Pharmacology Review Video Notes

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A comprehensive set of question-and-answer flashcards covering key concepts from digoxin and cardiac drugs, antidepressants, antipsychotics, angina therapies, coagulation and lipids, respiratory medications, sleep aids, pain management, anesthesia, and related topics as presented in the video notes.

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108 Terms

1
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What is the recommended trough range for digoxin to minimize toxicity?

0.5-0.8 ng/dL (narrow therapeutic window; 0.5-2.0 ng/dL is broader; aim for 0.5-0.8 to reduce toxicity risk).

2
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How should you determine whether to administer digoxin based on the pulse?

Count the pulse for one full minute and do not give digoxin if the pulse is less than 60.

3
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How is digoxin typically administered and monitored?

Orally or IV slowly; monitor cardiac status during therapy.

4
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List common side effects of digoxin.

Dysrhythmias from hypokalemia, anorexia, nausea/vomiting, visual disturbances (yellow halos around lights).

5
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What signs suggest digoxin toxicity requiring a provider call?

Rapid weight gain, irregular pulse, N/V, yellow halos, unusual fatigue, swelling in ankles/legs/fingers.

6
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What do beta blockers ('olol') do in the heart and lungs, and what are common uses?

Block beta-1 in the heart and beta-2 in the lungs; used for angina, hypertension, dysrhythmias, MI, HF, hyperthyroidism.

7
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Provide examples of nonselective and cardioselective beta blockers.

Nonselective: propranolol; cardioselective (beta-1): metoprolol (at high doses may affect beta-2).

8
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What are common adverse effects of ACE inhibitors?

First-dose hypotension; persistent dry cough and angioedema; hyperkalemia; potential renal failure; neutropenia; avoid in pregnancy.

9
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What is the significance of Peak and Trough levels in pharmacology?

Peak time is when the drug concentration is highest (often 1 hour after dose finish for some meds); trough is the lowest concentration just before the next dose and helps avoid toxicity.

10
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How long should antidepressant efficacy be waited before judging effectiveness?

4-8 weeks.

11
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What is the general approach to antidepressant dosing if initial response is inadequate?

Start low, gradually increase; if not effective, switch to another drug or add a second drug.

12
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Should patients discontinue antidepressants if symptoms resolve?

No—continue medication even if no symptoms are present.

13
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Why is monitoring for suicide risk important with antidepressants?

Antidepressants can increase suicide risk in some patients; monitor closely.

14
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What is the MOA of SSRIs such as fluoxetine?

Inhibit the reuptake of serotonin in monoamine neurotransmitters.

15
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List uses for SSRIs beyond depression.

Depressive disorders, bipolar disorder, OCD, panic disorder, bulimia, premenstrual dysphoric disorder.

16
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What is notable about fluoxetine’s half-life and onset of steady effects?

Long half-life; steady effects take about 4 weeks.

17
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What are common SSRI side effects and what syndrome can occur with certain combinations?

Weight gain, sexual dysfunction; serotonin syndrome can occur when combined with other antidepressants, lithium, or St. John’s Wort.

18
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Define Serotonin Syndrome and list its symptoms.

A potentially life-threatening condition from excess serotonin; symptoms include agitation, diarrhea, tachycardia, hypertension, hallucinations, and hyperthermia.

19
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Why is antidepressant switching sometimes necessary?

If a medication is not effective after an adequate trial, switch to another drug or add a second drug.

20
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What is the MOA of amitriptyline and what receptor systems does it affect besides NE/5-HT reuptake?

Blocks reuptake of norepinephrine and serotonin; also blocks histamine, acetylcholine, and alpha-1 receptors.

21
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What are common indications for amitriptyline?

Depression, bipolar disorder, OCD, ADHD, neuropathic pain, fibromyalgia, insomnia.

22
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Why should therapeutic trials with TCAs last several weeks?

Long half-life; relief may take weeks; do not judge failure until at least a month of therapy.

23
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Name common TCA side effects.

Sedation (histamine blockade); orthostatic hypotension (alpha-1 blockade); anticholinergic effects; cardiac toxicity; seizures; hypomania.

24
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Which drug interactions with TCAs increase risk of severe hypertension and cardiac stimulation?

MAOIs.

25
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How does smoking affect TCA effectiveness?

Smoking decreases the effectiveness of TCAs.

26
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What are overdose symptoms of TCAs and their treatment?

Cardiac dysrhythmias, hyperthermia, flushing, dry mouth, confusion, agitation, seizures, coma, death; treat with gastric lavage, activated charcoal, IV sodium bicarbonate for metabolic acidosis.

27
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What is the rationale for caution with TCAs in the elderly?

Increased risk of anticholinergic effects, orthostatic hypotension, confusion, and falls.

28
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What are MAOIs used for and what are their dietary precautions?

