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Bloc F - Defense > Pharmacology > Flashcards

Pharmacology Flashcards

(51 cards)

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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?

Study These Flashcards
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?

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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?

Study These Flashcards
A
  1. Allergies: allergic rhinitis, atopic dermatitis, hay fever, urticaria
  2. Motion sickness: vestibular disturbances
  3. Sedation and hypnotics
25
First generation of antihistamines drugs?
* DIPHENHYDRAMINE (Benadryl), CLEMASTINE * TRIPELENNAMINE * CHLORPHENIRAMINE * PROMETHAZINE * HYDROXYZINE, MECLIZINE, CYCLIZINE
26
Side effects of first generation of antihistamine?
* 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
Why are first generation antihistamine drugs used?
* Allergy * Motion sickness
28
Constraindication for the use of first generation of antihistamine drugs?
* Don’t mix with other drugs with muscarinic effects * Cross placenta
29
Second generation antihistamine drugs?
* CETIRIZINE (Zyrtec) * FEXOFENADINE (Allegra) * LORATADINE (Claritin) * DESLORATADINE (Clarinex) * LORATADINE (Claritin Hives Relief) * AZELASTIN (Intranasal Spray)
30
Constraindications of second generation antihistamines drugs?
**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
What Inflammatory pathways are linked to metabolic parameters in cardiovascular diseases?
* **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
What is the most important risk factor of cardiovascular diseases and why?
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
What is the mechanism of action of statins?
* 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
Which types of immunosuppresive agents are used for autoimmune disease such as Rheumatoid Arthritis and Lupus?
* Glucocortidoids * Anti-cell Proliferation * Interferons (TNK and IL-2 antagonists and S1P receptors)
35
What are the class of immunosuppressive agents used to treat Isoimmune disease (Rh hemolytic disease of the newborn)?
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
What type of immunosupressive therapy is used for organ transplantation?
Prevention and preparation of patient and selected donor + multitier immunosuppressive therapy (intensive induction therapy)
37
What type of immunosuppressive agent is used with a coronary stents?
Prevention of cell proliferation drug on the stent itself (drug-coated stent)
38
How does glucocorticoids work?
* 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
Name of Cytotoxic drugs and their mechanism of action
* **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
What is the mechanism of action of T cell targets immunosuppressive drugs?
Calcineurin inhibitors: * Cyclosporine and Tacrolimus: --\> Inhibits the phosphatase --\> inhibits NAFAT --\> no cytokines --\> no IL-2 * Sirolimus: effects cell cycle
41
What are the different types of antibody immunosuppressive drugs and their mechanism of action?
* **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 modulato**r: Fingolimod & Multiple Sclerosis --\> sequestration of lymphocytes into lymph nodes, away from the circulation
42
What is a biologic drug?
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
Biological drugs that can be used for the treatment of chronic resistant asthma?
* Omalizumab * Mepolizumab * Dupilumab * Lebrikizumab --\> Decreases inflammation and allergic reaction
44
When and why do we use steroids for the mangament of Rheumatoid arthritis?
* 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
How do we use new biological drugs named Modifying Anti-Rheumatic Drugs (DMARDs) for the treatement of Rheumatoid arthritis?
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
What are the second line biologic drugs used in the management of Rheumatoid arthritis?
* TNF Inhibitors * IL-1 Inhibitors * T-Cell Co-Stimulatory Blockade * B-Cell Depletion * JAK1/JAK3 inhibitor
47
What drug target can be used in the management of cardiovascular diseases?
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
What promissing novel biological therapies are available for cancer treatment ?
* Cancer vaccines * Promotes tumour rejection by antigen presenting modulation * Blockage of checkpoints molecules
49
What is an Adverse Drug Reactions (ADR)?
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
What are the subtypes of T cell delayed response?
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
What are the types of Drug hypersensitivity reactions (HDR)?
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 2. P-i: Pharmacological Stimulation of Immune Receptors Inert, labile interaction with the T cell receptor 3. Pseudo-allergic (Non-Immune-Mediated DH) Not immune mediated, no preexposure, dose dependent

Bloc F - Defense (7 decks)

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