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Bloc F - Defense > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are the functions of NSAIDs?

A
  1. ANTI-PYRETIC ACTION: blocks the production of PGE2 to reset the hypothalamic temperature set point:
  2. ANTI-PLATELET/ANTI-THROMBOTIC: decreases platelet production irreversibly of TXA2 by COX-1 to limit platelet aggregation and vasoconstriction
  3. ANTI-INFLAMMATORY
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2
Q

Which NSAIDs is not used as anti-platelet drug?

A

Ibuprophen

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3
Q

Side effects of NSAIDs?

A
  • GI bleedings, ulceration and obstruction: loss of cytoprotective actions or gastric prostaglandins, ++ < 65 y-o and alcohol
  • Pregnancy: prolonged gestation, antepartum and postpartum effect
  • Renal effects (ibuprophen ++): pressure, weight, Na retention, no effect on normal kidneys
  • Sensitivity reactions (histamine release pathway)
  • AVOID for children in viral illness (Reye’s syndrome)
  • Bleeding
  • All due to alteration of normal prostaglandin physiology
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4
Q

An overdose of NSAIDs is the result of what physiological mechanisms?

A

Combined metabolic acidosis & respiratory alkalosis

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5
Q

Functions of acetaminophen?

A
  1. Analgesic and anti-pyretic via inhibition of neuronal & vascular PGE2 generation
  2. Weak anti-inflammatory & anti-platelet activity: failure to inhibit platelet TXA2 or inflammatory PGE2 synthesis
  3. NO ANTI-INFLAMMATORY EFFECT
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6
Q

Side effects of acetaminophen?

A
  • Little GI toxicity
  • Potentially hepatotoxic or nephrotoxic
  • No sensitivity reaction
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7
Q

Acute lymphoblastic leukemia management?

A
  • Vincristine
  • Prednisone
  • Doxorubicin or Daunorubicin
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8
Q

Chronic myelogenous leukemia (Philadelphia chromosome) management?

A

Imatinib

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9
Q

Hodgkin Lymphoma management?

A

DBVD

Doxorubicin (Adriamycin)

Bleomycin

Vinblastine

Dacarbazine

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10
Q

Non-Hodgkin Lymphoma management?

A

CHOP

Cyclohosphamide

Doxorubicin (H)

Vincristine (O)

Prednisone

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11
Q

Principal chemotherapeutic agents?

A
  • DNA alkylation (Cyclophosphamide and Dacarbazine)
  • Antimetabolites (Methotrexate and 5-Fluorouracil)
  • Microtubules (Vincristine, Vinblastine and Taxols)
  • Topoisomerase inhibitors (Daunorubicin and Bleomycin)
  • Steroid hormone receptors: glucocorticoid - prednisone
  • Enzymes involved in cell signaling: tyrosine kinase inhibitor (matinib)
  • Antibodies
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12
Q

How do DNA alkylation chemotherapeutic agents work?

A
  • Toxicity of alkylating agents to rapidly proliferating cells (hematopoietic system, GI tract, gonads)
  • You can develop a resistance to alkylating agents
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13
Q

How do Antimetabolites chemotherapeutic agents work?

A
  • Starves the cell of thymidilate, can’t make DNA
  • Can be combined for better effect
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14
Q

How do Microtubules chemotherapeutic agents work?

A
  • Block the assembling of the microtubules or glues them together which blocs the mitosis
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15
Q

How do Topoisomerase inhibitors chemotherapeutic agents work?

A
  • Causes the DNA to break –> DNA damage –> the cell dies
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16
Q

How to steroids hormones receptors work?

A

Inhibits the expression of a variety of genes

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17
Q

How do tyrosine kinase inhibitors work?

A

Attacks cells that have translated chromosomes –> no phosphorylation –> kills the cells that have this translocation (CML and ALL)

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18
Q

Types of antibodies and how they work?

A
  • Anti-CD20 – Rituximab: destroys both normal and malignant B cells
  • Anti-CD30 – Brentuximab vedotin: kills specific lymphomas
  • Anti-PD1 – Pembrolizumab: activates programed death receptor that were blocked by the tumour
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19
Q

What are Autocoids?

A

Autocoids only act locally for a certain period of time, are like local hormones

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20
Q

Types of autocoids?

A
  • Histamine
  • Serotonin
  • Endogenous peptides
  • Prostaglandins
  • Leukotrienes
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21
Q

Histamine receptors?

A
  • H1 Receptor Antagonists (1st and 2nd generation)
  • H2 Receptor Antagonists (Ranitidine, Cimetidine)
  • H3 Receptor Agonist and Antagonists (potential new drugs being developed)
  • Mast Cell Stabilizers (Cromolyn Na, Nedocromil-Tilade, Albuterol)
22
Q

Primary physiological effects of histamines?

