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IHO Mike Rose > Drugs Exam 5 > Flashcards

Drugs Exam 5 Flashcards

1
Q

Diphenhydramine (Benadryl) OTC

A

Class: first generation antihistamine

MOA: Blockade H1, muscarinic, alpha adrenergic, and 5HT receptors.

PK: well absorbed orally. Widely distributed including CNS.

Can be used as opthalmic solutions.

Side effects:

  • Sedation (can potentiate other CNS depressants)
  • Drying of secretions
  • GI disturbances (N/V, diarrhea, constipation –> give w/ meals)

Acute poisoning treatment is symptomatic and supportive (dilated pupils, flushed face, fever, dry mouth, excitation, hallucinations, in-coordination, coma, CV collapse.)

Diphenydramine is specific for low incidence of GI side effects and causing sedation.

Uses: Allergy (rhinitis, urticaria, and atopic dermatitis),motion sickness, and sleep aid

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2
Q

Chlorpheniramine (OTC)

A

Most suitable first generation anithistamine for day time use

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3
Q

Cetrizine OTC

A

(Zyrtec)

Class: Second generation (non-sedating)

Only a small amount cross BBB. They are also actively effluxed by P-glycoprotein from the CNS.

MOA: inverse agonists and act as competitive inhibitors of histamine. No anticholinergic properties.

Therapeutic uses:
Allergy (rhinitis, urticaria, and atopic dermatitis),

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4
Q

Ibuprofen

A

Fewer GI side effects than aspirin.

Reversible COX inhibitor

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5
Q

Naproxen

A

Longer half life

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6
Q

Ketorolac

A

Given IV

Analgesia and anti-inflammatory

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7
Q

Ketopfofen

A

Related to Ibuprofen

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8
Q

Indomethacin

A

Most potent NSAID

Uses: Severe frontal headache and blood disorders. Also PDA

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9
Q

Piroxicam

A

Once a day administration, but can cause dose related serious GI bleeding.

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10
Q

Celecoxib

A

10-20x more selective for COX-2.

200mg/day

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11
Q

Acetaminophen

A

not an NSAID

Analgesic, antipyretic, but NOT antiinflammatory. Effectively inhibits COX in brain, but not in periphery.

OD can cause hepatic injury. Lower TI.

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12
Q

NSAIDs

A

Block COX 1 & COX 2 causing a decrease in prostaglandins, thromboxanes, and prostacyclins. Analgesic, antiinflammatory, antipyretic.

Platelets don’t have COX 2

Adverse effects: GI ulceration, prolongation of gestation, decreased renal function, increased bleeding time. hypersensitivity (Aspirin = 3-10% of asthmatics.

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13
Q

Acetylsalicylate (aspirin)

A

Irreversibly inhibits COX (8-10 days). Used in 81mg doses for heart patients.

Adverse effects: Reye’s syndorme (encpephalopathy, and fatty liver), hypersensitivity in 3-10% of asthmatics.

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14
Q

Zileuton

A

MOA: Inhibits the enzyme 5-lipoxygenase and thus prevents the synthesis of LTB4 as well as the peptide leukotrienes.

Decreases the use of beta-agonists.

Moderately effective in maintenance treatment of chronic asthma.

PK: metabolized by cyp 450

Toxicities: monitor for hepatic toxicity.

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15
Q

Zafirlukast

A

MOA: luekotriene receptor antagonoist (LTD4 receptor, Cys LTR1)

PK: inhibits CYP450.

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16
Q

Montelukast

A

MOA: luekotriene receptor antagonoist (LTD4 receptor, Cys LTR1)

Perscribed more because once daily administration w/o meal restrictions.

17
Q

Hydrocortisone

A

MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.

Antinflammtory (compared to cortisol) - 1
Sodium retention (compared to cortisol) - 1

Duration: Short (8-12 hours)

PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.

18
Q

Betamethasone

A

MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.

Antinflammtory (compared to cortisol) - 25
Sodium retention (compared to cortisol) - 0

Duration: long (36-72 hours)

PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.

19
Q

Dexamethasone

A

MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.

Antinflammtory (compared to cortisol) - 25
Sodium retention (compared to cortisol) - 0

Duration: Long (36-72 hours)

PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.

20
Q

Methylprednisolone

A

MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.

Antinflammtory (compared to cortisol) - 5
Sodium retention (compared to cortisol) - 0.5

Duration: Intermediate (12-26 hours)

PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.