Second- or third-line antidepressants for atypical depression; avoid tyramine-containing foods to prevent hypertensive crisis; no rapid dietary changes; wait 2 weeks before switching to another antidepressant.

29
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List high-tyramine foods.

Avocados, cheese, figs, fermented foods, soy, banana, smoked or processed meats, beer, certain wines, chocolate, beans.

30
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What is the mechanism of MAOIs and why must patients follow a tyramine-restricted diet?

MAO enzymes metabolize NE, serotonin, and dopamine; tyramine can trigger massive NE release causing hypertensive crisis if MAOIs are present.

31
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What are common adverse effects of MAOIs besides hypertensive crisis?

CNS stimulation, orthostatic hypotension, potential hypertensive crisis.

32
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Why is lithium used in bipolar disorder and how is it excreted?

Mood stabilizer that reduces euphoria and hyperactivity; excreted by kidneys; renal function essential.

33
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How does sodium balance affect lithium excretion and toxicity risk?

Low sodium increases lithium reabsorption in the kidney, raising toxicity risk; dehydration also raises levels.

34
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What are the maintenance and desired serum lithium levels?

Maintenance 0.4-1.0 mEq/L; desired 0.6-0.8 mEq/L.

35
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When should lithium levels be drawn and how often should monitoring occur?

Draw 12 hours after the evening dose; monitor every 2-3 days at treatment start, then every 3-6 months during maintenance.

36
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What is a key feature of antipsychotic-associated EPS and NMS?

EPS includes acute dystonia, parkinsonism, akathisia, and tardive dyskinesia; NMS is a rare, life-threatening syndrome with lead-pipe rigidity and fever.

37
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Describe acute dystonia and its management.

Early onset dystonic reaction (hours to days) with severe muscle spasms; treat with benztropine or diphenhydramine IM/IV.

38
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What are the characteristics of Parkinsonism as an EPS, and how is it managed?

Bradykinesia, mask-like facies, tremor, rigidity; managed with anticholinergics, sometimes self-resolves.

39
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What is akathisia and when can it develop?

Pacing and inner restlessness; typically develops within 2 months of starting therapy.

40
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What is tardive dyskinesia and why is it especially concerning?

Irreversible involuntary movements (lip smacking, tongue movements, choreoathetoid movements) that can develop after long-term therapy; prevention with lower doses.

41
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What is the recommended dosing pattern for antipsychotics to start?

Initial daily divided doses, then once at bedtime to promote sleep and adherence; may be higher initially but use lowest effective long-term dose.

42
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What defines stable and variant angina?

Stable angina is activity-triggered and relieved with rest; Prinzmetal (variant) angina is due to coronary vasospasm and can occur at any time.

43
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What is the medical emergency status of unstable angina?

Unstable angina is a medical emergency; requires immediate measures to maintain oxygen and reduce demand.

44
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What does OMNA stand for in acute angina/MI management?

Oxygen, Morphine, Nitroglycerin, Aspirin.

45
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What are the routes of nitroglycerin administration and their uses?

Sublingual tablets/powders, translingual spray for acute angina; oral capsules and transdermal patches for sustained release; IV for hypertension; apply patch with patch-free interval to prevent tolerance.

46
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How is nitroglycerin tolerance managed and what must be avoided?

Patch-free 8-10 hours daily (10-12 hours typically) to prevent tolerance; avoid sildenafil/cialis due to dangerous hypotension.

47
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What precautions should be taken with NTG administration in relation to vital signs?

Assess BP and pulse prior to administration; do not give if BP or pulse is too low.

48
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What are common beta-blockers and calcium channel blockers used for angina?

Beta-blockers such as propranolol and metoprolol; calcium channel blockers such as diltiazem, verapamil, nifedipine.

49
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What is ranolazine used for in angina and what is a key characteristic?

Used to decrease angina episodes; does not reduce heart rate or blood pressure.

50
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Explain the difference between anticoagulants and antiplatelets.

Anticoagulants (e.g., warfarin) inhibit clot formation; antiplatelets (e.g., ASA, Plavix) prevent platelet aggregation to stop arterial thrombus formation.

51
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What is the role of aspirin (ASA) in thrombotic risk management and its cautions?

Irreversibly inhibits COX to prevent platelet aggregation; avoid in patients with current GI bleeding; discontinue 5-7 days before surgery; increases bleeding risk.

52
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What is the mechanism of clopidogrel (Plavix) and its clinical use?

ADP receptor antagonist; inhibits platelet aggregation; used to reduce atherosclerotic events and to prevent stent thrombosis; stop 1 week before surgery; watch for bleeding and TTP.

53
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What are key monitoring parameters and antidotes for warfarin therapy?

Monitor PT/INR; therapeutic INR typically 2-3; antidote Vitamin K or FFP for excessive bleeding.

54
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What are thrombolytics and when are they used?