A
  • Primary cellular mediator of immediate hypersensitivity reaction and acute inflammatory response
  • Anaphylaxis
  • Seasonal allergies (asthma?)
  • Duodenal ulcers Þ can block release of gastrin + other enzymes
  • Systemic mastocytosis
  • Gastrinoma (Zollinger-Ellison Syndrome) Þ could be a target for anti-histamines because there are more cells in these conditions that are sensitive to histamines
23
Q

Therapeutic uses for Kay-LEEN-X?

A
  1. Allergies: allergic rhinitis, atopic dermatitis, hay fever, urticaria
  2. Motion sickness: vestibular disturbances
  3. Sedation and hypnotics
24
Q
A
25
Q

First generation of antihistamines drugs?

A
  • DIPHENHYDRAMINE (Benadryl), CLEMASTINE
  • TRIPELENNAMINE
  • CHLORPHENIRAMINE
  • PROMETHAZINE
  • HYDROXYZINE, MECLIZINE, CYCLIZINE
26
Q

Side effects of first generation of antihistamine?

A
  • Sedation (paradoxical excitation in children)
  • Dizziness
  • Fatigue
  • Tachydysrhythmias in overdose - rare
  • Allergic reactions with topical use
  • Potentiate CNS depressants
  • Peripheral anti-muscarinic effects
  • Dry mouth
  • Blurred vision
  • Constipation
  • Urinary Retention
27
Q

Why are first generation antihistamine drugs used?

A
  • Allergy
  • Motion sickness
28
Q

Constraindication for the use of first generation of antihistamine drugs?

A
  • Don’t mix with other drugs with muscarinic effects
  • Cross placenta
29
Q

Second generation antihistamine drugs?

A
  • CETIRIZINE (Zyrtec)
  • FEXOFENADINE (Allegra)
  • LORATADINE (Claritin)
  • DESLORATADINE (Clarinex)
  • LORATADINE (Claritin Hives Relief)
  • AZELASTIN (Intranasal Spray)
30
Q

Constraindications of second generation antihistamines drugs?

A

Erythromycin, grapefruit juice and ketoconazole inhibit the metabolism of fexofenadine and loratadine in healthy subjects- this causes no adverse effects.

Terfenadine (Seldane) and Fexofenadine (Allegra) should not be taken with grapefruit juice or erythromycin or other drugs that inhibit the enzyme.

31
Q

What Inflammatory pathways are linked to metabolic parameters in cardiovascular diseases?

A
  • Pattern Recognition Receptor (PRR)–> Toll Like Receptors (TLRs)
    Following activation in the inflammasomes (NLPR3) by lipoproteins and lipopolysaccharides (FAT THAT YOU EAT) –> IL-1β is secreted into the circulation where it exerts effects in the brain, and on bone and endothelial cells –> causes INFLAMMATION
  • TH1 receptor
    Plaque activation & rupture is linked to TH1 effects (oxidatively modified LDL and B2-glycoprotein I)
  • B cells
    Contribute to anti-atherosclerotic activity by specific antibodies against plaque antigens and binding of antibodies to inhibitory Fc receptors
32
Q

What is the most important risk factor of cardiovascular diseases and why?

A

AGE:

  • More inflammation everywhere (bones, bronchioles, brain, skin and vessels)
  • Age related changes of CD28 expression on Lymphocytes found in age-related chronic diseases
33
Q

What is the mechanism of action of statins?

A
  • Reduces cholesterol
  • Interfere with antigen presentation inhibiting MHC Class II, CD40, CD80/CD86 upregulation
  • Induce Fox P3 expression on naïve CD4+ T cells Þ functional CD4 + Fox P3 + regulatory T cells
  • Reduction of macrophage work in vessels and replace it by collagen (stable plaque)
34
Q

Which types of immunosuppresive agents are used for autoimmune disease such as Rheumatoid Arthritis and Lupus?

A
  • Glucocortidoids
  • Anti-cell Proliferation
  • Interferons (TNK and IL-2 antagonists and S1P receptors)
35
Q

What are the class of immunosuppressive agents used to treat Isoimmune disease (Rh hemolytic disease of the newborn)?

A

Initial response is blocked if specific Ab (RhD IgG, with a high Ab titer to RhD Ag) is administered to the mother at 28 weeks gestation and/or within 72 hrs offf birth of 1st baby

36
Q

What type of immunosupressive therapy is used for organ transplantation?

A

Prevention and preparation of patient and selected donor + multitier immunosuppressive therapy (intensive induction therapy)

37
Q

What type of immunosuppressive agent is used with a coronary stents?

A

Prevention of cell proliferation drug on the stent itself (drug-coated stent)

38
Q

How does glucocorticoids work?

A
  • Decrease transcription of pro-inflammatory genes ( IL-1, IL-2, IL-6)
  • Increase expression of anti-inflammatory genes

The net result is a decrease in immune cell signaling and proliferation

39
Q

Name of Cytotoxic drugs and their mechanism of action

A
  • Azathioprine: metabolized to 6-mercaptopurine; inhibits purine synthesis, blocks DNA and RNA synthesis
  • Mycophenolate mofetil: Inhibits inosine mono-phosphate dehydrogenase –> blocks de novo purine synthesis –> inhibits T and B cell proliferation and functions
  • Methotrexate: inhibits folic acid metabolic enzymes –> starves cells of thymidine (DNA building blocks)
40
Q

What is the mechanism of action of T cell targets immunosuppressive drugs?

