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PCP Pharm Review > Module 9 > Flashcards

Module 9 Flashcards

1
Q

What are the properties of NSAIDs?

A

Analgesic, anti-inflammatory, antipyretic, aspirin-platelet inhibition.

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2
Q

What are the types of NSAIDs?

A

Salicylates (e.g., aspirin), acetic acid derivatives (e.g., diclofenac, ketorolac), COX-2 inhibitors (e.g., celecoxib), propionic acid derivatives (e.g., ibuprofen, naproxen).

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3
Q

What are the indications for NSAIDs?

A

Pain, arthritis, fever, inflammation.

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4
Q

What are the adverse effects of NSAIDs?

A

GI bleeding, renal impairment, cardiovascular issues.

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5
Q

What are the contraindications for NSAIDs?

A

Allergies, bleeding disorders, severe liver/kidney disease.

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6
Q

What are the drug interactions with NSAIDs?

A

Alcohol (↑ GI bleeding), anticoagulants (↑ bleeding tendency).

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7
Q

What special topic is associated with aspirin?

A

Antiplatelet effects; risk of Reye’s Syndrome in children.

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8
Q

What is included in gout treatment?

A

NSAIDs and specific drugs like allopurinol and colchicine.

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9
Q

What are the classifications of bacteria based on Gram stain?

A

Gram (+): Stain purple; e.g., Staphylococcus. Gram (−): Stain pink; e.g., E. coli.

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10
Q

What are the cell shapes of bacteria?

A

Rod (bacilli), spherical (cocci), spiral (spirilla).

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11
Q

What are the mechanisms of action of antibiotics?

A

Inhibit cell wall synthesis (e.g., penicillins, cephalosporins), inhibit protein synthesis (e.g., tetracyclines, macrolides), disrupt nucleic acids (e.g., fluoroquinolones), antimetabolites (e.g., sulfonamides).

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12
Q

What are the classes of antibiotics?

A
  1. Penicillins: Broad spectrum; common allergy risks. 2. Cephalosporins: 5 generations; effective for Gram +/− infections. 3. Macrolides: Alternative for penicillin-allergic patients. 4. Tetracyclines: Broad spectrum; avoid in pregnancy/children under 8. 5. Aminoglycosides: Potent; risk of nephrotoxicity, ototoxicity. 6. Quinolones: Broad spectrum; risk of tendon rupture. 7. Sulfonamides: Bacteriostatic; used for UTIs and respiratory infections.
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13
Q

What are superinfections?

A

Secondary infections due to disrupted normal flora.

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14
Q

What is prophylactic therapy?

A

Preventative antibiotic use before surgery.

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15
Q

What is the mechanism of antiviral agents?

A

Suppress viral replication (e.g., acyclovir for HSV).

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16
Q

What are key antiviral drugs?

A

Oseltamivir (Tamiflu): Treats influenza A/B. Antiretrovirals: Treat HIV (e.g., HAART regimen).

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17
Q

What should be taught about antivirals?

A

Take antivirals early; some drugs (e.g., rifampin) discolor body fluids.

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18
Q

What are the types of fungal infections?

A

Systemic (e.g., aspergillosis) vs. superficial (e.g., athlete’s foot).

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19
Q

What are key antifungal drugs?

A

Amphotericin B: Treats severe infections but has high toxicity. Fluconazole: Crosses blood-brain barrier for CNS infections.

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20
Q

What is the mechanism of antifungal agents?

A

Interfere with cell membrane synthesis or function.

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21
Q

What causes malaria?

A

Caused by Plasmodium species.

22
Q

What are the treatments for malaria?

A

Chloroquine, artemisinin derivatives.

23
Q

What are treatments for non-malarial protozoa?

A

Treated with metronidazole.

24
Q

What are first-line antitubercular drugs?

A

Isoniazid, rifampin, pyrazinamide, ethambutol.

25
Q

What are the adverse effects of isoniazid?

A

Hepatotoxicity, neuropathy.

26
Q

What is a notable effect of rifampin?

A

Discolors body fluids.