Clot-busting agents (e.g., tPA) that dissolve clots; used in evolving MI, CVA, and PE; risk of bleeding; antidote Amicar for coagulation reversal.

55
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What are basic lipid goals and major contributors to CHD?

Total cholesterol <200 mg/dL; LDL is the greatest contributor; HDL is protective; screen every 5 years starting at age 20.

56
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Which statin is given as an example and what is its key MOA and dosing consideration?

Atorvastatin (Lipitor); MOA: inhibits HMG-CoA reductase; take at night; avoid during pregnancy.

57
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What are common statin adverse effects and monitoring requirements?

Headache, memory changes, GI upset; myopathy/rhabdomyolysis; monitor liver enzymes (LFTs) and CK if symptoms arise; avoid grapefruit juice.

58
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What is the role and caveat of fibrates and ezetimibe in lipid management?

Fibrates lower TGs and raise HDL with little LDL effect; can increase bleeding risk with warfarin; ezetimibe reduces cholesterol by blocking intestinal absorption.

59
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What are the major inhaler types and their administration principles?

Metered-dose inhalers (MDIs) with spacers; dry powder inhalers (DPIs) breath-activated; nebulizers for solution delivery; follow priming and spacing steps.

60
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What are key steps for correct MDI technique?

Shake for 5 seconds; prime on first use; exhale fully; place mouthpiece, inhale while pressing canister; inhale 3-5 seconds; hold 10 seconds; exhale slowly; wait 1 minute before second puff.

61
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What are bronchodilators and their general function in respiratory therapy?

Beta-2 agonists (short-acting and long-acting) that bronchodilate and may suppress histamine release; often used with inhaled corticosteroids for inflammation control.

62
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What are the adverse effects and considerations for albuterol?

Can cause tachycardia; monitor heart rate; avoid in patients with certain dysrhythmias or angina.

63
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What are the main corticosteroids used in asthma and their key adverse effects?

Inhaled glucocorticoids reduce airway inflammation; principal adverse effects: thrush and dysphonia; rinse mouth after use; systemic steroids can cause hyperglycemia, adrenal suppression, leukocytosis.

64
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What is montelukast (Singulair) used for and its notable adverse effect?

Leukotriene receptor antagonist for asthma prophylaxis and exercise-induced bronchospasm; adverse effect: depression and suicidal ideation.

65
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What are the main classes of sedatives/hypnotics and their general cautions?

Benzodiazepines (e.g., alprazolam, lorazepam); risk of dependence, sedation, memory impairment; avoid alcohol; antagonist is flumazenil for overdose.

66
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Name three non-benzodiazepine sedative-hypnotics used for insomnia and a key usage note.

Zolpidem (Ambien), Zaleplon (Sonata), Eszopiclone (Lunesta); all are short-term except Lunesta; may cause daytime drowsiness and other side effects.

67
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What nonprescription and herbal options are mentioned for sleep, and what is the most effective therapy for chronic insomnia?

Melatonin and mild herbs (valerian, chamomile, etc.); Cognitive Behavioral Therapy is the most effective and safest treatment for chronic insomnia.

68
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What expectorant is used to thin and loosen mucus in coughs?

Guaifenesin (Mucinex).

69
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What are antitussives and examples?

Cough suppressants; opioids: codeine; non-opioid: dextromethorphan (Robitussin).

70
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What are common nasal decongestants and their risk?

Oxymetazoline (Afrin); vasoconstriction with rebound nasal swelling if overused.

71
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What is the general action of antihistamines and how are generations differentiated?

Block H1 receptors to reduce edema, flushing, itching, pain, and rhinorrhea; 1st generation sedates (e.g., diphenhydramine, promethazine); 2nd generation less sedating (e.g., loratadine); 3rd generation very minimally sedating (e.g., levocetirizine).

72
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What are neuromuscular blocking agents and their clinical uses?

Paralytics that prevent ACh from activating nicotinic receptors, causing skeletal muscle relaxation; used in surgery and mechanical ventilation; require two-RN checks; risk of malignant hyperthermia.

73
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Differentiate nondepolarizing (e.g., pancuronium) from depolarizing (succinylcholine) agents.

Nondepolarizing block neural transmission by competing with ACh at receptors; rapid onset, lasts 20-45 minutes; depolarizing causes initial contractions then paralysis; very short action (1-10 minutes).

74
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What is the risk and management of malignant hyperthermia (MH)?

Life-threatening reaction to certain anesthetics; muscle rigidity and fever; treat with IV dantrolene, call for help, hydrate, O2, cooling measures.

75
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What is the primary opioid receptor and the common strong opioid used for analgesia?

Mu (μ) receptor; morphine is a strong opioid commonly used for analgesia in various settings.

76
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List common adverse effects of opioids mediated by mu receptor activation.

