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Pharmacology > Antihistamines > Flashcards

Antihistamines Flashcards

1
Q

Histamine storage

A
  1. Stored in granules within mast cells and basophils
    -used for inflammatory response, allergy and anaphylactic shock
  2. Also stored in GI, CNA, dermis, other tissues
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2
Q

Histamine receptors

A
  1. H1
    -high affinity
    -activated at low histamine dose
  2. H2
    -smooth muscle contraction (bronchioles> GI tract> urinary tract)
    -smooth muscle relaxation- dilation of arterioles, capillaries = swelling, heat
    *lower affinity but longer duration. Remember H2 blockers are for GI anti ulcer drugs
  3. H3
  4. H4
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3
Q

Histamine role in allergic reactions

A

Typically local cutaneous response
-foreign antigen cross links with IgE on dermal mast cells, causes activation and mast cell degranulation= histamine release= cardinal signs of inflammation

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4
Q

Cardinal signs of inflammation

A

-redness
-swelling
-pain
-heat
-loss of function

**occurs from H1 receptor activation: vasodilation (redness), capillary dilation (edema, swelling), stimulates nerve endings (pain, pruritis)

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5
Q

Anaphylaxis

A

Severe, systemic histamine release and widespread activation of H1 receptors

-hypotension: vasodilation, decreased peripheral resistance
-bronchoconstriction: bronchiole smooth muscle contraction

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6
Q

Mainstay drug for hypotension and bronchoconstriction

A

Epinephrine
**emergency!

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7
Q

Peripheral release of histamine

A

-stimulates sensory neurons
-recognized as pruritus and pain

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8
Q

H1-blocking antihistamines

A

“Reversible competitive inhibition”
-compete with histamine for H1 receptor binding site
-counteracted by high histamine concentrations
-may stabilize H1 receptor in non-active state= prevents histamine-H1 receptor activation

**no impact on H2 receptors

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9
Q

H1-blocking antihistamines pharmacokinetics

A

-limited oral bioavailability
-lipid soluble and high volume of distribution

-hepatic metabolism

-drug interactions in human med (not in vet med)
>because we don’t use them long term in animals
>can induce an increased clearance after repeated dosing
>elimination may be inhibited by P-gp substrates

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10
Q

1st generation H1 blockers/antihistamines effects

A

-Both antihistamines and anti cholinergic
**can cause sedation (low dose) or CNS excitement (high dose)

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11
Q

Pyrilamine (antihist)

A

-1st generation H1 blocker
-vet formulations
-injectable and oral formulations

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12
Q

Diphenhydramine

A

Benadryl
-1st generation H1 blocker
-

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13
Q

Dimenhydrinate

A

Gravol, Dramamine
-1st generation H1 blocker
-just diphenhydramine + chlorotheophylline
-

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14
Q

Trimeprazine

A

-anti pruritic
-found in Vanectyl-P (very old drug for treating skin allergies in animals… also contains prednisolone)

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15
Q

2nd generation H1 blocking antihistamines

A

-more selective for peripheral H1 receptors; no sedation/drowsy because no antihistamine and anticholinergic effects from getting into CNS (P-gp substrates)
-longer half life and dosing intervals

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16
Q

2nd generation H1 blocking antihistamine drug options

A
  1. Cetirizine (Zyrtec)
  2. Loratidine (claritin)
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17
Q

3rd generation H1 blocking antihistamines

A

-contains only the active moiety
*active enantiomer and active metabolite

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18
Q

Clinical use of H1 blocker antihistamines

A

Modulate allergic reaction, but wont stop allergen exposure or histamine release
-more useful if given before allergen contact and histamine release

**does not stop histamine release from mast cells, just modulates/blocks H1 receptors

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19
Q

H1 blocking antihistamines for atopic dermatitis

A

-may decrease pruritus for short time
-could be that the sedative component (H1 receptors in CNS) were actual reason that decreased pruritus

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20
Q

H1 blockers- uses other than antihistamines

A
  1. bronchoconstriction- limited efficacy
  2. antidote for extrapyramidal rxns
  3. Adjunctive therapy for anaphylaxis, insect bites
    **but does not replace Epi
  4. Adjunctive therapy for dogs with mast cell tumours
    *help prevent pruritus due to degranulation
    *diphenhydramine prior to working on mast cells
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21
Q

Anticholinergic effects of 1st generation H1 blockers

A

Block muscarinic receptors (eg. parasympatholytic signs)
-dry mouth & mucous membranes
-tachycardia
-ileus
-mydriasis

-CNS depression (low dose) or excitement (high dose)

**these drugs do not replace the use of atropine!

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22
Q

Systemic antifungals

A

-Amphotericin B

Azoles:
-Ketoconazole
-Iraconazole
-Fluconazole

23
Q

Topical antifungals

A

Azoles:
-miconazole
-clotrimazole

-Terbinafine

24
Q

Types of fungal infections

A
  1. superficial mycoses
  2. systemic (invasive) mycoses
25
Q

Superficial mycoses

A

-affect the skin, hair, and nails

26
Q

Systemic (invasive) mycoses

A

-involve the internal organs
-primary vs. opportunistic
-prolonged duration of therapy typically required

27
Q

Targets for antifungal therapy

A
  1. Cell membrane
    -fungi use ergosterol instead of cholesterol
  2. DNA synthesis
    -some compounds selectively activated by fungi, arresting DNA synthesis
  3. Cell Wall
    -unlike mammalian cells, fungi have cell wall with chitin
28
Q

Amphotericin B

A

-injectable solution (human formulations), only for IV use in clinic
-for severe systemic fungal infections; no effect on bacteria/rickettsia

29
Q

Mechanism of Amphotericin B

A

Binds to sterols in fungal cell membrane
-alters membrane, causes K to leak out

*can also affect mammal cell cholesterol= TOXIC

30
Q

Toxicity of Amphotericin B

A

Very toxic
-Especially CATS
-nephrotoxic- reversible at first, then irreversible with prolonged use
-anorexia, vomiting, anemia

**used, but not typically the 1st line of therapy

31
Q

What fungi is Amphotericin B used for?