27
Q

What is important patient teaching for antitubercular drugs?

A

Adherence is critical; treatment can last 6-12 months.

28
Q

What are general tips for patient teaching?

A

Complete full antibiotic/antiviral course. Report severe side effects (e.g., bleeding, rash). Take with food or water to reduce GI upset (if applicable). NSAIDs: Avoid alcohol; monitor for bleeding. Antibiotics: Watch for allergic reactions; monitor stool/urine for unusual changes.

29
Q

What is the purpose of the immune system?

A

Protects the body from antigens (e.g., bacteria, viruses, cancer) and distinguishes self from non-self.

30
Q

What are the lines of defense in the immune system?

A
  1. Physical/Chemical Barriers: Skin, mucous membranes, gastric secretions.
  2. Inflammatory Response: Phagocytosis.
  3. Adaptive Immune Response: Involves T cells, B cells, and natural killer cells.
31
Q

What is Natural Active immunity?

A

Body produces antibodies after infection (e.g., chickenpox).

32
Q

What is Artificial Active immunity?

A

Vaccination with weakened/dead antigens (e.g., flu shot).

33
Q

What is Natural Passive immunity?

A

Antibodies passed from mother to baby (e.g., IgG in breast milk).

34
Q

What is Artificial Passive immunity?

A

Antibodies given (e.g., rabies antiserum).

35
Q

What are toxoids?

A

Weakened bacterial toxins (e.g., tetanus toxoid) that stimulate production of specific antibodies.

36
Q

What are the types of vaccines?

A
  1. Live Attenuated: Weakened microorganisms.
  2. Inactivated: Dead microorganisms.
37
Q

What are common adverse effects of vaccines?

A

Minor: Fever, soreness, rash.
Severe: Encephalitis, anaphylaxis.

38
Q

What is the purpose of immunosuppressants?

A

Suppress immune response to prevent transplant rejection or treat autoimmune diseases.

39
Q

What are the classes of immunosuppressants?

A
  1. Glucocorticoids: Inhibit T-cell activation.
  2. Calcineurin Inhibitors: Block T-cell production (e.g., cyclosporine).
  3. Antimetabolites: Inhibit T-cell proliferation (e.g., azathioprine).
  4. Biologics: Target T-cell function (e.g., basiliximab).
40
Q

What are common adverse effects of immunosuppressants?

A

Hypertension, nephrotoxicity, neurotoxicity, infections.

41
Q

What are DMARDs?

A

Disease-Modifying Anti-Rheumatic Drugs that treat Rheumatoid Arthritis (RA) by slowing disease progression.

42
Q

What is the onset of action for DMARDs?

A

Weeks to months.

43
Q

What are examples of DMARDs?

A

Methotrexate, hydroxychloroquine.

44
Q

What do biological response modifiers do?

A

Alter immune system to target diseases (e.g., cancer, MS).

45
Q

What are interferons used for?

A

Enhance immune response and inhibit cancer/viral replication; used for MS, cancer, viral infections.

46
Q

What are hematopoietic drugs?

A

Promote blood cell production in bone marrow.

47
Q

What is the purpose of antineoplastic agents?

A

Treat cancer by killing or stopping cancer cell growth.

48
Q

What are common adverse effects of antineoplastic agents?

A

Common: Nausea, fatigue, hair loss.
Serious: Low blood counts, infections.

49
Q

What is the role of hormonal agents in cancer treatment?

A

Block or compete with hormones to treat hormone-sensitive cancers (e.g., Tamoxifen for breast cancer).

50
Q

What are general patient teaching tips for vaccines?

A

Warm compress for soreness; rest; report severe reactions.

51
Q

What are general patient teaching tips for immunosuppressants?

A

Avoid infection risks; adhere to therapy; monitor for adverse effects.

52
Q

What are general patient teaching tips for antineoplastic drugs?

A

Avoid alcohol and spicy foods; practice good oral hygiene; encourage hydration, proper nutrition, and adherence to prescribed therapies.

PCP Pharm Review (10 decks)

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