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Block 4 Pharmacology > Pharmacology of anti-inflammatories and immune suppression > Flashcards

Pharmacology of anti-inflammatories and immune suppression Flashcards

1
Q

Cardinal signs of inflammation

A 
Rubor 
Tumor 
Calor
Dolore 
Functio laesa
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2
Q

causes of acute inflammation

A

Infections (viral, bacterial, parasitic)
Trauma and foreign bodies
Chemical, physical, endogenous agents -> cell death
Acute immune reactions (Allergy

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3
Q

causes of chronic inflammation

A

Persisting infections
Chronic exogenous or endogenous toxicity
Chronic immune reactions
(Autoimmunity & transplant rejection)

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4
Q

examples of the immune driven inflammation

A 
Allergies
Contact dermatitis
Celiac disease
Autoimmune disease
Organ rejection
Clearing bacterial and viral infections 
Graft vs Host disease
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5
Q

name 5 NSAIDS

A

Aspirin, Indomethacin, Paracetamol, Ibuprofen, Diclofenac

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6
Q

when are NSAIDS taken

A

Prescribed for pain & chronic inflammation

OTC for minor aches and pains.

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7
Q

what symptoms do NSAIDS treat

A

anti-inflammatory
analgesic
antipyretic

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8
Q

what are the significant adverse effects of NSAIDS on the GI tract

A

abdominal discomfort, dyspepsia
Stomach / duodenal ulceration
Myocardial infarction

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9
Q

which is the only NSAID to irreversibly inactivate both isoforms of the COX enzymes (COX-1 and COX-2)

A

Aspirin

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10
Q

which NSAID Acetylates the catalytic serine residue in position 529.

A

Aspirin

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11
Q

at which levels does aspirin affect COX2 expression

A

at both transcriptional and posttranscriptional levels

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12
Q

in what way does COX-2 acetylation modifies the enzyme

A

enzyme in such a way that it performs an incomplete reaction ultimately resulting in the generation of lipoxins

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13
Q

what else does Aspirin do?

A

Inhibits IκB kinase and prevents NF-κB activation

Acetylates many proteins and RNA

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14
Q

what are the two COX inhibitors

A

Aspirin and Ibuprofen

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15
Q

how does ibuprofen block the antiplatelet effect?

A

by blocks the activity of aspirin

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16
Q

Side effect of asprin

A

Nausa Stomach pain Heart burn Vomitting

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17
Q

more serious side effects of Aspirin

A

swelling of eyes, face,lips,tongue,throat
wheezing, difficulty breathing, horseness, fast breathing
fast heart beat
cold clammy skin
hives rash
bright red blood in stools, black or tarry stolols
ringing in the ears, loss of hearing
bloody vomit, vomit resembling coffee grounds

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18
Q

what are coxibs

A

family of drugs more targeted to COX-2

Selective anti-inflammatory

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19
Q

example of a coxibs

A

Celecoxib

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20
Q

where is cox 2 found

A

in cancer cells/Vascular endothelium/kidney

21
Q

why were coxibs made?

A

to minimise gastric problems

22
Q

what concurrent use of celecoxib increase the risk of

A

Hyponatraemia low sodium
Nephrotoxicity
Hyperkalaemia high potassium
bleeding

23
Q

what are NO-NSAIDs (nitric oxide-donating NSAID)

A

New class of NSAIDs having a gastro-protective effect and increased anti-inflammatory activity.

24
Q

SAIDS:glucocorticoids examples

A

hydrocortisone, prednisolone and dexamethasone

25
Q

what are SAIDS based on

A

Based on adrenal steroids

26
Q

what are SAIDS synthesized from

A

synthesized from cholesterol

27
Q

when are SAIDS released

A

released as needed under the influence of ACTH

28
Q

when are SAIDS used

A

Used clinically in many inflammatory disease

29
Q

when are SAIDS used Topically

A

low toxicity

30
Q

when are SAIDS used Acutely

A

acceptable toxicity

31
Q

when are SAIDS used Chronically

A

severe side effects and toxicity.

32
Q

when do you normally experience side effects of glucocorticods

A

Occurring mainly with prolonged systemic use as anti-inflammatory or immunosuppressive

33
Q

side effects of glucocorticoids

A

Suppression of response to infection
Suppression of endogenous glucocorticoid synthesis.
Metabolic actions (effecting carbohydrate and proteins metabolism)
Iatrogenic Cushing’s Syndrome
Osteoporosis

34
Q

Lewis triple response of histamine

A

Reddening -> Vasodilatation -small arterioles and pre-capillary vessels

Wheal -> Increased permeability of post- capillary venules

Flare -> antidromic stimulation of local nerve resulting in the release of vasodilators

35
Q

what receptors does Histamine affect?

A

H1, H2, H3 and H4 GPCRs

36
Q

what cells release histamine

A

mast cells

37
Q

when are histamines released

A

by exocytosis during inflammatory and allergic reactions

38
Q

what do histamines cause

A 
Stimulation of gastric secretion 
Contraction of smooth muscle (other than that of blood vessels) 
Cardiac stimulation	
Vasodilation
Increased vascular permeability
39
Q

Sedating Antihistamines H1, H2

A

Chlorphenamine

promethazine

40
Q

Non Sedating Antihistamines H1, H2

A

Cetrizine

fexofenadine

41
Q

what do antihistamines do

A

Reduce the increased vascular permeability caused by histamine

42
Q

when are antihistamines used

A

Allergic rhinitis (hay fever), urticaria, insect bites, drug sensitivitiesTopical preparations (e.g. for eye, nose)As a adjunct to adrenaline in emergency treatment of anaphylaxis

43
Q

other effects of antihistamines

A

5-hydroxytryptamine (5-HT) receptors, α!-adrenoreceptors and ACH muscarinic receptors

44
Q

Immunosuppression

A

Tissue rejection
Psoriasis
Rheumatoid arthritis

Corticosteroids +

45
Q

Immunosuppressive drugs

A

Cyclosporine A
Tacrolimus (F506)
Rapamycin

46
Q

Two therapies for rheumatoid arthritis, psoriasis, asthma, Crohn’s, MS

A

Monoclonal Antibody therary

Disease Modifying Anti-Rheumatic Drugs (DMARDs):

47
Q

whar are monoclonal antibodies

A

Humanized or human monoclonal antibodies. Inhibit cytokines, receptors, adhesion molecules

48
Q

da foq

A 
TNF: Cimzia, Humira, Remicade, Simponi
IL6:  Actemra
IL12 and IL23:  Stelara
IL1α: Illaris
IgE: Xolair
α4 and α4β7:  Tysabri, Entyvio
CD11a: Raptiva
CD20: Rituxan, Mabthera
Other biologics:  Anakinra,  recombinant human IL-1RA; Enbrel, Human TNFR2–Fc fusion protein

Block 4 Pharmacology (16 decks)

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