damage.
72
What are β-blockers also known as?
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β-adrenergic antagonists
73
What is the indication for using Metoprolol as a β-blocker?
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Tachyarrhythmias caused by increased sympathetic activity
74
What is the mechanism of action (MOA) of β-blockers?
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Target pacemaker cells, prolong AV conduction and decrease heart rate & contractility
75
What is the mechanism of action (MOA) of Class III potassium channel blockers?
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Prevent potassium outflux during repolarization, leading to prolonged refractory period in cardiomyocytes.
76
What is the indication for Class III potassium channel blockers?
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Broad-spectrum antiarrhythmic medication, effective in severe ventricular tachyarrhythmias.
77
What is the dental side effect of Amiodarone?
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altered taste sensation
78
What are the adverse effects of Amiodarone?
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pulmonary fibrosis, neuropathy, and hepatotoxicity
79
How does Amiodarone interact with other drugs?
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It can inhibit several members of the cytochrome P450 family, leading to possible adverse interactions with several drug groups such as codeine and fentanyl. Amiodarone reduces codeine metabolism.
80
What are the main mechanisms of action (MOA) of non-dihydropyridine calcium channel blockers like Diltiazem and Verapamil?
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They block the L-type calcium channels in the myocardium, preventing the repolarization stage in pacemaker cells, which slows conduction in the AV and SA nodes, thus prolonging the effective refractory period.
81
What are the key adverse effects of non-dihydropyridine calcium channel blockers?
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Bradycardia, hypotension, and gingival hyperplasia.
82
What is the mechanism of action of Atropine in managing bradyarrhythmia?
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Blocks the effects of acetylcholine, increasing sinus rate, AV nodal and SA conduction velocity, and decreasing the refractory period.
83
What are the indications for using Atropine in managing bradyarrhythmia?
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Bradyarrhythmias
84
What is orthostatic hypotension?
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A sudden drop in blood pressure when a person stands up from a lying or sitting position.
85
Why should epinephrine use be monitored in arrhythmia patients?
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Because epinephrine has an excitatory action that could exacerbate arrhythmias.
86
What dental condition can be caused by calcium channel blockers?
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Gingival hyperplasia.
87
What is the potential role of oral inflammation in atrial fibrillation?
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Oral inflammation can lead to bacteremia, which triggers an immune response and systemic inflammation, potentially contributing to atrial fibrillation.
88
List the shared risk factors for oral inflammation and atrial fibrillation.
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Hypertension, metabolic syndrome, cigarette smoking, obesity, diabetes, and genetic predisposition.
89
What is heart failure?
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Heart failure is a condition in which the heart is unable to pump enough blood to meet the body's needs.
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What are the two types of heart failure?
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Heart failure can be classified as either systolic or diastolic dysfunction.
91
What are the two main categories of heart failure?
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Right heart failure and left heart failure
92
What is systolic heart failure?
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Heart failure with reduced ejection fraction (HFrEF), due to impaired ability of ventricles to eject blood (can’t pump).
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What is diastolic heart failure?
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Heart failure with preserved ejection fraction (HFpEF), due to impaired ability of ventricles to adequately fill with blood (ventricular stiffness=can’t fill).
94
What is the physiological response to heart failure in terms of preload?
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Increase preload by increasing ventricular filling to increase systemic perfusion.
95
What are the two key physiological responses to heart failure mentioned in the slide?
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Myocardial remodeling and hypertrophy to work harder, and neuroendocrine system release vasopressin and norepinephrine.
96
What are the therapeutic goals of drugs used for heart failure?
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Improve contractility and reduce cardiac workload to alleviate symptoms, normalize HR and rhythm, slow disease progression, and improve patient survival.
97
List the categories of drugs used for heart failure.
By enhancing cardiac contractility and increasing stroke volume
101
What is the mechanism of action (MOA) of digoxin?
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Digoxin inhibits the Na+/K+ exchange by Na+/K+-ATPase, leading to increased intracellular Na+ and Ca2+ levels, which promotes stronger cardiomyocyte contraction.
102
How does digoxin affect the Na+/Ca2+ exchange?
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Increased intracellular Na+ decreases the driving force for the Na+/Ca2+ exchange, resulting in decreased extrusion of Ca2+ into the extracellular space.
103
What are the indications for using Digoxin?
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Digoxin is used for heart failure (with reduced ejection fraction) and for rhythm control (Afib).
104
What are the early signs of toxicity from Digoxin?
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Nausea, vomiting, confusion, and blurred vision are early signs of toxicity.
105
What is the narrow therapeutic index of digoxin?
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Toxicity is seen at >2 ng/ml.
106
What antibiotics can increase the absorption of digoxin and increase the risk of toxicity?
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Macrolides and tetracycline antibiotics.
107
What effect do CYP 450 inducers have on the concentrations of the active drug?
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They may lower the concentrations.
108
What is a Sodium Glucose co-transporter inhibitor?