21
Q

Prednisone

A

MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.

Antinflammtory (compared to cortisol) - 4
Sodium retention (compared to cortisol) - 0.8

Duration: Intermediate (12-36 hours)

PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.

22
Q

Corticosteroids General

A

MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.

Bind glucocorticoid receptors which are located intracellularly changing DNA transcription of glucocorticoid response elements (GREs).

Also interact with NF-kB and AP-1.

Time lag in steroid action.

Cell movement: More neutrophils (demarginalization and increased produciton). Lymphopenia, decreased monocytes and eosinophils.

Effects on inflammatory mediators:
-reduced COX 2 espression, decreased arachadonic release from phospholipids, inhibits degranulaiton, inhibits synthesis and release of TNF, IL-1, IL-2, and IFN.

Side effects: immunosuppression (microbial and fungal infxs.), ulcers, behavioral disurbances, cataracts, osteoporosis, inhibition of growth.

From withdrawal w/o taper: acute adrenal insufficiency –> fever, myalgia, arthralgia, malaise, death from hypotension and shock

Therapeutic principles:

  • trial and error for proper dose
  • singe dose = no harmful effects
  • prolonged therapy increases incidence of lethal effects
  • risk of adrenal insufficiency with abrupt cessation of prolonged, high-dose therapy.
  • dosage varies greatly with condition.

PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.

23
Q

Autograft

A

Self to self.

i.e. skin graft

24
Q

Isograft

A

Syngeneic. Between two identical twins

25
Q

Allograft

A

Between genetically different individuals

26
Q

Xenograft

A

Between two species

i.e. porcine heart valve

27
Q

Fexofenadine

A

Class: Second generation (non-sedating)

Only a small amount cross BBB. They are also actively effluxed by P-glycoprotein from the CNS.

MOA: inverse agonists and act as competitive inhibitors of histamine. No anticholinergic properties.

Therapeutic uses:
Allergy (rhinitis, urticaria, and atopic dermatitis),

28
Q

Loratadine

A

Clariton

Class: Second generation (non-sedating)

Only a small amount cross BBB. They are also actively effluxed by P-glycoprotein from the CNS.

MOA: inverse agonists and act as competitive inhibitors of histamine. No anticholinergic properties.

Therapeutic uses:
Allergy (rhinitis, urticaria, and atopic dermatitis),

29
Q

Cyclosporine

A

MOA: Binds to cyclophilin resulting in the inhibition of calcineurin which inhibits NFAT –> decreased IL-2 –> decreased T-cell production.

PK: metabolized in the liver

Use: long term therapy for transplantation.

Toxicity: renal toxicity (must distinguished from rejection in kidney transplantation).

30
Q

Tacrolimus

A

Binds to FK binding protein resulting in the inhibition of calcineurin activity which inhibits NFAT –> decreased IL-2 –> decreased IL-2 –> decreased T-cell production.

100x more potent than cyclosporine.

Toxicity: renal toxicity (must distinguished from rejection in kidney transplantation).

31
Q

Sirolimus

A

AKA rapamycin

MOA: Binds FKBP to inhibit MTOR blocking cell cycle progression from G1 to S. Also decreases bioenergetics, and more.

Use: Used in combination therapy for organ transplant rejection.

32
Q

Mycophenolate Mofetil

A

MOA: A metabolite that inhibits ionosine monophosphate DH (IMPDH) decreasing guanine nucleotide synthesis which decreases B and T cell production (other cells can use salvage pathways more).

Toxicity: Leukopenia, diarrhea, and vomiting.

33
Q

Anti-thymocite globulin (ATG)

A

Bind to thymocytes in the circulation resulting in lymphopenia and impaired T cell immune responses.

Toxicity: serum sickness and nephritis.

34
Q

Muromonab CD3

A

Binds to E chain of CD3. Causes TCR to be internalized preventing antigen recognition.

Initially causes cytokine release. Thus main toxicity is cytokine storm (flu-like sx to fatal hypotesnion)

35
Q

Daclizumab

A

Anti IL-2 receptor antibodies.

Used in organ transplantation

Toxicities: less –> no cytokine storm

36
Q

Basiliximab

A

Anti IL-2 receptor antibodies.

Used in organ transplantation

Toxicities: less –> no cytokine storm.

IHO Mike Rose (20 decks)

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