A

Calcineurin inhibitors:

  • Cyclosporine and Tacrolimus: –> Inhibits the phosphatase –> inhibits NAFAT –> no cytokines –> no IL-2
  • Sirolimus: effects cell cycle
41
Q

What are the different types of antibody immunosuppressive drugs and their mechanism of action?

A
  • Anti-thymocyte globulin (ATG): Rapid depletion of peripheral lymphocytes –> prevent initial graft rejection
  • Murine monoclonal Ab-Muromonab (OKT3): Anti-CD3 –> Blocks antigen recognition –> used to reverse acute allograft rejection
  • Humanized Anti-IL2-receptor α (CD25): Daclizumab –> targets antigen-activated T cells by binding to alpha chain of IL-2 R (CD25) –> used with calcineurin inhibitors to prevent acute organ rejection
  • Humanized Anti-CD52 Ab: Alemtuzumab –> binds CD52 on B and T cells, macrophages, NK cells Þ induces cell lysis and leukopenia
  • Sphingosine 1-phosphate (S1P) receptor modulator: Fingolimod & Multiple Sclerosis –> sequestration of lymphocytes into lymph nodes, away from the circulation
42
Q

What is a biologic drug?

A

The term “biologics” is used for a class of medications (either approved or in development) produced by means of biological processes involving recombinant DNA technology. Three types:

  1. Substances that are (nearly) identical to the body’s own key signalling proteins (ex. insulin)
  2. Monoclonal antibodies
  3. Receptor constructs (fusion proteins), usually based on a naturally-occurring receptor linked to the immunoglobulin frame
43
Q

Biological drugs that can be used for the treatment of chronic resistant asthma?

A
  • Omalizumab
  • Mepolizumab
  • Dupilumab
  • Lebrikizumab

–> Decreases inflammation and allergic reaction

44
Q

When and why do we use steroids for the mangament of Rheumatoid arthritis?

A
  • Might be used as a bridge until other DMARDs begin to have their effects
  • Might be used if it is just one or two specific joints
  • Not suitable for long-term use because of adrenal suppression
45
Q

How do we use new biological drugs named Modifying Anti-Rheumatic Drugs (DMARDs) for the treatement of Rheumatoid arthritis?

A

They are first line and can be used from mono to triple therapy:

  • Triple Therapy
    Methotrexate, Sulfasalazine, Hydroxychloroquine
  • Double Therapy
    Methotrexate & Leflunomide
    Methotrexate & Sulfasalazine
    Methotrexate & Hydroxychloroquine
    Methotrexate & Gold
    Sulfasalazine & Plaquenil
  • Monotherapy
46
Q

What are the second line biologic drugs used in the management of Rheumatoid arthritis?

A
  • TNF Inhibitors
  • IL-1 Inhibitors
  • T-Cell Co-Stimulatory Blockade
  • B-Cell Depletion
  • JAK1/JAK3 inhibitor
47
Q

What drug target can be used in the management of cardiovascular diseases?

A

Humanized IgG1 and IgG2 monoclonal antibody against PCSK9: Decreases LDL cholesterol in setting of atherosclerotic cardiovascular disease, heterozygous familial hypercholesterolemia, or homozygous familial hypercholesterolemia

48
Q

What promissing novel biological therapies are available for cancer treatment ?

A
  • Cancer vaccines
  • Promotes tumour rejection by antigen presenting modulation
  • Blockage of checkpoints molecules
49
Q

What is an Adverse Drug Reactions (ADR)?

A

An noxious, unintended and undesired drug effect

  1. Predictable (type A)
  2. Unpredictable (type B): in susceptible individuals –> called drug hypersensitivity reactions (HDR) when involve the immune system
50
Q

What are the subtypes of T cell delayed response?

A
  1. CDA Th1: maculopapular rash
  2. CD4 Th2: Maculopapular rash and bullous exanthemas
  3. Cytotoxic T lymphocytes (CD4/CD8): Maculopapular and pustular bullous
  4. T cell (IL-8): pustular exanthema
  5. CD8 > CD4: Non-immediate urticaria (>1h to 48 h)
51
Q

What are the types of Drug hypersensitivity reactions (HDR)?

A
  1. Allergic immune

Hapten (chemically reactive) and Prohapten (requires metabolization to become hapten in cell)

Exogenous compounds are presented on MHC II –> CD4 T cells reponse

Endogenous compounds are presented on MHC I –> CD8 T cells reponse

  1. P-i: Pharmacological Stimulation of Immune Receptors
    Inert, labile interaction with the T cell receptor
  2. Pseudo-allergic (Non-Immune-Mediated DH)
    Not immune mediated, no preexposure, dose dependent

Bloc F - Defense (7 decks)

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