Decreased respiration, orthostatic hypotension, euphoria, sedation, miosis, constipation, urinary retention, nausea.

77
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What is the role of naloxone (Narcan) and how is it administered?

Opioid antagonist that reverses analgesia and respiratory depression; routes include IV, IM, SubQ, intranasal; onset rapid; may precipitate withdrawal in opioid-dependent patients.

78
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What is the dosing and use of naloxone in emergency settings (forms and onset)?

IV effects immediate and ~1 hour duration; IM/SubQ effects in 2-5 minutes; intranasal also available; half-life ~2 hours; Evzio auto-injector available.

79
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What are general anesthesia inhaled agents and their MAC concept?

Isoflurane (a halogenated volatile agent) with low MAC indicating high potency; MAC is the minimum alveolar concentration; lower MAC means higher potency.

80
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What are key inhalation anesthesia agents and their roles/risks?

Isoflurane (potent but can cause hypotension/bradycardia); Nitrous oxide provides analgesia and is used as adjunct; Rare MH risk; may require O2 due to diffusion hypoxia.

81
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What is the role of propofol in anesthesia?

Non-barbiturate hypnotic with sedation and amnesia but no analgesia; must be given with analgesic; avoid in patients with soy/egg allergy.

82
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What is ketamine’s unique property as an anesthetic?

Dissociative state with rapid induction and emergence; may cause delirium or hallucinations; requires MD/CRNA for administration.

83
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What are the main regional anesthesia techniques and their general effects?

Nerve block, regional anesthesia (distal limb), epidural (spinal roots), spinal (intrathecal); monitor for neonatal depression with neuraxial blocks.

84
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What is a common complication of neuraxial anesthesia and its management?

Hypotension; strategies include adjusting patient position (head down), IV fluids, and monitoring; ensure airway and perfusion.

85
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What is the role of lidocaine and local anesthetics, and what are ester vs amide types?

Block nerve impulses by blocking sodium channel permeability; lidocaine is an amide local anesthetic; often co-administered with epinephrine to extend effect; esters vs amides differ in metabolism and allergy risk.

86
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What are the contraindications for certain local anesthetics?

Hypersensitivity to amide-type local anesthetics, sulfites, or methylparaben.

87
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What is the action of dysrhythmia antiarrhythmics on cardiac conduction?

Drugs can treat tachy- or bradydysrhythmias but may also cause dysrhythmias; monitor continuously during therapy.

88
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How is adenosine used in SVT and what is its key administration note?

Increases AV node refractory period and decreases SA node automaticity; push rapidly IV near the heart, followed by saline flush; rapid short-acting with very brief half-life.

89
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What is amiodarone’s role and its major adverse effects?

Amiodarone reduces automaticity, conduction, and can widen QRS and prolong PR/QT; used for life-threatening arrhythmias not responsive to other therapies; long half-life with several possible adverse effects including pulmonary toxicity and thyroid issues.

90
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When is atropine used in cardiac care?

Used to treat bradycardia.

91
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What is the goal of thrombolytic therapy and its major risk?

Break down formed clots by converting plasminogen to plasmin; used for evolving MI, CVA, and PE; major risk is bleeding; antidote Amicar for coagulation reversal.

92
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What is the general pathway of coagulation that leads to a clotted plug?

Coagulation pathways converge to activate thrombin, which converts fibrinogen to fibrin to form a stable clot; platelets form the initial plug and fibrin reinforces it.

93
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What are the components of the coagulation tests PT, aPTT, and INR?

PT measures extrinsic pathway clotting; aPTT measures intrinsic pathway; INR standardizes PT to monitor warfarin therapy.

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What is the significance of an INR greater than 4?

Increased risk of bleeding.

95
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What are the antidotes for excessive anticoagulation with warfarin?

Vitamin K (PO/IV) or fresh frozen plasma (FFP).

96
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What are major lipid-lowering drug classes and their general actions?

Statins (HMG-CoA reductase inhibitors) lower cholesterol; fibrates lower TGs and raise HDL; ezetimibe blocks intestinal cholesterol absorption.

97
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What is the main teaching point for statin administration timing and safety?

Take at night; avoid use in pregnancy; monitor liver enzymes and watch for myopathy; avoid grapefruit juice due to metabolism interactions.

98
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What is the mechanism and clinical use of montelukast?

Leukotriene receptor antagonist; prophylaxis and maintenance therapy in asthma and exercise-induced bronchospasm; not for acute relief; monitor for depressive symptoms and suicidality.

99
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What is the difference between MDIs and DPIs in terms of administration?

MDIs require hand-breath coordination and spacers; DPIs are breath-activated and easier to use with less coordination required.

100
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What is the general purpose of bronchodilators, and what is a common side effect to monitor?

Bronchodilators relax bronchial smooth muscle; monitor for tachycardia with beta-agonists.