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A type of medication that promotes glucosuria and decreases preload, used to manage heart failure and type 2 diabetes.
109
What is the example of a Sodium Glucose co-transporter inhibitor?
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Dapagliflozin (Farxiga®)
110
What dental consideration should be taken into account when using Sodium Glucose co-transporter inhibitors?
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Orthostatic hypotension and risk of stress-induced hypoglycemia in diabetic patients.
111
What is the mechanism of action (MOA) of β-adrenergic agonists?
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β-Adrenergic agonists improve cardiac function by positive inotropic effects (β1) and vasodilation (β2).
112
What are the indications for β-adrenergic agonists?
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IV for management of acute decompensated HF in hospital setting.
113
What is the mechanism of action (MOA) of phosphodiesterase-3 inhibitors?
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Increase cyclic AMP (cAMP), activate calcium channels, leading to elevated intracellular Ca2+ levels and enhanced excitation contraction.
114
What are the indications for phosphodiesterase-3 inhibitors?
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Ionotropic support, acute heart failure. Used in acute settings as IV infusion.
115
What is hypertension?
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Hypertension is a chronic condition characterized by persistently elevated blood pressure.
116
What are the two main categories of hypertension?
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Primary hypertension and secondary hypertension.
117
What are the two physiological mechanisms that control blood pressure?
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Baroreceptor reflex and Renin-angiotensin-aldosterone system
118
How does the Baroreceptor reflex control blood pressure?
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It changes the activity of the sympathetic and parasympathetic nervous system.
119
What is the therapeutic goal in treating hypertension?
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Reducing the volume overload, reducing sympathetic influence, and vasodilation to decrease resistance.
120
What are the blood pressure goals when treating hypertension?
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Systolic blood pressure <130 mm Hg and diastolic blood pressure <80 mm Hg.
121
What are the four main categories of antihypertensive agents?
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Sympatholytic agents, vasodilators, diuretics, and antagonizing the renin-angiotensin-aldosterone pathway
122
What are the subcategories of the antagonizing the renin-angiotensin-aldosterone pathway category?
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Renin inhibitors, ACE inhibitors, and Angiotensin II blockers
123
What is the function of α1-adrenergic receptors?
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Vasoconstriction, increased peripheral resistance, and blood pressure
124
What is the function of β1-adrenergic receptors?
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Increase heart rate and force of contraction, increase renin release
125
What is the mechanism of action (MOA) of α1-blockers?
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Causes a decrease in peripheral vascular resistance through the relaxation of both arterial and venous smooth muscle.
126
What are the adverse effects of α1-blockers?
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Reflex tachycardia and orthostatic hypotension.
127
What is the mechanism of action (MOA) of an α2-agonist?
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Acts centrally as an α2 agonist to decrease the sympathetic outflow (NE and Ach), reducing total peripheral resistance.
128
What are the adverse effects of an α2-agonist?
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Xerostomia, orthostatic hypotension, sedation, and confusion.
129
What is the mechanism of action (MOA) of β-blockers?
Show answer
Antagonist for β-receptors; blocks β1-receptors in heart and kidney
130
What are the examples of β-blockers mentioned in the slide?
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Propranolol, Metoprolol, Atenolol
131
What are the indications for the treatment mentioned in the slide?
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Treatment of hypertension, especially in patients with other heart conditions. Can be used for angina, arrhythmia, and heart failure.
132
What are the adverse effects mentioned in the slide?
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Bradycardia, insomnia, orthostatic hypotension.
133
What are calcium channels?
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Voltage-gated ion channels found in various types of cells including cardiac muscle and vascular smooth muscles.
134
How are calcium channel blockers classified?
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They are classified into Dihydropyridine type and Non-dihydropyridines.
135
What are the non-dihydropyridine calcium channel blockers?
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Diltiazem and Verapamil.
136
What is the mechanism of action (MOA) of dihydropyridine type calcium channel antagonists?
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They act as calcium channel antagonists to block calcium entry, leading to vasodilation of arterioles.
137
What are the examples of dihydropyridine type calcium channel antagonists?
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Nifedipine (Adalat®) and amlodipine (Norvasc®).
138
What are the indications for dihydropyridine type calcium channel antagonists?
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Treatment of hypertension and angina.
139
What are the adverse effects of Nifedipine and amlodipine?
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Dizziness and orthostatic hypotension.
140
Which dihydropyridine does not cause gingival hyperplasia?
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Isradipine [DynaCirc].
141
How long after treatment with amlodipine (5 mg) did gingival hyperplasia occur in the patient?
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3 months.
142
What is the potential risk associated with using nonselective beta-blockers like propranolol in patients with multiple local anesthesia containing epinephrine?
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The risk is an increase in the risk for acute hypertensive episodes.
143
What is the consequence of using NSAIDs for more than 5 days in patients taking beta-blockers?
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It may diminish the antihypertensive efficacy of beta-blockers.
144
What is the side effect of centrally acting agents like clonidine?