A

-dogs, cats, horses

-Aspergillosis, Blastomycosis, Cryptococcus, Candida

32
Q

Azole mechanism of actions

A

-Binds to cytochrome P450 enzyme complex
-inhibits the synthesis of ergosterol resulting in fungal cell membrane damage

**also effect normal function of mammal CYP enzymes

33
Q

Itraconazole

A

-only vet formulation
-for cats

**other azoles used human formulations. Fine for dogs, but cats are much smaller

34
Q

Azole impact on mammal CYP enzymes

A
  1. CYP used to convert lanosterol to cholesterol
  2. required for synthesis of steroid hormones (including cortisol and reproductive steroids)
    *means that Ketoconazole can be used to treat hyperadrenocorticism.. but better options available
  3. Drug interactions because impact on CYP enzymes
    eg. cyclosporine
35
Q

Azole pharmacokinetics

A

-concentration-independent fungistatic agents
*candida albicans

Goal: maintain 1-2x minimal inhibitory concentration of fungal species for entire dosing interval
-product label says 1x a day, but may have increased efficiency with 2x a day

36
Q

Azole fungi resistance

A
  1. Fungal species finds way to avoid drug accumulation in the pathogen
    -decrease drug influx, increase drug efflux
  2. Changes in drug interaction with target enzymes in ergosterol synthesis pathway
37
Q

Ketaconazole

A

Formulations: oral tablets and suspensions, topical creams and shampoos
*systemic all prescription
*all human products

38
Q

What is ketoconazole used for in vet med?

A

-yeast (Malazzezia)- but other products available

-systemic fungi (coccidioidomycosis, blastomycosis, histoplasmosis, cryptococcosis)

-dermatophytes

39
Q

Adverse effects of Ketoconazole

A
  1. hepatic toxicity
    -dose dependent
    -monitor liver enzymes
    -drug interactions possible
  2. GI: nausea, vomiting, anorexia
    -dose dependent
    -decrease adverse events if administered with food
40
Q

Itraconazole (sporonox)

A

-Itrafungol oral solution licensed for cats

-treatment for feline dermatophytosis from Microsporum canis

-expensive, but safer than other antifungals
-compounded itraconazole= very sketchy

41
Q

PK of Itraconazole

A

-increased oral bioavailability when given with food!

-high volume of distribution accumulates in hair/skin

42
Q

Itraconazole compared to Ketaconazole

A

-more potent antifungal activity
-similar adverse effects but generally less severe
-similar hepatic CYP450 metabolism and drug interactions

43
Q

Clinical uses of Itraconazole on label

A

-Dermatophytes (Trichophyton spp, Microsporum spp

-yeasts (candida, Malassezia)

-various dimorphic fungi, zygomycetes and eumycetes (Aspergillus spp)

44
Q

Clinical uses of Itraconazole extralabel

A

-systemic fungal diseases (Blastomycosis in dogs AND cryptococcus in cats)

-horses: gutteral pouch mycosis, nasal aspergillosis, fungal keratitis

45
Q

Fluconazole

A

-no vet formulations available

-expensive

-good oral bioavailability, limited protein binding
*penetrates well into tissues and crosses BBB

-limited hepatic metabolism, mostly excreted in urine

-generally safe- mild GI effects

46
Q

Uses for Fluconazole

A

-good for Condida, Cryptococcus, Coccidioides
eg. fungal menigitis

-limited for systemic fungal species (Blastomycosis, Histoplasma, Sporothrix)

-no activity against Aspergillus

47
Q

Topical Azoles

A

-Miconazole
-Clotrimazole

48
Q

Miconazole drugs in clinic

A

-surolan
-easotic
-microderm
-otizole

49
Q

Clotrimazole drugs in clinic

A

-otomax
-Aurizon
-Mometamaxx

50
Q

Miconazole and Clotrimazole

A

-licensed for topical use against superficial skin/ear mycotic infections in small animals
*products often include an antibiotic and steroid

51
Q

Why not used miconazole and clotrimazole systemically?

A

-rapid hepatic enzyme induction (increased drug clearance)

-serious adverse events

52
Q

Terbinafine (Osurnia, Claro)

A

-topical gel/solution for mycotic/bacterial otic infections in dogs and cats
*also includes florfenicol antibiotic and steroids

-inhibits enzymes involved in ergosterol synthesis

-less frequent dosing (2 doses every 7days, or monthly)

53
Q

Iodophors

A

-Betadine and chlorhexidine
-considered antifungal as well by different method= cleaning or drying the skin/removing dirt that fungus is living in

Pharmacology (33 decks)

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